Lower Arterial Pressure Research Articles

Comparative evaluation of the effects of pregabalin, dexmedetomidine, and their combination on the hemodynamic response and anesthetic requirements in patients undergoing laparoscopic cholecystectomy: A randomized double-blind prospective study

Background:In this study, we evaluated the efficacy of premedication with dexmedetomidine, pregabalin, and dexmedetomidine-pregabalin combination for attenuating the haemodynamic stress response to laryngoscopy and intubation and pneumoperitoneum (primary outcome), and for reducing anaesthetic requirement (secondary outcome) in patients undergoing laparoscopic cholecystectomy.Methods:Ninety ASA physical status classes I-II patients, between 18 to 65 years of age, of either sex, scheduled to undergo laparoscopic cholecystectomy were included in this randomised double blind study. Morbidly obese patients and those with history of hypertension, cardiac, renal, hepatic, endocrine or pulmonary dysfunction were excluded. Patients were randomized to three groups – Group P- received oral pregabalin (150 mg) one hour before induction and 100 mL of i.v normal saline (0.9%) over 10 minutes, 10 minutes before induction; Group D- received i.v dexmedetomidine (1 μg.kg−1) prepared in 100 mL of 0.9% normal saline and given over 10 minutes, 10 minutes before induction, and an oral placebo tablet one hour before induction; and Group C-received a combination of oral pregabalin 75 mg one hour before induction, and IV dexmedetomidine (0.5 μg.kg−1) prepared in 100 mL of 0.9% normal saline over 10 minutes, 10 minutes before induction.Results:Dexmedetomidine significantly attenuated the stress response to laryngoscopy and intubation and pneumoperitoneum and reduced anaesthetic requirement as compared to the other two groups. Dexmedetomidine was associated with significantly lower mean arterial pressures and higher sedation score in the preoperative and postoperative period and significantly lower heart rate and arterial pressures and reduced anaesthetic requirement in the intraoperative period as compared to the other groups.Conclusion:Dexmedetomidine is a valuable adjunct to the technique of balanced anaesthesia for maintaining haemodynamic stability.

Показники гемодинаміки при артропластиці кульшового суглоба в умовах різних методів знеболювання

Мета. Порівняння гемодинамiчних профілів пацієнтів при артропластиці кульшового суглоба (КС) в умовах різних методів знеболювання.
 Матеріали і методи. У 132 пацієнтів у ході виконання артропластики КС оцінювали показники гемодинаміки в періопераційному періоді в залежності від методики інтраопераційної анестезії та післяопераційної аналгезії.
 Результати. На тлі спінальної анестезії спостерігали суттєве зниження артеріального тиску (АТ) з тенденцією до брадикардії, що потребувало вазопресорної підтримки. Загальна анестезія супроводжувалась досить стабільним рівнем АТ з епізодами тахікардії. Найбільш стабільною була гемодинаміка на тлі паравертебральної і каудальної епідуральної анестезії та блокад нервів (поперекового сплетення та сідничного нерва). В післяопераційному періоді гемодинаміка була найбільш стабільною на тлі пролонгованих реґіональних методів аналгезії.
 Висновки. Пролонговані паравертебральні блоки є оптимальним варіантом знеболювання при артропластиці КС з точки зору забезпечення гемодинамічної стабільності.

Risk indicators for acute kidney injury in cardiogenic shock

PurposeIn critical illness, the relation between the macrocirculation, microcirculation and organ dysfunction, such as acute kidney injury (AKI), is complex. This study aimed at identifying predictors for AKI in patients with cardiogenic shock. Materials and methodsThirty-nine adult cardiogenic shock patients, with an admission creatinine <200 μmol l−1, and whose microcirculation was measured within 48 h were enrolled. Patient data were analyzed if AKI stage ≥1 developed according to the Kidney Disease/Improving Outcomes classification within 48 h after admission. Variables with a p < .05 in the univariate analysis were considered for analysis with logistic regression. ResultsTwenty-four patients (61.5%) developed AKI within 48 h. The group that developed AKI had higher central venous pressures (CVP), lower diastolic arterial blood pressures and mean perfusion pressures, higher maximum ventilator pressures as well as positive end expiratory pressures and were treated with higher dosages of dobutamine. There was no difference of the microcirculation. In the multivariate logistic regression analysis, CVP was the only independent predictor for AKI (OR 1.241; 95% CI 1.030–1.495; p = .023). ConclusionsIn this population of patients with cardiogenic shock, CVP was associated with the development of AKI.

