Low Perfusion Pressure Research Articles

MULTIPLE RENAL ARTERIES AS A RISK FACTOR FOR SEVERE HYPERTENSION IN YOUNG ADULTS?

Objective: The significance of multiple renal arteries (MRAs) in arterial hypertension (AH) is not fully understood. Lower perfusion pressure due to longer length and narrower caliber of MRAs could cause segmental hyperreninemia sufficient to result in renin-dependent systemic hypertension. Sympathetic renal nerve activity might be affected by hyperreninema as well. The aim of the study was to examine the characteristics of young adult hypertensives in relation to the existence of MRAs that were diagnosed during evaluation for secondary arterial hypertension. Design and method: 32 patients underwent routine evaluation for secondary hypertension and target organ damage. Patients were divided into two groups, one with MRAs and the other without MRAs. Data were presented as mean +standard deviation and compared by the Indipendent-Sample t-test. Results: The mean age was 38 years, and 13 patients were diagnosed with MRAs. There were more men in the MRAs group, otherwise, there were no significant differences in baseline characteristics between the groups (BMI, smoking, family history). None of them were diagnosed with secondary endocrine hypertension or renal artery stenosis. MRAs group showed significantly higher values of office SBP/DBP (p < 0,012) and 24-hour SBP/DBP (p < 0,001), and nonsignificantly higher values of heart rate. Although nonsignificant, direct renin concentrations were slightly higher in the MRAs group, while insulin levels were higher in the non-MRAs group. Dyslipidemia was diagnosed in most patients, without significant differences between groups. Electrocardiographic and echocardiographic changes suggesting hypertensive heart remodeling were found in 55% of patients in MRAs compared to 32% in non-MRAs, there were no significant differences in NTproBNP levels. A nonsignificant reduction in glomerular filtration rate was noticed in the MRAs group, while there were no significant differences in 24-hour albuminuria (p 0,308; p 0,614). Conclusions: The significance of MRAs in arterial hypertension is a matter of debate. In our study of young patients with arterial hypertension and MRAs, we observed features of more severe hypertension with already existing hypertensive target organ damages. Proper medical treatment with antihypertensive agents is crucial. Future studies will answer the question about interventional therapeutic procedures’ role in preventing cardiovascular complications.

Mitochondria and renal microvascular dysfunction following ischemia-reperfusion in rats

The pathophysiological mechanisms underlying ischemia-reperfusion (IR) induced acute kidney injury (AKI) remain poorly understood. Preglomerular microvessels (PGMV), specifically afferent arterioles, possess an intrinsic autoregulatory ability that is vital for ensuring stable renal hemodynamics. Our recent study indicates that renal autoregulation is impaired in IR rats due to reactive oxygen species (ROS) accumulation. We hypothesized that mitochondria-derived ROS (mtROS) in preglomerular microvessels contribute to renal autoregulatory impairment in IR rats. Blood-perfused juxtamedullary nephron experiments were performed on kidneys of male Sprague-Dawley rats 24 hours after IR induction (60-min, bilateral renal artery clamping). Afferent arteriolar autoregulation was assessed as perfusion pressure (PP) was increased from 65 to 170 mmHg in 15 mmHg increments. Afferent arterioles of sham-operated control rats (n=7) established pressure-mediated autoregulatory responses. Baseline diameter (100 mmHg) averaged 13.2±0.4 μm and increased to 114±4% of baseline when PP decreased from 100 to 65 mmHg. Diameter decreased to 65±3% of baseline when PP increased to 170 mmHg. In contrast, afferent arterioles from IR rats lost autoregulatory capability and remained between 90 and 100% of baseline diameter over 65-170 mmHg (n=8). Addition of Mito-Tempo (mitochondria-targeted antioxidant, 0.1 mM, n=3) to the perfusate restored autoregulation in IR rats at lower PP (65-125 mmHg, P>0.05 vs sham) and partially restored it over 140-170 mmHg. Superfusion with oligomycin (ATP synthase inhibitor, 2.5 μM) in normal kidneys evoked vasodilation to 178±13% baseline and blunting of autoregulatory reactivity. Renal autoregulation is linked to ATP-sensitive P2X1-receptor signaling. Changes in ATP-induced intracellular calcium concentration ([Ca2+]i) were assessed in isolated PGMV myocytes using Fura-2 fluorescent dye. IR markedly attenuated [Ca2+]i responses to 10 and 100 μM ATP by 46±11% and 57±15%, respectively (P<0.05, n=3-4 rats/group), and blunted ATP-induced afferent arteriolar vasoconstriction ( P<0.05 vs. sham, n=3/group). IR markedly increased the fluorescence intensity of mitoROS (MitoSOX™ kit) in PGMV compared to sham rats. Mitochondrial respiratory function was assessed using High Resolution Respirometry in freshly isolated PGMV (n=3/group). IR significantly reduced basal respiration (20±4 vs. 58±9 pmol/s·ml in sham, P<0.05) and oxidative phosphorylation capacity (51±10 vs. 219±37 pmol/s·ml in sham, P<0.05). The percentage of ATP-linked respiration was also reduced in PGMV of IR (60±2% vs. 75±2% in sham, P<0.05). In conclusion, mitochondria of PGMV are involved in regulating renal microvascular tone and autoregulation. IR leads to autoregulatory dysfunction by causing mitochondrial dysfunction in PGMV, increased mtROS production and suppression of ATP-dependent calcium signaling. This study is supported by grants R01DK106500. This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Cerebral blood flow velocity progressively decreases with increasing levels of verticalization in healthy adults. A cross-sectional study with an observational design.

