Mm Hg Change Research Articles

The Role of Blood Pressure Variability in the Development of Nephropathy in Type 1 Diabetes

OBJECTIVEIncreases in blood pressure and visit-to-visit variability have both been found to independently increase the likelihood of cardiovascular events in nondiabetic individuals. This study has investigated whether each may also influence the development of microvascular complications in type 1 diabetes by examining data from the Diabetes Control and Complications Trial (DCCT).RESEARCH DESIGN AND METHODSUsing binary longitudinal multiple logistic regression, mean systolic (SBP) and diastolic (DBP) blood pressure as well as annual visit-to-visit variability (SD.SBP and SD.DBP, respectively) was related to the risk of the development/progression of nephropathy and retinopathy in initially normotensive subjects who did not become pregnant during the DCCT.RESULTSMean SBP and SD.SBP were independently predictive of albuminuria (odds ratio 1.005 [95% CI 1.002–1.008], P < 0.001 and 1.093 [1.069–1.117], P < 0.001, respectively, for 1 mmHg change), although SBP variability did not add to mean SBP in predicting retinopathy (0.999 [0.985–1.013], P = 0.93). DBP variability was also independently predictive of nephropathy (1.102 [1.068–1.137], P < 0.001) and not of retinopathy (0.991 [0.971–1.010], P = 0.37). Mean SBP was poorly related to SD.SBP (r2 < 0.01) as was mean DBP with SD. DBP (r2 < 0.01).CONCLUSIONSVisit-to-visit variability in blood pressure consistently independently added to mean blood pressure in predicting the risk of nephropathy, but not retinopathy, in the DCCT. This observation could have implications for the management and treatment of blood pressure in patients with type 1 diabetes.

Masked hypertension, nocturnal blood pressure and retinopathy in normotensive patients with type 1 diabetes

Aim To analyze the prevalence of masked hypertension and its possible association with microvascular complications in patients with type 1 diabetes (T1D). Methods A cross-sectional study was conducted in 188 consecutive normotensive patients at the office with T1D without renal replacement therapy or previous renal transplant. All patients were assessed regarding the presence of diabetic retinopathy (DR) (direct and indirect fundoscopy), urinary albumin excretion rate (immunoturbidimetry), and ambulatory blood pressure monitoring (ABPM) (Spacelabs 90207). Results Masked hypertension was observed in 14 (13.6%) out of 103 clinical normotensive patients and in 7.4% of the entire cohort. Twenty-three percent of patients with clinical normotension had masked nocturnal hypertension. DR was associated with night systolic and diastolic BP [OR of each 5 mmHg change 1.41 (95%CI: 1.09–1.83, P = 0.009) and 1.40 (95%CI: 1.02–1.93, P = 0.04), respectively] and with masked nocturnal hypertension [OR: 3.23 (95%CI: 1.29–8.11, P = 0.01)]. Conclusions In T1D patients with clinic BP < 130/80 mmHg, masked hypertension and especially masked nocturnal hypertension are present. Normotensive patients with nocturnal BP > 120/70 mmHg have higher presence of DR, and only will be identified through ABPM.

Changes in blood pressure before the development of nosocomial acute kidney injury

Blood pressure is an important determinant of renal perfusion and acute kidney injury (AKI) is common in hospital patients. However, there is limited knowledge concerning the incidence of relative hypotension prior to its development in general wards. We compared blood pressure recordings in a cohort of consecutive patients with no change in renal function to a cohort of patients with acute changes in renal function according to RIFLE classes R, I and F for AKI. We assessed blood pressure over a 3-day period before the development of AKI in index patients and a similar 3-day period in controls. We excluded patients with absolute hypotension [systolic blood pressure (SBP) <90 mmHg]. Patients were old (mean age 76.1 +/- 15.1) and mostly female (57.1%). Those who developed AKI had a lower diastolic blood pressure (P = 0.01), a trend towards lower mean arterial pressure (P = 0.077) and a greater decrease in mean systolic (P < 0.0001), mean diastolic (P < 0.0001) and mean arterial pressure (P < 0.0001) compared to controls. On multivariate logistic regression analysis, a decrease in SBP relative to pre-morbid value was a significant independent predictor of the development of AKI and of RIFLE classes I and F (odds ratio 1.084 for every -1 mmHg change in SBP). Relative hypotension is more common in ward patients who develop nosocomial AKI than in controls. In these patients, a decrease in SBP relative to pre-morbid value is a significant independent predictor of the development of severe AKI.