Abstract 102: Inhaled Nitric Oxide Mitigates Pulmonary Hypertension and Improves Cerebral Hemodynamics During Prolonged Cardiopulmonary Pesuscitation in a Swine Model of Pediatric Cardiac Arrest

Introduction: Pulmonary hypertension may play a role in preventing ROSC during prolonged CPR. Targeted pulmonary vasodilation with inhaled nitric oxide (iNO) during CPR may improve pulmonary blood flow and improve outcomes. The purpose of this study was to study the effects of iNO in a randomized, blinded, placebo controlled, pediatric swine model of asphyxial cardiac arrest. Hypothesis: Animals treated with iNO will have lower pulmonary artery pressure, improved systemic hemodynamics, and increased cerebral blood flow during prolonged CPR compared to control. Methods: Four-week-old piglets (n=10) that underwent seven minutes of asphyxia, induction of VF, and 10 minutes of CPR were randomized to either iNO (20 ppm) or placebo in a blinded fashion starting one min into CPR and needed more than 1 defibrillation attempt. Defibrillation was attempted after 10 minutes of CPR. Animals that did not achieve ROSC by 20 minutes were euthanized. Invasive pulmonary and systemic hemodynamics, and both invasive and noninvasive cerebral hemodynamics were continuously measured. Data described as mean ± SD and compared using a generalized estimating equation regression model. Results: All 5 iNO-treated animals and 2/5 placebo-treated animals achieved ROSC. Those treated with iNO had lower mean pulmonary artery pressures (29.5 ± 9.1 vs. 48.3 ± 5.6 mmHg, p=0.04); higher mean aortic pressures (51.9 ± 6.4 vs. 35.5 ± 4.4 mmHg, p=0.01); higher cerebral blood flow (invasive: 230.4 ± 57.4 vs. 28.7 ± 42.1 % baseline, p&lt;0.001; noninvasive: 58.4 ± 10.9 vs. 32.4 ± 8.1 % baseline, p=0.02); and higher cerebral tissue oxygenation (invasive: 33.1 ± 13.0 vs. 1.2 ± 9.8 mmHg, p=0.01; noninvasive: 38.0 ± 4.2 vs. 26.2 ± 3.1%, p=0.005) compared with placebo. Conclusions: Treatment with iNO during prolonged CPR results in lower pulmonary artery pressure, improved systemic hemodynamics, and increased cerebral blood flow and oxygenation. Pulmonary vasodilation may have an important role during prolonged CPR for asphyxial cardiac arrests.

Pathological and Transcriptome Changes in the ReninAAV db/ db uNx Model of Advanced Diabetic Kidney Disease Exhibit Features of Human Disease.

The ReninAAV db/db uNx model of diabetic kidney disease (DKD) exhibits hallmarks of advanced human disease, including progressive elevations in albuminuria and serum creatinine, loss of glomerular filtration rate, and pathological changes. Microarray analysis of renal transcriptome changes were more similar to human DKD when compared to db/db eNOS-/- model. The model responds to treatment with arterial pressure lowering (lisinopril) or glycemic control (rosiglitazone) at early stages of disease. We hypothesized the ReninAAV db/db uNx model with advanced disease would have residual disease after treatment with lisinopril, rosiglitazone, or combination of both. To test this, ReninAAV db/db uNx mice with advanced disease were treated with lisinopril, rosiglitazone, or combination of both for 10 weeks. All treatment groups showed significant lowering of urinary albumin to creatinine ratio compared to baseline; however, only combination group exhibited lowering of serum creatinine. Treatment improved renal pathological scores compared to baseline values with residual disease evident in all treatment groups when compared to db/m controls. Gene expression analysis by TaqMan supported pathological changes with increased fibrotic and inflammatory markers. The results further validate this model of DKD in which residual disease is present when treated with agents to lower arterial pressure and glycemic control.