Autoregulation of the cerebral vasculature keeps brain perfusion stable over a range of systemic mean arterial pressures to ensure brain functioning, e.g., in different body positions. Verticalization, i.e., transfer from lying (0°) to upright (70°), which causes systemic blood pressure drop, would otherwise dramatically lower cerebral perfusion pressure inducing fainting. Understanding cerebral autoregulation is therefore a prerequisite to safe mobilization of patients in therapy. We measured the impact of verticalization on cerebral blood flow velocity (CBFV) and systemic blood pressure (BP), heart rate (HR) and oxygen saturation in healthy individuals. We measured CBFV in the middle cerebral artery (MCA) of the dominant hemisphere in 20 subjects using continuous transcranial doppler ultrasound (TCD). Subjects were verticalized at 0°, -5°, 15°, 30°, 45° and 70° for 3-5 min each, using a standardized Sara Combilizer chair. In addition, blood pressure, heart rate and oxygen saturation were continuously monitored. We show that CBFV progressively decreases in the MCA with increasing degrees of verticalization. Systolic and diastolic BP, as well as HR, show a compensatory increase during verticalization. In healthy adults CBFV changes rapidly with changing levels of verticalization. The changes in the circulatory parameters are similar to results regarding classic orthostasis. ClinicalTrials.gov, identifier: NCT04573114.

Lung Injury Risk in Traumatic Brain Injury Managed With Optimal Cerebral Perfusion Pressure Guided-Therapy.

Management of traumatic brain injury (TBI) has to counterbalance prevention of secondary brain injury without systemic complications, namely lung injury. The potential risk of developing acute respiratory distress syndrome (ARDS) leads to therapeutic decisions such as fluid balance restriction, high PEEP and other lung protective measures, that may conflict with neurologic outcome. In fact, low cerebral perfusion pressure (CPP) may induce secondary ischemic injury and mortality, but disproportionate high CPP may also increase morbidity and worse lung compliance and hypoxia with the risk of developing ARDS and fatal outcome. The evaluation of cerebral autoregulation at bedside and individualized (optimal CPP) CPPopt-guided therapy, may not only be a relevant measure to protect the brain, but also a safe measure to avoid systemic complications. We aimed to study the safety of CPPopt-guided-therapy and the risk of secondary lung injury association with bad outcome. Single-center retrospective analysis of 92 severe TBI patients admitted to the Neurocritical Care Unit managed with CPPopt-guided-therapy by PRx (pressure reactivity index). During the first 10 days, we collected data from blood gas, ventilation and brain variables. Evolution along time was analyzed using linear mixed-effects regression models. 86% were male with mean age 53±21 years. 49% presented multiple trauma and 21% thoracic trauma. At hospital admission, median GCS was 7 and after 3-months GOS was 3. Monitoring data was CPP 86±7mmHg, CPP-CPPopt -2.8±10.2mmHg and PRx 0.03±0.19. The average PFratio (PaO2/FiO2) was 305±88 and driving pressure 15.9±3.5cmH2O. PFratio exhibited a significant quadratic dependence across time and PRx and driving pressure presented significant negative association with PFRatio. CPP and CPPopt did not present significant effect on PFratio (p=0.533; p=0.556). A significant positive association between outcome and the difference CPP-CPPopt was found. Management of TBI using CPPopt-guided-therapy was associated with better outcome and seems to be safe regarding the development of secondary lung injury.