The Relationship Between Baseline Blood Pressure and Computed Tomography Findings in Acute Stroke

High blood pressure (BP) is present in approximately 80% of patients with acute ischemic stroke and is independently associated with poor outcome. There are few data examining the relationship between admission BP and acute CT findings. TAIST was a randomized controlled trial assessing 10 days of treatment with tinzaparin versus aspirin in 1489 patients with acute ischemic stroke (<48 hr) with admission BP of </=220/120 mmHg. CT brain scans were performed before randomization and after 10 days. The relationships between baseline BP and adjudicated CT findings were assessed. Odds ratios per 10 mmHg change in BP were calculated. Higher systolic BP (SBP) was associated with abnormal CT scans because of independent associations with chronic changes of leukoariosis (OR, 1.12; 95% CI, 1.05-1.17) and old infarction (OR, 1.12; 95% CI, 1.06-1.17) at baseline, and signs of visible infarction at day 10 (OR, 1.06; 95% CI, 1.00-1.13). A lower SBP was associated with signs of acute infarction (OR, 0.94; 95% CI, 0.89-0.99). Hemorrhagic transformation, dense middle cerebral artery sign, mass effect, and cerebral edema at day 10 were not independently associated with baseline BP. Although high baseline BP is independently associated with a poor outcome after stroke, this was not shown to be through an association with increased hemorrhagic transformation, cerebral edema, or mass effect; trial design may be suboptimal to detect this. Higher SBP is associated with visible infarction on day 10 scans. The influence of changing BP in acute stroke on CT findings is still to be ascertained.

Human cerebrovascular and ventilatory CO2 reactivity to end‐tidal, arterial and internal jugular vein PCO2

This study examined cerebrovascular reactivity and ventilation during step changes in CO(2) in humans. We hypothesized that: (1) end-tidal P(CO(2)) (P(ET,CO(2))) would overestimate arterial P(CO(2)) (P(a,CO(2))) during step variations in P(ET,CO(2)) and thus underestimate cerebrovascular CO(2) reactivity; and (2) since P(CO(2)) from the internal jugular vein (P(jv,CO(2))) better represents brain tissue P(CO(2)), cerebrovascular CO(2) reactivity would be higher when expressed against P(jv,CO(2)) than with P(a,CO(2)), and would be related to the degree of ventilatory change during hypercapnia. Incremental hypercapnia was achieved through 4 min administrations of 4% and 8% CO(2). Incremental hypocapnia involved two 4 min steps of hyperventilation to change P(ET,CO(2)), in an equal and opposite direction, to that incurred during hypercapnia. Arterial and internal jugular venous blood was sampled simultaneously at baseline and during each CO(2) step. Cerebrovascular reactivity to CO(2) was expressed as the percentage change in blood flow velocity in the middle cerebral artery (MCAv) per mmHg change in P(a,CO(2)) and P(jv,CO(2)). During hypercapnia, but not hypocapnia, P(ET,CO(2)) overestimated P(a,CO(2)) by +2.4 +/- 3.4 mmHg and underestimated MCAv-CO(2) reactivity (P < 0.05). The hypercapnic and hypocapnic MCAv-CO(2) reactivity was higher ( approximately 97% and approximately 24%, respectively) when expressed with P(jv,CO(2)) than P(a,CO(2)) (P < 0.05). The hypercapnic MCAv-P(jv,CO(2)) reactivity was inversely related to the increase in ventilatory change (R(2) = 0.43; P < 0.05), indicating that a reduced reactivity results in less central CO(2) washout and greater ventilatory stimulus. Differences in the P(ET,CO(2)), P(a,CO(2)) and P(jv,CO(2))-MCAv relationships have implications for the true representation and physiological interpretation of cerebrovascular CO(2) reactivity.