RF70 RESULTS FROM AN IN VIVO COMPARISON OF THE OPTIFLOW AND EZ GLIDE AORTIC DISPERSION CANNULAE

Background: Morbidity associated with embolization during cannulation in coronary artery bypass grafts (CABG) is strongly related to patient characteristics/comorbidities, the arterial cannulation site and the shape of the arterial cannula tip.. The desired features of an arterial cannula should be to prevent those morbid effects and focus on achieving higher flows with lower cannula pressures. Methods: To evaluate the in vivo performance of two aortic dispersion flow cannulas: Optiflow (Sorin Group, Italy) and EZ Glide (Edwards Lifesciences, USA) in relation to cannula pressures, pump flow rates and plasma free hemoglobin. Over a 12 month period we collected data on a prospective, randomized (1:1), non-blinded, monocentric study with a cohort of 30 patients (Optiflow group N = 15; EZ Glide group N = 15). Results: The Optiflow cannula was found to have decreasing cannula pressures as pump flow rates increased (112.3 ± 10.9 mmHg vs 131.1 ± 11.4 mmHg, p &lt; 0.0001). Results also indicated no significant differences between groups in plasma free hemoglobin increases (p = 0.41) or total microembolic signals counts during cardiac surgery (p = 0.63). Conclusions: Both Optiflow and EZ Glide dispersion flow arterial cannulas performed well, but the Optiflow cannula demonstrated an ability to increase pump flow rates with lower arterial line and cannula pressures than the EZ Glide cannula. This implies an ability to improve peripheral perfusion while reducing cannula shear stress and reducing the risk of endothelial damage in an area where the cannula jet hits the intraluminal aortic wall, thereby having the potential to reduce the risk of atherosclerotic plaque dislodgement.

Surveying the Literature

Surveying the Literature

Diabetes mellitus attenuates the pressure response against hypotensive stress by impairing the sympathetic regulation of the baroreflex afferent arc

Patients with diabetes mellitus (DM) often show arterial pressure (AP) lability associated with cardiovascular autonomic neuropathy. Because the arterial baroreflex tightly regulates AP via sympathetic nerve activity (SNA), we investigated the systematic baroreflex function, considering the control theory in DM by open-loop analysis. We used Zucker diabetic fatty (ZDF) rats as a type 2 DM model. Under general anesthesia, we isolated the carotid sinuses from the systemic circulation, changed intracarotid sinus pressure (CSP), and recorded SNA and AP responses. We compared CSP-AP (total loop), CSP-SNA (afferent arc), and SNA-AP (efferent arc) relationships between ZDF lean ( n = 8) and ZDF fatty rats ( n = 6). Although the total loop gain of baroreflex (ΔAP/ΔCSP) at the operating point did not differ between the two groups, the average gain in the lower CSP range was markedly reduced in ZDF fatty rats (0.03 ± 0.01 vs. 0.87 ± 0.10 mmHg/mmHg, P < 0.001). The afferent arc showed the same trend as the total loop, with a response threshold of 139.8 ± 1.0 mmHg in ZDF fatty rats. There were no significant differences in the gain of efferent arc between the two groups. Simulation experiments indicated a markedly higher AP fall and lower total loop gain of baroreflex in ZDF fatty rats than in ZDF lean rats against hypotensive stress because the efferent arc intersected with the afferent arc in the SNA unresponsive range. Thus, we concluded that impaired baroreflex sympathetic regulation in the lower AP range attenuates the pressure response against hypotensive stress and may partially contribute to AP lability in DM. NEW & NOTEWORTHY In this study, we investigated the open-loop baroreflex function, considering the control theory in type 2 diabetes mellitus model rats to address the systematic mechanism of arterial pressure (AP) lability in diabetes mellitus. The unresponsiveness of baroreflex sympathetic regulation in the lower AP range was observed in type 2 diabetic rats. It may attenuate the baroreflex pressure-stabilizing function and induce greater AP fall against hypotensive stress.