Isolated Mitochondria State after Myocardial Ischemia-Reperfusion Injury and Cardioprotection: Analysis by Flow Cytometry

Mitochondria are key organelles involved in cell survival and death during the acute phenomena of myocardial ischemia-reperfusion (i.e., myocardial infarction). To investigate the functions of isolated mitochondria such as calcium retention capacity, oxidative phosphorylation, and reactive oxygen species (ROS) production, already established methods are based on extramitochondrial measurements of the whole mitochondria population. The aim of this study was to develop a reliable and well-characterized method for multiparametric analysis of isolated single mitochondrion by flow cytometry (FC) in the context of myocardial infarction. The advantage of FC is the possibility to give a simultaneous analysis of morphological parameters (side and forward scatters: SSC and FSC) for each mitochondrion, combined with intramitochondrial measurements of several biological markers, such as ROS production or membrane potential (Δφm), using specific fluorescent probes. For this study, a rat model of ischemia-reperfusion and a protective approach of post-conditioning using low reperfusion pressure was used. Thanks to the use of specific probes (NAO, MTR, TMRM, DilC1, and DHR123) combined with flow cytometry, we propose a method: (i) to identify mitochondrial populations of interest based on quality criteria (NAO/TMRM double staining); (ii) to monitor their morphological criteria, especially during swelling due to calcium overload; and (iii) to compare mitochondrial functions (membrane potential and ROS production) in different experimental groups. Applied to mitochondria from ischemic hearts, these measurements revealed that individual mitochondria are altered and that cardioprotection by low-pressure reperfusion reduces damage, as expected. Our results highlight FC as a reliable and sensitive method to investigate changes in mitochondrial functions and morphology in pathological conditions that disrupts their activity such as the case in ischemia-reperfusion. This methodological approach can be extended to other pathologies involving mitochondrial dysfunctions. Moreover, FC offers the possibility to work with very small amounts of isolated mitochondria, a factor that may limit the use of classical methods.

DIAGNOSTIC VALUE OF PROCALCITONIN IN PREDICTING SEPSIS IN BURNS PATIENTS

Patients who have suffered from burns are at an increased risk of dying from sepsis. The combination of a systemic inammatory response and a recognised infection is what medical professionals call sepsis. If the infection is not treated, then it will lead to severe sepsis, which is characterised by organ dysfunction, low perfusion, and low blood pressure. The systemic inammatory response syndrome, often known as SIRS, may have an infectious or a noninfectious origin. When dealing with patients who have suffered serious trauma or burns, it is often difcult to determine whether SIRS is the consequence of the injury itself or whether it is related to a superimposed infection. In patients with SIRS, the majority of the clinical symptoms of infection, including fever, tachycardia, and leukocytosis, were also present. As a result, in order to circumvent this problem, the American Burns Association established a consensus panel, and criteria were drafted in order to dene sepsis in burns patients. In the past, a number of research have been carried out to determine the value of the PCT in both burns and non-burns related situations . Even in the absence of sepsis, the value of PCT may be modestly elevated due to the localised infection. Therefore, the diagnostic threshold for sepsis is quite low when using the cut off value that was examined in the earlier investigations. This study was carried out to determine the PCT value in burns patients and also to locate a threshold value that may be used to suspect sepsis in its early stages. We intend to incorporate this threshold value as a protocol into our existing set up

Abstract WP141: The Combined Effect Of Blood Pressure And Translesional Pressure Ratio Impacts The Stroke Mechanisms Of Intracranial Atherosclerosis

Introduction: ICAS confers the greatest risk of stroke, but the pathophysiology of stroke mechanismremains unclear. Essentially, plaque rupture is a physical process of structural failuredue to destructive biomechanics, and hypoperfusion is due to low perfusion pressure,which act as 2 major stroke mechanisms in sICAS. Notably, blood pressure (BP)plays key role in determining both biomechanics and perfusion of ICAS. Hypothesis: ICAS could result in significant BP change which may further influence strokemechanism. High local pressure gradient across ICAS may cause plaque rupture andthe subsequent artery-to-artery embolism, whereas low perfusion pressure atpost-stenosis area may restrict perfusion and induce the subsequent borderzoneinfarcts (Fig) . Method: A total of 339 sICAS patients due to 50-99% stenosis in MCA or ICA were includedfrom CNSR3. By Newton-Krylov-Schwarz method, CFD models were built based onTOF-MRA (Fig) . Translesional pressure ratio (PR) across ICAS was calculated as:pressurepoststenotic/pressureprestenotic. SBP gradient was calculated as: SBPх(1-PR),indicating the SBP drop across ICAS. Perfusion pressure at post-stenosis area wascalculated as: MAPхPR. Results: After adjustment, high SBP gradient and low perfusion pressure was shown tocorrelate with cortical infarcts (p=0.041) and borderzone infarcts (borderlinesignificant, p=0.059) (Fig) . Between the 2 parameters, Pearson correlation coefficient=-0.854, p <.0001. The cutoff of SBP gradient and perfusion pressure for the above 2stroke mechanisms was 14.4mmHg and 94.4mmHg, respectively. Conclusions: We demonstrated the hemodynamic hypothesis of stroke mechanism in sICAS thatartery-to-artery embolism and hypoperfusion could be attributed to the combinedeffect of blood pressure and translesional PR. Accordingly, a double-edged role of high BP level in sICAS may further surface, which can induce destructivebiomechanics but relieve hypoperfusion simultaneously.