Do vasoregulatory mechanisms in exercising human muscle compensate for changes in arterial perfusion pressure?

We tested the hypothesis that vasoregulatory mechanisms completely counteract the effects of sudden changes in arterial perfusion pressure on exercising muscle blood flow. Twelve healthy young subjects (7 female, 5 male) lay supine and performed rhythmic isometric handgrip contractions (2 s contraction/ 2 s relaxation 30% maximal voluntary contraction). Forearm blood flow (FBF; echo and Doppler ultrasound), mean arterial blood pressure (arterial tonometry), and heart rate (ECG) were measured. Moving the arm between above the heart (AH) and below the heart (BH) level during contraction in steady-state exercise achieved sudden approximately 30 mmHg changes in forearm arterial perfusion pressure (FAPP). We analyzed cardiac cycles during relaxation (FBF(relax)). In an AH-to-BH transition, FBF(relax) increased immediately, in excess of the increase in FAPP (approximately 69% vs. approximately 41%). This was accounted for by pressure-related distension of forearm resistance vasculature [forearm vascular conductance (FVC(relax)) increased by approximately 19%]. FVC(relax) was restored by the second relaxation. Continued slow decreases in FVC(relax) stabilized by 2 min without restoring FBF(relax). In a BH-to-AH transition, FBF(relax) decreased immediately, in excess of the decrease in FAPP (approximately 37% vs. approximately 29%). FVC(relax) decreased by approximately 14%, suggesting pressure-related passive recoil of resistance vessels. The pattern of FVC(relax) was similar to that in the AH-to-BH transition, and FBF(relax) was not restored. These data support rapid myogenic regulation of vascular conductance in exercising human muscle but incomplete flow restoration via slower-acting mechanisms. Local arterial perfusion pressure is an important determinant of steady-state blood flow in the exercising human forearm.

Cerebrovascular reactivity to hypercapnia is unimpaired in breath‐hold divers

Hypercapnic cerebrovascular reactivity is decreased in obstructive sleep apnoea and congestive heart disease perhaps as a result of repeated apnoeas. To test the hypothesis that repeated apnoeas blunt cerebrovascular reactivity to hypercapnia, we studied breath hold divers and determined cerebrovascular reactivity by measuring changes in middle cerebral artery velocity (MCAV, cm s(-1)) per mmHg change in end-tidal partial pressure of CO2(PET,CO2 ) in response to two hyperoxic hypercapnia rebreathing manoeuvres (modified Read protocol) in elite breath-hold divers (BHD, n=7) and non-divers (ND, n=7). In addition, ventilation and central (beat-to-beat stroke volume measurement with Modelflow technique) haemodynamics were determined. Ventilatory responses to hypercapnia were blunted in BHD versus ND largely due to lower breathing frequency. Cerebrovascular reactivity did not differ between groups (3.7 +/- 1.4 versus 3.4 +/- 1.3% mmHg(-1) in BHD and ND, respectively; P=0.90) and the same was found for cerebral vascular resistance and MCAV recovery to baseline after termination of the CO2 challenge. Cardiovascular parameters were not changed significantly during rebreathing in either group, except for a small increase in mean arterial pressure for both groups. Our findings indicate that the regulation of the cerebral circulation in response to hypercapnia is intact in elite breath-hold divers, potentially as a protective mechanism against the chronic intermittent cerebral hypoxia and/or hypercapnia that occurs during breath-hold diving. These data also suggest that factors other than repeated apnoeas contribute to the blunting of cerebrovascular reactivity in conditions like sleep apnoea.