Consenso de expertos sobre el manejo clínico de la hipertensión arterial en Colombia. Sociedad Colombiana de Cardiología y Cirugía

In 2017, the American College of Cardiology (ACC) and the American Heart Association (AHA) concurrently established new guidelines for the prevention, detection, assessment and management of arterial hypertension in adults, based on new scientific evidence supporting its intensive treatment.The formal recommendation was to use lower arterial pressure thresholds for initiating antihypertensive treatment. This consideration arose from studies which related the achievement of lower arterial pressure figures with a significant decrease in the risk of cardiovascular disease and mortality in the hypertensive population.In light of this new definition of arterial hypertension, Muntner et al. consider that the prevalence of hypertension in the United States would be 45.6%, compared with 31.9% if the previously accepted and implemented parameters from the JNC7 were applied. According to this committee, the percentage of American adults recommended for antihypertensive treatment would go from 34.3% to 36.2%, while the percentage of hypertensives not achieving the established goals would increase from 39 to 53.4%.Meanwhile, Bundy et al. reached similar conclusions, calculating that 45.4% of adult Americans over the age of 20 (105.3 million) would have hypertension according to the new classification, compared to data from 2014, which considered 32.0% (74.1 million) to be hypertensive. This 13.5% difference amounts to 31.3 million people who would be classified as hypertensive.In Colombia, the application of the new classification would mean going from a prevalence of 22.0% in 2016 to an estimated 43.3%, currently, just by changing the cut-off value for being considered hypertensive, which would amount to classifying approximately 21 million people as sick.

A3938 Renal angiotensin generation depends on hepatic angiotensinogen (AGT)

Objectives: AGT synthesis is believed to occur in liver, kidney, brain and adipocytes, so that selectively deleting hepatic AGT may not alter renal angiotensin (Ang) levels. Here we investigated whether arterial pressure lowering with liver-targeted AGT siRNA versus renin-Ang system (RAS) blockers affects renal function and Ang levels. Methods: Arterial pressure was measured via radiotelemetry in spontaneously hypertensive rats during vehicle, valsartan, captopril (both p.o.), siRNA (fortnightly s.c. injection), siRNA + valsartan or captopril + valsartan treatment for 4 weeks. Transcutaneous measurement of glomerular filtration rate (GFR) and 24 h urinary excretory function was assessed at 2 and 4 weeks. Renal Ang levels were measured by mass spectrometry. Results: Dual RAS blockade synergistically lowered arterial pressure compared to monotherapy. Valsartan increased AngI (P < 0.05), while captopril ± valsartan did not affect AngI. siRNA ± valsartan lowered AngI by > 30% (both P < 0.01). In contrast, neither siRNA nor valsartan lowered AngII. Captopril modestly lowered AngII while dual RAS blockade greatly reduced AngII (all P < 0.05). The renal AngII/I ratio was increased 4-fold after siRNA, reduced by > 70% after valsartan and captopril ± valsartan (all P < 0.05) and unaltered after siRNA + valsartan. No treatment affected GFR, natriuresis or albuminuria. Conclusion: The lowering of renal AngI after liver-targeted AGT siRNA suggests that hepatic rather than renal AGT determines renal Ang generation. Upregulation of ACE and/or AT1 receptors may allow renal AngII to remain intact after siRNA, and only dual RAS blockade annihilates renal AngII. AGT siRNA synergistically lowers arterial pressure when combined with existing RAS blockers and may be a novel treatment for hypertension without apparent negative effects on renal function.

Abstract P110: Renal Angiotensin Generation Depends on Hepatic Angiotensinogen: Evidence From a Preclinical Study With RNAi Therapeutics Targeting Liver Angiotensinogen