The Effects of Different Doses of Sildenafil on Coronary Blood Flow and Oxidative Stress in Isolated Rat Hearts.

The dose-response relationship of sildenafil effects on cardiac function is not completely elucidated. The aim of this study was to assess the effects of different doses of sildenafil on coronary flow and oxidative stress in isolated rat hearts. Coronary flow and markers of oxidative stress, including nitrite outflow, and superoxide anion production in coronary effluent, were determined for isolated rat hearts. The experiments were performed during control conditions and in the presence of sildenafil (10, 20, 50, 200 nM) alone or with Nω-nitro-L-arginine monomethyl ester (L-NAME) (30 μM). Sildenafil was shown to result in a significant increase in coronary flow at lower coronary perfusion pressure (CPP) values at all administered doses, whereas, with an increase in CPP, a reduction in coronary flow was observed. An increase in nitric oxide (NO) was most pronounced in the group treated with the lowest dose of sildenafil at the highest CPP value. After the inhibition of the NO-cyclic guanosine monophosphate (cGMP) signaling (NOS) system by L-NAME, only a dose of 200 nM sildenafil was high enough to overcome the inhibition and to boost release of O2-. That effect was CPP-dependent, with statistical significance reached at 80, 100 and 120 mmHg. Our findings indicate that sildenafil causes changes in heart vasculature in a dose-dependent manner, with a shift from a vasodilatation effect to vasoconstriction with a pressure increase. The highest dose administered is capable of producing superoxide anion radicals in terms of NOS system inhibition.

Experience with clinical cerebral autoregulation testing in children hospitalized with traumatic brain injury: Translating research to bedside.

To report our institutional experience with implementing a clinical cerebral autoregulation testing order set with protocol in children hospitalized with traumatic brain injury (TBI). After IRB approval, we examined clinical use, patient characteristics, feasibility, and safety of cerebral autoregulation testing in children aged <18 years between 2014 and 2021. A clinical order set with a protocol for cerebral autoregulation testing was introduced in 2018. 25 (24 severe TBI and 1 mild TBI) children, median age 13 years [IQR 4.5; 15] and median admission GCS 3[IQR 3; 3.5]) underwent 61 cerebral autoregulation tests during the first 16 days after admission [IQR1.5; 7; range 0-16]. Testing was more common after implementation of the order set (n = 16, 64% after the order set vs. n = 9, 36% before the order set) and initiated during the first 2 days. During testing, patients were mechanically ventilated (n = 60, 98.4%), had invasive arterial blood pressure monitoring (n = 60, 98.4%), had intracranial pressure monitoring (n = 56, 90.3%), brain-tissue oxygenation monitoring (n = 56, 90.3%), and external ventricular drain (n = 13, 25.5%). Most patients received sedation and analgesia for intracranial pressure control (n = 52; 83.8%) and vasoactive support (n = 55, 90.2%) during testing. Cerebral autoregulation testing was completed in 82% (n = 50 tests); 11 tests were not completed [high intracranial pressure (n = 5), high blood pressure (n = 2), bradycardia (n = 2), low cerebral perfusion pressure (n = 1), or intolerance to blood pressure cuff inflation (n = 1)]. Impaired cerebral autoregulation on first assessment resulted in repeat testing (80% impaired vs. 23% intact, RR 2.93, 95% CI 1.06:8.08, p = 0.03). Seven out of 50 tests (14%) resulted in a change in cerebral hemodynamic targets. Findings from this series of children with TBI indicate that: (1) Availability of clinical order set with protocol facilitated clinical cerebral autoregulation testing, (2) Clinicians ordered cerebral autoregulation tests in children with severe TBI receiving high therapeutic intensity and repeatedly with impaired status on the first test, (3) Clinical cerebral autoregulation testing is feasible and safe, and (4) Testing results led to change in hemodynamic targets in some patients.