Individual Differences in Blood Pressure Changes after Endurance and Resistance Training

PURPOSE: Large individual differences in the responsiveness of systolic blood pressure (SBP) to regular endurance training have been observed in healthy normotensive subjects. The training induced changes have ranged from a +20 increase to a −40 mmHg decrease. The individual effect of exercise training mode to decrease SBP among the healthy subjects is not well known. We tested the hypothesis that subjects with a poor responsiveness to endurance training might benefit from resistance training in terms of SBP. METHODS: The study population consisted of sedentary normotensive (SBP<150 mmHg) healthy male and female subjects (n=73, 42±5 year). The randomized crossover study design included a 2-week lab oratory-controlled endurance or resistance training period with a 2-month detraining period between the interventions. SBP was measured at resting condition and during a 5 min passive head-up tilt test. RESULTS: Large individual differences were observed in the changes of SBP (?SBP) after both the endurance (average −3±7 mmHg, P=0.001, range −20 to +13 mmHg) and resistance training (average −2±7 mmHg, P=0.034, range −31 to +16 mmHg) in resting condition. The average decrease in ?SBP between genders was similar after both the endurance and resistance training (P=ns between males and females). There was no linear relationship between the δSBP after each training intervention (r=−.06, P=ns). On the contrary, when the study group was divided into quartiles according to the endurance training response (+6±3, −1±2, −5±2, and −12±3 mmHg change in resting SBP, P<0.0001), the group with the increased SBP after endurance training (+6±3 mmHg, n=1 8) decreased SBP after the resistance training intervention (−2±3 mmHg, P<0.0001, compared with endurance training response). The same difference in ?SBP was also observed during a sympathetic stimulation caused by the head-up tilting (+4±8 mmHg vs. −1±5 mmHg, P=0.052, after endurance and resistance training, respectively). CONCLUSIONS: The individual responsiveness of SBP to exercise training is related to the mode of training. The healthy subjects whose SBP increase after endurance training intervention results in a decreased SBP after resistance training intervention. Supported by the Ministry of Education, Helsinki, Finland.

Cerebral vascular reactivity to hypercapnia is unchanged in apnea divers

Hypercapnic cerebrovascular reactivity is decreased in obstructive sleep apnea and congestive heart disease patients. Ventilatory response to hypercapnia and/or hypoxia is blunted in apnea divers, whereas cerebrovascular reactivity to hypercapnia is presently unknown. We hypothesized that cerebrovascular reactivity to hypercapnia is increased in elite apnea divers, compared to control subjects, as a part of the O2 conserving mechanism to maintain adequate brain O2 supply. In the present study we determined cerebrovascular reactivity by measuring change in middle cerebral artery velocity per mmHg change in PETCO2 in response to two hyperoxic hypercapnia rebreathing maneuvers in seven elite apnea divers and seven control subjects. Ventilatory response to hypercapnia was blunted in divers compared to controls. Hypercapnia-induced ventilation increase was significantly lower in divers due to lower respiratory frequency. Cerebrovascular reactivity was unchanged in both groups (3.7±1.4 vs 3.4±1.3 %/mmHg PETCO2 in divers and controls) and the same was found for cerebral vascular resistance and a time for middle cerebral artery velocity recovery to baseline value. Results indicate that the regulation of the cerebral circulation in response to hypercapnia shows no difference between divers and controls serving as protective mechanism against chronic intermittent cerebral hypoxia/hypercapnia. This study was supported by Croatian Ministry of Science, Education and Sports.