Angiotensinogen (AGT) synthesis is proposed to occur not only in the liver, but also in kidney, brain and adipocytes. Selectively deleting hepatic AGT might therefore not affect renal angiotensin (Ang) levels. Here we investigated whether arterial pressure lowering with liver-targeted AGT siRNA versus renin-Ang system (RAS) blockers affects renal function and Ang levels. Arterial pressure was measured via radiotelemetry in spontaneously hypertensive rats during vehicle, valsartan, captopril (both p.o.), siRNA (s.c. fortnightly injection), siRNA+valsartan or captopril+valsartan treatment for 4 weeks. Transcutaneous measurement of glomerular filtration rate (GFR) and 24h urinary excretory function was assessed at 2 and 4 weeks. Renal Ang levels were measured by mass spectrometry. Dual RAS blockade synergistically lowered arterial pressure compared to monotherapy. Valsartan and captopril increased AngI (1096±205 and 939±128 fmol/g, respectively versus 413±46 fmol/g in vehicle-treated; both P&lt;0.01 vs. vehicle), while captopril+valsartan did not affect AngI (260±42 fmol/g). siRNA and siRNA+valsartan lowered AngI (59±6 and 12±3 fmol/g, respectively; P&lt;0.0001 versus vehicle). Conversely, neither siRNA nor valsartan lowered AngII (228±15 and 338±39 fmol/g versus 431±48 fmol/g in vehicle-treated). Captopril modestly lowered AngII while dual RAS blockade with siRNA+valsartan or captopril+valsartan greatly reduced AngII (115±20, 15±5 and 9±3 fmol/g, respectively; all P&lt;0.0001). The renal AngII/I ratio was increased 4-fold after siRNA (P&lt;0.001), reduced by &gt;70% after valsartan, captopril and captopril+valsartan (all P&lt;0.001) and unaltered after siRNA+valsartan. No treatment affected GFR, natriuresis or albuminuria. In conclusion, the lowering of renal AngI after liver-targeted AGT siRNA suggests that hepatic rather than renal AGT determines renal Ang generation. Upregulation of ACE and/or AT 1 R may allow renal AngII to remain intact after AGT siRNA, and only dual RAS blockade significantly reduces renal AngII. AGT siRNA synergistically lowers arterial pressure when combined with existing RAS blockers and may be a novel treatment for hypertension without apparent negative effects on renal function.

Habitual physical activity and central artery stiffening in older adults: the Atherosclerosis Risk in Communities study.

Regular physical activity appears to attenuate or even reverse age-related arterial stiffening. Yet, it is not clear if the reduced stiffening associated with habitual physical activity is also observed in community-dwelling older adults. Among 3893 older adults in a prospective cohort study, we associated physical activity with measures of central arterial stiffness (via carotid-femoral pulse wave velocity or cfPWV) and pressure pulsatility (via central pulse pressure or cPP). We also examined the association of long-term habitual physical activity, measured as persistence in physical activity levels from mid-life to late-life, with cfPWV and cPP among 1747 participants. The adjusted mean difference in cfPWV was lower, reflecting less arterial stiffness, for those with moderate (ß = -0.30 m/s) or high (ß = -0.38 m/s) physical activity compared with no physical activity. The adjusted mean difference in cPP was also lower for those with high (ß = -2.49 mmHg) physical activity, relative to no physical activity. Stronger effect estimates were observed among those with persistent physical activity from mid-life to late-life. Higher physical activity in late-life, and habitual physical activity from mid-life to late-life, is associated with lower central arterial stiffness and pressure pulsatility in a large population-based sample of community-dwelling older adults.

Hypotension and a positive fluid balance are associated with delirium in patients with shock.

The pathogenesis of delirium in critically ill patients is multifactorial. How hypotension and hypoxemia affect brain function and whether they can promote delirium remains unclear. A high cumulative positive fluid balance may also have a negative effect on brain function and promote delirium. We hypothesized that delirium would be more likely to develop in patients with low systemic arterial pressure, hypoxemia and a higher positive fluid balance, and investigated these associations in a prospective observational cohort study in patients with shock. After initial resuscitation, episodes of hypotension, defined as a mean arterial pressure (MAP) <65 mmHg or diastolic pressure <60 mmHg, and hypoxemia, defined as peripheral oxygen saturation (SpO2) <90% for more than one minute or any arterial oxygen concentration (PaO2) <90 mmHg, were recorded during the first 5 days of the ICU stay. Fluid balance was evaluated daily and the 5-day cumulative fluid balance recorded. Delirium was assessed using the Confusion Assessment Method for the ICU. A total of 252 patients were admitted with shock during the study period; 185 (73%) developed delirium. Patients who developed delirium also had more episodes of hypotension with a low MAP (p = 0.013) or diastolic pressure (p = 0.018) during the first five days of the ICU stay than those who did not. Patients with a higher cumulative fluid balance during the same period were also more likely to develop delirium (p = 0.01); there was no significant difference in the occurrence of hypoxemia between groups. Joint modeling, combining a linear-mixed model and an adjusted Cox survival model showed that low diastolic pressure (alpha effect = -0.058±0.0013, p = 0.043) and a positive cumulative fluid balance (alpha effect = 0.04±0.003, p = 0.021) were independently associated with delirium. In conclusion, low diastolic pressure and a cumulative positive fluid balance but not hypoxemia were independently associated with development of delirium in patients with shock.