The Clinical Experience of 22 Years Analysis of Therapeutic and Surgical Treatment of the Early Glaucoma

The article presents the clinical case of a 22-year follow-up of a patient with early glaucoma whose visual functions were stabilized during the first 12 years after trabeculectomy and during the next 10 years of therapeutic treatment due to poor compliance the disease progressed to advanced glaucoma. As a result, in 2021 there were pronounced changes in the visual field of the left eye, the main cause, probably, was a vascular accident against the background of low perfusion pressure and uncompensated IOP. After a thorough analysis and scrupulous selection of eyedrops, IOP was compensated with laser and instillation of Dortimol Antiglau, which showed the best results of tolerability and achievement of tolerant pressure. This article presents data from clinical and instrumental studies and analyzes factors reflecting the importance of assessing the level of compliance in reducing the glaucoma progression.

Системная гипотония и низкое перфузионное давление как факторы прогрессирования первичной открытоугольной глаукомы

Glaucoma progression is still a relevant issue in up-to-date ophthalmology. An important prerequisite for stabilizing glaucoma is the achievement of the target intraocular pressure (IOP). However, many patients with primary open-angle glaucoma (POAG) continue to suffer vision loss despite IOP reduction. Additional factors are also important for glaucoma progression, e.g., blood pressure (BP) and ocular perfusion pressure (OPP). Multiple published data have shown a decrease in blood flow velocity in the retrobulbar vessels, choroid, retina, and optic nerve in patients with glaucoma. A decrease in OPP is a predictor of insufficient intraocular blood supply. Systemic BP has a strong effect on OPP. Intensive treatment for hypertension significantly reduces BP, decreases OPP, and prevents the progression of glaucomatous optic neuropathy. A new paradigm shift that implies a personalized approach to the choice of diagnostic and treatment strategy for glaucoma is emerging. This paper reviews current published data on the effect of systemic hypotension and low OPP on POAG progression. KEYWORDS: glaucoma, intraocular pressure, blood pressure, hypertension, hypotension, perfusion pressure. FOR CITATION: Мyakonkaya O.S., Sarkisyan A.S., Seleznev A.V., Kuroyedov A.V., Brezhnev A.Yu. Systemic hypotension and low perfusion pressure as risk factors for primary open-angle glaucoma progression. Russian Journal of Clinical Ophthalmology. 2023;23(4):202–206 (in Russ.). DOI: 10.32364/2311-7729-2023-23-4-5.

PS-C12-4: OPEN-ANGLE GLAUCOMATOUS OPTIC DAMAGE ASSOCIATED WITH DAYTIME AND NOCTURNAL DIPS IN BLOOD PRESSURE

Background: Impaired ocular perfusion pressure via systemic hypoperfusion plays a pivotal role in the pathogenesis of open-angle glaucoma (OAG). Extreme dips in mean arterial pressure (MAP) during 24-h are associated with OAG, however, whether this is driven by diurnal or nocturnal dips remains undocumented. We aimed this study to investigate the association of OAG damage with daytime and nocturnal dips in MAP. Methods: We conducted a retrospective longitudinal study that included 110 primary OAG patients who underwent 24-h ambulatory blood pressure monitoring. OAG damage was defined as changes in mean deviation (MD) of visual field tests during follow-up. MAP variability independent of the mean (VIMmap) was computed for daytime and nighttime. Dips were the five daytime and three nighttime lowest drops in MAP. We also calculated the night-to-day ratio and defined low diurnal and nocturnal MAP levels. We applied mixed models to evaluate changes in MD (expressed as decibels [dB]) during follow-up in relation to diurnal and nocturnal variability and dips in MAP. Results: The mean age was 64.0y (53% women). The median follow-up was nine years. In adjusted mixed models, every + 3 mmHg increase in daytime VIMmap was associated with a -2.57 dB longitudinal change in MD (P &lt; 0.001). The longitudinal changes in MD associated with daytime dip measures ranged from -2.56 dB (95% confidence interval [CI], -3.61 to -1.51; P &lt; 0.001) to -3.19 dB (95% CI, -4.53 to -1.84; P &lt; 0.001). For nighttime measures, the MD changed -0.71 dB (CI, -1.24 to -0.17; P = 0.009) per every -5 decrease in the nighttime MAP level. Nocturnal MAP level &lt; 74 mmHg and every 0.05 decrease in the night-to-day ratio were related to -7.23 (P = 0.003) and -0.96 (P = 0.011) changes in MD. Nighttime VIMmapP and nocturnal dips were not associated with changes in MD (P &gt; 0.097). Conclusions: Extreme daytime dips in MAP relate to OAG damage independently of the MAP level. Whereas, the association between OAG damage and nocturnal measures is driven by the nocturnal MAP level rather than variability or dips in MAP. The assessment of diurnal patterns in MAP might offer an opportunity to understand the pathogenesis of OAG. This is also critical as the perfusion pressure to the eyes is physiological 30% lower than at the brachial level in the standing or sitting positions. Therefore, a physiological lower perfusion pressure combined with extreme diurnal dips in MAP would exacerbate the hypoperfusion state in the optic nerve, leading to further glaucoma damage.