REBUTTAL FROM DR. ROTHE

POINT-COUNTERPOINTREBUTTAL FROM DR. ROTHEPublished Online:01 Oct 2006https://doi.org/10.1152/japplphysiol.00561b.2006MoreSectionsPDF (43 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInEmailWeChat Hainsworth and Drinkhill (2) concluded that active venoconstriction is not important in raising end-diastolic volume (EDV) or stroke volume during exercise and orthostasis. They do admit that active venoconstriction exists, but in their last paragraph, they conclude that it only provides a small venous return enhancement. I fully agree with the following. 1) The skeletal muscle pump during exercise can provide the major part of the maintenance or increase in EDV (7). 2) Active venoconstriction occurs primarily in the abdominal splanchnic bed. 3) Skin and skeletal muscle venous responses are minimal. 4) The spleens of dogs are much larger than that of humans. 4) In response to changes in flow and venous distending pressure, passive changes in venous volume are indeed important.However, Hainsworth and Drinkhill did not support the assumption that constant pressure perfusion eliminates concurrent active venoconstriction in assessing the magnitude of the passive venous responses. Changing the carotid sinus pressure between 60 and 195 mmHg, Hainsworth and Drinkhill (2) claim a 3 ml/kg change in effective circulatory volume (the total stressed volume) of the liver and intestinal bed. In conjunction with a total body compliance of 2.5 ml·kg−1·mmHg−1, this would change the Pmcf by 1.2 mmHg. Assuming that the Pra at equilibrium would be increased by the same amount, they then claim, using “Guyton's curves,” that this would increase the cardiac output by only 20%. Herndon and Sagawa (Ref. 3, Fig. 7) suggest that the sensitivity of cardiac output to changes in Pra is 52 ml·min−1·kg−1 change in flow per millimeter mercury change in Pra. Thus a change in cardiac output from a 1.2 mmHg change in Pra would be a much larger increase of 60 ml·min−1·kg−1. Other studies have reported much larger active venous changes than the 3 ml/kg. For example, for dogs, carotid baroreceptor changes, a 7.0 ml/kg change (1); maximum sympathetic simulation, with spleen intact 7.2 ml/kg, without spleen 4.3 ml/kg (4); carotid sinus pressure changes, with spleen 8.4 ml/kg, without spleen 7.2 ml/kg (8).They also claim (Ref. 2; Fig. 2) that the intestinal bed provides a negligible active venoconstriction response based on the data from the study by Noble et al. (4). We (6) evaluated active and passive venoconstriction in segments of dog jejunum. Norepinephrine caused an active change in intestinal blood volume of 24% and a passive change of 62%. Active venoconstriction is important.REFERENCES1 Brunner MJ, Shoukas AA, and MacAnespie CL. The effect of the carotid sinus baroreceptor reflex on blood flow and volume redistribution in the total systemic vascular bed of the dog. Circ Res 48: 274–285, 1981.Crossref | PubMed | ISI | Google Scholar2 Hainsworth R and Drinkhill MJ. Counterpoint: Active venoconstriction is not an important adjunct to maintaining or raising end-diastolic volume and stroke volume during exercise and orthostasis. J Appl Physiol. In Press.Google Scholar3 Herndon CW and Sagawa K. Combined effects of aortic and right atrial pressure on aortic flow. Am J Physiol 217: 65–72, 1969.Link | ISI | Google Scholar4 Karim F and Hainsworth R. Responses of abdominal vascular capacitance to stimulation of splanchnic nerves. Am J Physiol 231: 434–440, 1976.Link | ISI | Google Scholar5 Noble BJ, Drinkhill MJ, Myers DS, and Hainsworth R. Reflex control of splanchnic blood volume in anesthetized dogs. J Physiol 513: 363–272, 1998.Google Scholar6 Rothe CF, Johns BL, and Bennett TD. Vascular capacitance of dog intestine using mean transit time of indicator. Am J Physiol Heart Circ Physiol 234: H7–H13, 1978.Link | ISI | Google Scholar7 Sheriff D. Point: The muscle pump raises muscle blood flow during locomotion. J Appl Physiol 99: 371–372, 2005.Link | ISI | Google Scholar8 Shoukas AA, MacAnespie CL, Brunner L, and Watermeier MJ. The importance of the spleen in blood volume shifts of the systemic vascular bed caused by the carotid sinus baroreceptor reflex in the dog. Circ Res 49: 759–766, 1981.Crossref | PubMed | ISI | Google Scholar Download PDF Previous Back to Top Next FiguresReferencesRelatedInformation More from this issue > Volume 101Issue 4October 2006Pages 1265-1266 Copyright & PermissionsCopyright © 2006 the American Physiological Societyhttps://doi.org/10.1152/japplphysiol.00561b.2006History Published online 1 October 2006 Published in print 1 October 2006 Metrics