Invasive Hemodynamic Characterization of the Portal-hypertensive Syndrome in Cirrhotic Rats.

This is a detailed protocol describing invasive hemodynamic measurements in cirrhotic rats for the characterization of portal hypertensive syndrome. Portal hypertension (PHT) due to cirrhosis is responsible for the most severe complications in patients with liver disease. The full picture of the portal hypertensive syndrome is characterized by increased portal pressure (PP) due to the increased intrahepatic vascular resistance (IHVR), hyperdynamic circulation, and increased splanchnic blood flow. Progressive splanchnic arterial vasodilation and increased cardiac output with elevated heart rate (HR) but low arterial pressure characterizes the portal hypertensive syndrome. Novel therapies are currently being developed that aim to decrease PP by either targeting IHVR or increased splanchnic blood flow - but side effects on systemic hemodynamics may occur. Thus, a detailed characterization of portal venous, splanchnic, and systemic hemodynamic parameters, including measurement of PP, portal venous blood flow (PVBF), mesenteric arterial blood flow, mean arterial pressure (MAP), and HR is needed for preclinical evaluation of the efficacy of novel treatments for PHT. Our video article provides the reader with a structured protocol for performing invasive hemodynamic measurements in cirrhotic rats. In particular, we describe the catheterization of the femoral artery and the portal vein via an ileocolic vein and the measurement of portal venous and splanchnic blood flow via perivascular Doppler-ultrasound flow probes. Representative results of different rat models of PHT are shown.

Weight loss improves arterial blood gases and respiratory parameters in obese dogs.

Canine obesity is a common medical disorder and a known risk factor for associated diseases; it can seriously influence various physiological functions, thereby limiting the longevity of the animal. In this study, we evaluated potential respiratory alterations in obese dogs before and after being subjected to caloric restriction to decrease their body weight by 20%, and compared those dogs with control dogs with ideal body condition score. The animals were divided into three experimental groups: GI (obese dogs; n=11); GII (obese dogs after weight loss, same animals as in GI); GIII (control dogs; n=11). We evaluated lung function by spirometry and arterial blood gases. Statistical analysis included paired or non-paired Student's t test. Compared with dogs within an ideal body condition score (GIII), obese dogs (GI) had a low arterial partial pressure of oxygen (p<0.05); decreased tidal volume (p<0.005), inspiratory time and expiratory time (p<0.05); and an increased respiratory rate (p<0.005). After losing weight (GII), no differences with control dogs (GIII) were verified. The results suggested that obese dogs have an improvement in respiratory function with weight loss, but further investigations in a larger group of dogs are advised to confirm these findings.

The Effects of Secondhand Smoke Exposure on Postoperative Pain and Ventilation Values During One-Lung Ventilation: A Prospective Clinical Trial