Macular and peripapillary microvascular changes in open angle glaucoma and ocular hypertension: A longitudinal study using optical coherence tomography angiography (OCT‐A)

AbstractPurpose: To investigate prospectively macular and peripapillary microvascular changes in patients with glaucoma and ocular hypertension.Methods: A 12‐month prospective longitudinal study was performed with 124 open‐angle‐glaucoma‐eyes (GE), 111 ocular‐hypertension‐eyes (OHE) and 98 gender and age matched control‐eyes (CE). Glaucomatous progression was defined as a decrease of ≥5 μm in average or ≥7 μm in a sector of RNFL thickness. OMAG OCT microangiography (Angioplex, HD OCT, Cirrus 5000, Zeiss) was used to analyse optic disc and macular regions. The statistical analysis was performed using Mann–Whitney‐Test with the SPSS version 23.0 statistical package (SPSS Inc., IL).Results: Among OHE and GE groups, 21.7% of eyes showed progression, being the decrease of Peripapillary Flux Index (PFI), Macular Vessel Density (MVD) and Macular Capillary Perfusion Density (MPD) greater (−0.0067; −0.696 mm/mm2 and −1.56%) compared to non‐progressive eyes (+0.0038; 0.527 mm/mm2 and 1.55%) being the nasal and inferior sectors for PFI, and the superior and temporal sectors for both MVD and MPD, the ones that showed greater differences [p = 0.015 and p &lt; 0.001 for the last two]. Furthermore, Peripapillary Perfusion Density (PPD) showed non‐significant greater decrease (−0.347) compared to non‐progressive eyes (−0.324) [p = 0.775]. Characteristics as increased vertical cup to disc ratio (CDV) (0.64 vs. 0.57), elevated intraocular pressure (IOP) (18.25 vs. 15.40 mmHg), thinner central corneal thickness (CCT) (520.18 vs. 541.67 μm) and lower ocular perfusion pressure (OPP) (47.81 vs. 48.95 mmHg) were significantly different in those progressive OHE and GE [p &lt; 0.05 for all]. Nevertheless, minimum ganglion cell layer thickness (GCLM) was only significantly lower in progressive GE (58.51 vs. 73.98 μm) [p = 0.036].Conclusions: Data showed that when glaucomatous progression took place, stronger microvascular changes occurred in the macular and peripapillary areas, as greater decrease of MVD, MPD and PFI, especially in superior and temporal sectors for the macular area, and in nasal and inferior sectors for the peripapillary area. Nevertheless, further research with larger population and larger follow‐up is needed to obtain stronger results.

ACE Question

Article| October 2022 ACE Question ASA Monitor October 2022, Vol. 86, 16. https://doi.org/10.1097/01.ASM.0000890044.70818.98 Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn MailTo Cite Icon Cite Get Permissions Search Site Citation ACE Question. ASA Monitor 2022; 86:16 doi: https://doi.org/10.1097/01.ASM.0000890044.70818.98 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll PublicationsASA Monitor Search Advanced Search Topics: anesthesiology continuing education (ace) Which of the following agents is MOST likely to decrease intraocular pressure? Ophthalmic surgeries are the most commonly performed surgical procedures in the United States. Intraocular pressure (IOP) is defined by the pressure exerted by different components of the globe to the containing wall. A normal IOP is 16 ± 5 mm Hg, and a value above 25 mm Hg is considered abnormal. A normal IOP is important for maintaining the normal integrity of orbital structures and proper refractory index. IOP is also important for maintaining ocular perfusion pressure, the difference between mean arterial pressure and intraocular pressure. Low ocular perfusion pressures (below 50 mm Hg) have been reported to cause irreversible injury to the retinal cells. Anesthetic agents and the overall management of anesthesia have relevant effects on IOP (Table). Knowledge of these factors is important to avoid the undue rise of IOP during anesthesia, especially during... You do not currently have access to this content.

Coronary perfusion pressure is associated with adverse outcomes in advanced heart failure.