To investigate the relationships between secondhand smoke (SHS) exposure and oxygenation during one-lung ventilation (OLV) in lobectomy surgery and between SHS exposure and postoperative analgesic consumption. Prospective study. University, Faculty of Medicine, operating room. Sixty adult patients with American Society of Anesthesiologists score II to III, aged 18 to 65 years, with a body mass index (BMI) <35 kg/m2 scheduled for lobectomy surgery by open thoracotomy. Patients were divided into 2 groups: the SHS group (n = 30) (urine cotinine level ≥6.0 ng/mL) and the NS (nonsmoker) group (n = 30) (urine cotinine level <6.0 ng/mL and no smoking history). SHS exposure was defined according to a previously published algorithm. Noninvasive blood pressure, electrocardiography, capnography, and peripheral oxygen saturation were monitored, and intra- and postoperative arterial oxygen tension (PaO2), arterial carbon dioxide tension (PaCO2), and intraoperative peak airway pressure were compared between the 2 groups. Postoperative analgesic consumption was calculated. No significant differences in demographics or preoperative data were noted between the 2 groups. PaO2 values 10 minutes after OLV onset and 10 minutes after the end of OLV were increased significantly in the NS group compared with those in the SHS group (p < 0.05). PaO2 values after 10 minutes of OLV in the NS and SHS groups were 285.5 ± 90 mmHg and 186.7 ± 66 mmHg, respectively. PaO2 values after OLV termination in the NS and SHS groups were 365.8 ± 58 mmHg and 283.6 ± 64 mmHg (p < 0.05), respectively. PaCO2 values 10 minutes after OLV onset, 10 minutes after the end of OLV, at the end of surgery, and upon arrival in the intermediate care unit were significantly different between the 2 groups (p < 0.05). The present study demonstrated that during OLV, patients exposed to SHS exhibited significantly lower arterial oxygen pressure compared with nonsmokers. Arterial carbon dioxide values were increased significantly in SHS-exposed patients. Morphine consumption for postoperative analgesia also was increased in patients exposed to SHS compared with that in nonsmokers.

Effects of losartan and allopurinol on cardiorespiratory regulation in obstructive sleep apnoea

What is the central question of this study? In sleep apnoea, a putative link between intermittent hypoxia and hypertension is the generation of oxygen radicals by angiotensinII and xanthine oxidase within the chemoreflex arc and vasculature. We tested whether chemoreflex control of sympathetic outflow, hypoxic vasodilatation and blood pressure are altered by angiotensin blockade (losartan) and/or xanthine oxidase inhibition (allopurinol). What is the main finding and its importance? Both drugs lowered blood pressure without altering sympathetic outflow, reducing chemoreflex sensitivity or enhancing hypoxic vasodilatation. Losartan and allopurinol are effective therapies for achieving blood pressure control in sleep apnoea. Chemoreflex sensitization produced by chronic intermittent hypoxia in rats is attenuated by angiotensinII type1 receptor (AT1 R) blockade. Both AT1 R blockade and xanthine oxidase inhibition ameliorate chronic intermittent hypoxia-induced endothelial dysfunction. We hypothesized that treatment with losartan and allopurinol would reduce chemoreflex sensitivity and improve hypoxic vasodilatation in patients with obstructive sleep apnoea. Eighty-six hypertensive patients with apnoea-hypopnoea index ≥25eventsh-1 and no other cardiovascular, pulmonary, renal or metabolic disease were randomly assigned to receive allopurinol, losartan or placebo for 6weeks. Treatment with other medications and/or continuous positive airway pressure remained unchanged. Tests of chemoreflex sensitivity and hypoxic vasodilatation were performed during wakefulness before and after treatment. Ventilation (pneumotachography), muscle sympathetic nerve activity (microneurography), heart rate (electrocardiography), arterial oxygen saturation (pulse oximetry), blood pressure (sphygmomanometry), forearm blood flow (venous occlusion plethysmography) and cerebral flow velocity (transcranial Doppler ultrasound) were measured during eupnoeic breathing and graded reductions in inspired O2 tension. Losartan and allopurinol lowered arterial pressure measured during eupnoeic breathing and exposure to acute hypoxia. Neither drug altered the slopes of ventilatory, sympathetic or cardiovascular responses to acute hypoxia. We conclude that losartan and allopurinol are viable pharmacotherapeutic adjuncts for achieving blood pressure control in hypertensive obstructive sleep apnoea patients, even those who are adequately treated with continuous positive airway pressure.

Renal function at the time of nephrology referral but not dialysis initiation as a risk for death in patients with diabetes mellitus.