Myocardial perfusion is an important determinant of cardiac function. We hypothesized that low coronary perfusion pressure (CPP) would be associated with adverse outcomes in heart failure. Myocardial perfusion impacts the contractile efficiency thus a low CPP would signal low myocardial perfusion in the face of increased cardiac demand as a result of volume overload. We analyzed patients with complete hemodynamic data in the Evaluation Study of Congestive Heart Failure and Pulmonary Artery Catheterization Effectiveness trial using Cox Proportional Hazards regression for the primary outcome of the composite risk of death, heart transplantation, or left ventricular assist device [(LVAD). DT × LVAD] and the secondary outcome of the composite risk of DT × LVAD and heart failure hospitalization (DT × LVADHF). CPP was calculated as the difference between diastolic blood pressure and pulmonary artery wedge pressure. Heart failure categories (ischemic vs non-ischemic) were also stratified based on CPP strata. The 158 patients (56.7 ± 13.6years, 28.5% female) studied had a median CPP of 40mmHg (IQR 35-52mmHg). During 6months of follow-up, 35 (22.2%) had the composite primary outcome and 109 (69.0%) had the composite secondary outcome. When these outcomes were then stratified based on the median, CPP was associated with these outcomes. Increasing CPP was associated with lower risk of both the primary outcome of DT × LVAD (HR 0.96, 95% CI 0.94-0.99 p = .002) and as well as the secondary outcome of DT × LVADHF (p = .0008) There was significant interaction between CPP and ischemic etiology (p = .04). A low coronary artery perfusion pressure below (median) 40mmHg in patients with advanced heart failure undergoing invasive hemodynamic monitoring with a pulmonary artery catheter was associated with adverse outcomes. CPP could useful in guiding risk stratification of advanced heart failure patients and timely evaluation of advanced heart failure therapies.

Border tissue morphology is associated with the pattern of visual field progression in open-angle glaucoma

The etiology of open-angle glaucoma (OAG) is yet unclear. This study investigated possible risk factors, such as the morphology of the border tissue that affect the pattern of visual field (VF) progression in eyes with OAG. 166 eyes of 166 OAG patients with an externally oblique border tissue (EOBT) at least in one direction were included. EOBT was obtained by analyzing enhanced depth imaging spectral-domain optical coherence tomography images. A pointwise linear regression was used to determine VF progression by measuring the deterioration rate of each point in the VF. The odds ratio of VF progression for each risk factor was estimated using logistic regression analysis. Seventy (42.2%) eyes showed VF deterioration. In multivariate analysis, longer follow-up period, higher baseline intraocular pressure (IOP), lower mean ocular perfusion pressure (MOPP), and smaller angular location of the longest EOBT were associated with VF progression (all p values were below 0.05). In the multivariate analysis, the location of the longest EOBT was significantly associated with inferior (p = 0.002) and central (p = 0.017) VF progression. In conclusion, VF progression pattern in OAG eyes is associated with the location of the longest EOBT as well as other known risk factors.

The influence of the composition of the gel Soderm®-Forte and the metabolic energy corrector cytoflavin on the course of the inflammatory process in the conditions of experimental periodontitis

The study explored the possibility of combining the multitargent means of gel Soderm®-Forte and the metabolic energy corrector Cytoflavin in conditions of inflammatory pathology of periodontal tissues on a model of induced experimental periodontitis in rats. It is shown that the conduct of complex pharmacotherapy with drugs with antimicrobial, anti-inflammatory, energy-correcting and antioxidant orientation helps to reduce inflammatory phenomena in periodontal tissues, normalize osmotic exudation of the gingival fluid of the sulcular region and restore the index assessment of the tissues of the periodontal complex.&#x0D; The paper substantiates and shows the significance of the use of these drugs that can have a prolonged therapeutic effect on the peripheral microvascular network in the region of the gingival groove, reducing the exudative component in the postcapillary venules and arterioles by lowering perfusion pressure and reducing their permeability and improving protective effects under hypoxia.

Behavioral and Neural Activity-Dependent Recanalization of Plugged Capillaries in the Brain of Adult and Aged Mice.

The capillaries of the brain, owing to their small diameter and low perfusion pressure, are vulnerable to interruptions in blood flow. These tiny occlusions can have outsized consequences on angioarchitecture and brain function; especially when exacerbated by disease states or accumulate with aging. A distinctive feature of the brain’s microvasculature is the ability for active neurons to recruit local blood flow. The coupling of neural activity to blood flow could play an important role in recanalizing obstructed capillaries. To investigate this idea, we experimentally induced capillary obstructions in mice by injecting fluorescent microspheres and then manipulated neural activity levels though behavioral or pharmacologic approaches. We show that engaging adult and aged mice with 12 h exposure to an enriched environment (group housing, novel objects, exercise wheels) was sufficient to significantly reduce the density of obstructed capillaries throughout the forebrain. In order to more directly manipulate neural activity, we pharmacologically suppressed or increased neuronal activity in the somatosensory cortex. When we suppressed cortical activity, recanalization was impaired given the density of obstructed capillaries was significantly increased. Conversely, increasing cortical activity improved capillary recanalization. Since systemic cardiovascular factors (changes in heart rate, blood pressure) could explain these effects on recanalization, we demonstrate that unilateral manipulations of neural activity through whisker trimming or injection of muscimol, still had significant and hemisphere specific effects on recanalization, even in mice exposed to enrichment where cardiovascular effects would be evident in both hemispheres. In summary, our studies reveal that neural activity bi-directionally regulates the recanalization of obstructed capillaries. Further, we show that stimulating brain activity through behavioral engagement (i.e., environmental enrichment) can promote vascular health throughout the lifespan.

The Effect of Autonomic Nervous System Dysfunction on the Progression of Primary Open-Angle Glaucoma.

PurposeTo study the effect of autonomic nervous system (ANS) dysfunction on glaucoma progression in patients with primary open angle glaucoma (POAG).Patients and MethodsA retrospective study of 40 cases of POAG patients who underwent regular reexamination for more than 3 years was performed. All participants were subjected to heart-rate variability (HRV) assessment. Patients were divided equally into the lowest and highest HRV groups according to the standard deviation value of the qualified normal to normal intervals (SDNN), a representative indicator of HRV. The lower the HRV, the more severe the ANS dysfunction with sympathetic predominance. Visual field (VF) parameters and retinal nerve fiber layer (RNFL) thickness were used to evaluate and compare the progression of glaucoma damage between the two groups.ResultsThere were 20 cases in the lowest HRV group and 20 cases in the highest HRV group. The thinning rate of RNFL in the lowest HRV group was significantly faster than that in the highest HRV group (1.44±1.58 vs 0.29±0.56 μm/year, P=0.00), accompanied by greater fluctuation of intraocular pressure (IOP) (P=0.04), lower diastolic blood pressure (P=0.01), mean blood pressure (P=0.04), and lower mean ocular perfusion pressure (P=0.04). Meanwhile, the incidence of central VF defects in the lowest HRV group was significantly higher than that in the highest HRV group (65.0% vs 30%, P=0.03). Linear regression analysis showed that there was a significant correlation between SDNN and the thickness loss rate of RNFL (P=0.01).ConclusionPOAG patients with lower HRV, which reflects ANS dysfunction with sympathetic predominance, presented faster glaucoma progression than patients with higher HRV. The more rapid progression of POAG with lower HRV may be explained by IOP and vascular risk factors.

Framework for Considering Abnormal Heart Rate Characteristics and Other Signs of Sepsis in Very Low Birth Weight Infants.

A heart rate characteristics index (HeRO score), incorporating low variability and superimposed decelerations, was developed as a sepsis risk indicator for preterm infants in the neonatal intensive care unit (NICU). A rise in the risk score should prompt consideration of other clinical changes that may be signs of sepsis to decide whether a workup and antibiotics are needed. We aimed to develop a framework to systematically consider signs potentially indicating sepsis in very low birth weight (VLBW) infants. We developed easy-recall acronyms for 10 signs of sepsis in VLBW infants. Over 12 months in a level IV NICU, neonatology fellows completed a brief survey after each shift to document changes prompting sepsis workups. We analyzed associations between survey data, hourly heart rate characteristic data, and the diagnosis of the workup, grouped as culture-positive sepsis (CXSEP, positive blood or urine culture), clinical sepsis (CLINSEP, negative cultures treated with antibiotics ≥5 days), or sepsis ruled out (SRO, negative cultures and <3 days antibiotics). We analyzed 93 sepsis workups in 48 VLBW infants (35 CXSEP, 20 CLINSEP, and 38 SRO). The most frequently cited changes prompting the workups were heart rate patterns and respiratory deterioration, which were common in all three categories. Low blood pressure and poor perfusion were uncommonly cited but were more likely to be associated with CXSEP than the other signs. A rise in the HeRO score ≥1 from 0 to 12 hours before compared with 12to 72 hours prior the blood culture occurred in 31% of workups diagnosed as CXSEP, 16% CLINSEP, and 31% SRO. The HeRO score can alert clinicians to VLBW infants at high or increasing risk of a sepsis-like illness, but heart rate characteristic patterns are highly variable in individual babies. The easy-recall NeoSEP-10 framework can assist clinicians in considering other clinical changes when making decisions about sepsis workups and the duration of antibiotics. · Abnormal heart rate characteristics can indicate sepsis or other pathologies in preterm infants.. · We developed a simple bedside tool to consider clinical signs potentially associated with sepsis.. · Considering vital sign trends together with clinical changes is a key to right-timing antibiotics..