ABSTRACTBackgroundRenal patients with diabetes mellitus are at very high risk of death before and after chronic dialysis initiation. Risk factors for death in this population are not clearly identified.MethodsWe performed a retrospective survival analysis in 861 patients with diabetes mellitus consecutively followed up in the 2000–13 period in a nephrology setting.ResultsThe mean age was 70 ± 10 years [men 65.2%; diabetes duration 13.7 ± 10.3 years; mean estimated glomerular filtration rate (eGFR) 42.4 ± 21.0 mL/min/1.73 m2). During follow-up (median 60 months; up 15 years), 263 patients died (184 before and 79 after dialysis initiation) and 183 started chronic dialysis. In multivariate analyses, age, elevated systolic and low diastolic arterial pressures, peripheral artery disease, cancer, loop diuretic use and atrial fibrillation at baseline and acute kidney injury (AKI), heart failure (HF) and amputation during follow-up were identified as risk factors for death. After adjustments on these parameters, eGFRs at the time of the first outpatient visit—eGFR <45 mL/min/1.73 m2 {hazard ratio [HR] 1.58 [95% confidence interval (CI) 1.15–2.17]}, P = 0.005 and eGFR <30 [HR 1.53 (1.05–2.05)], P = 0.004, but not eGFR <60—were powerful risk factors for death. When initiation of dialysis was entered into the multivariate models, it was not associated with a risk of premature death [HR 1.19 (95% CI 0.91–1.55), P = 0.2069], even in patients >80 years of age [HR 1.08 (95% CI 0.64–1.81), P = 0.7793].ConclusionsIn patients with diabetes mellitus, high systolic and low diastolic arterial pressure, peripheral artery disease and development of AKI and HF are significant risk factors for death. In addition to these parameters, eGFR <45 mL/min/1.73 m2 at the time of referral is also a powerful risk factor for death.

Heart transplant outcomes in patients with Chagas cardiomyopathy in the United States.

Chagas cardiomyopathy (CC) is one of the chronic manifestations of Trypanosoma cruzi (T.cruzi) infection and is among the leading reasons for heart transplantation (HT) in Latin America. Chagas disease is also present in areas with large Hispanic communities in the United States. Our objective is to evaluate the outcomes of cardiac allograft recipients with the diagnosis of CC in the United States. We identified 25 adult patients with CC and 15930 with idiopathic dilated cardiomyopathy (IDCMP) who underwent HT between 1987 and 2015. CC patients were mostly Hispanics, had lower mean pulmonary artery pressure (23 vs 29mmHg, P=.035) and lower BMI (24 vs 26, P=.007). Patients with CC were more likely to be supported with a total artificial heart (TAH) as bridge to transplant (P=.009). There were no statistical differences for overall mortality and graft survival between CC and IDCMP cardiac allograft recipients. Induction therapy and mycophenolate mofetil (MMF) use were associated with higher rate of infection in Chagas patients. Heart transplantation recipients with CC diagnosis appear to have similar outcomes to IDCMP patients. Induction therapy and MMF use may be associated with higher risk of infection in CC patients who underwent transplantation.

Epidural Spinal Cord Stimulation of Lumbosacral Networks Modulates Arterial Blood Pressure in Individuals With Spinal Cord Injury-Induced Cardiovascular Deficits.

Disruption of motor and autonomic pathways induced by spinal cord injury (SCI) often leads to persistent low arterial blood pressure and orthostatic intolerance. Spinal cord epidural stimulation (scES) has been shown to enable independent standing and voluntary movement in individuals with clinically motor complete SCI. In this study, we addressed whether scES configured to activate motor lumbosacral networks can also modulate arterial blood pressure by assessing continuous, beat-by-beat blood pressure and lower extremity electromyography during supine and standing in seven individuals with C5-T4 SCI. In three research participants with arterial hypotension, orthostatic intolerance, and low levels of circulating catecholamines (group 1), scES applied while supine and standing resulted in increased arterial blood pressure. In four research participants without evidence of arterial hypotension or orthostatic intolerance and normative circulating catecholamines (group 2), scES did not induce significant increases in arterial blood pressure. During scES, there were no significant differences in electromyographic (EMG) activity between group 1 and group 2. In group 1, during standing assisted by scES, blood pressure was maintained at 119/72 ± 7/14 mmHg (mean ± SD) compared with 70/45 ± 5/7 mmHg without scES. In group 2 there were no arterial blood pressure changes during standing with or without scES. These findings demonstrate that scES configured to facilitate motor function can acutely increase arterial blood pressure in individuals with SCI-induced cardiovascular deficits.