COUNTERPOINT: ACTIVE VENOCONSTRICTION IS NOT IMPORTANT IN MAINTAINING OR RAISING END-DIASTOLIC VOLUME AND STROKE VOLUME DURING EXERCISE AND ORTHOSTASIS

Veins were considered merely as passive conduits of blood until Mellander ([13][1]) reported that stimulation of sympathetic nerves supplying the cat's hindquarters resulted in a decrease in regional blood volume. This and other work led Folkow and Mellander ([4][2]) to assert that veins were “at

Variability in time delay between two models of pulse oximeters for deriving the photoplethysmographic signals

Pulse oximetry is commonly used as an arterial blood oxygen saturation (SaO2) measure. However, its other serial output, the photoplethysmography (PPG) signal, is not as well studied. Raw PPG signals can be used to estimate cardiovascular measures like pulse transit time (PTT) and possibly heart rate (HR). These timing-related measurements are heavily dependent on the minimal variability in phase delay of the PPG signals. Masimo SET® Rad-9™ and Novametrix Oxypleth oximeters were investigated for their PPG phase characteristics on nine healthy adults. To facilitate comparison, PPG signals were acquired from fingers on the same hand in a random fashion. Results showed that mean PTT variations acquired from the Masimo oximeter (37.89 ms) were much greater than the Novametrix (5.66 ms). Documented evidence suggests that 1 ms variation in PTT is equivalent to 1 mmHg change in blood pressure. Moreover, the PTT trend derived from the Masimo oximeter can be mistaken as obstructive sleep apnoeas based on the known criteria. HR comparison was evaluated against estimates attained from an electrocardiogram (ECG). Novametrix differed from ECG by 0.71 ± 0.58% (p < 0.05) while Masimo differed by 4.51 ± 3.66% (p > 0.05). Modern oximeters can be attractive for their improved SaO2 measurement. However, using raw PPG signals obtained directly from these oximeters for timing-related measurements warrants further investigations.

Blood pressure dipping is reproducible in clinical practice

Blood pressure dipping pattern has clinical and prognostic consequences. However, reproducibility of night-time blood pressure fall during 24-h ambulatory blood pressure monitoring is considered limited. This limited reproducibility is possibly a result of inadequate day-night definitions. We retrospectively examined the reproducibility of blood pressure dipping in clinical practice, applying a method that accounts for sleep-awake states and does not rely on arbitrary day-night definitions. We also examined dipping repeatability in subjects with changing blood pressure. Of 962 consecutive ambulatory measurements performed in our unit during a 3-year period, 100 patients (age 60+/-15) had a prior session, and were the subjects of this study. Based on patients' report we defined 'awake blood pressure' as the average of pressure recordings while the subject was awake, including night-time arousals, and 'sleep blood pressure' as the average of pressure recordings while the subject was sleeping, including afternoon naps. We found systolic blood pressure dipping not less reproducible than 24-h, awake- and sleep systolic blood pressure, as evaluated by both Pearson correlations (r=0.52 versus 0.5, 0.5, 0.49, respectively, P < or =0.0002 in all), and Bland-Altman repeatability. In a subgroup of 35 subjects (age 63+/-15) with at least 10 mmHg change in systolic blood pressure between the two sessions, systolic blood pressure dipping remained reproducible (r=0.45, P<0.007). When interpreted in a way that accounts for sleep-awake pattern, sleep-induced systolic blood pressure dipping in clinical practice is a very reproducible feature of ambulatory blood pressure monitoring, in accordance with its vital prognostic implications.

Dynamic cardiorespiratory interaction during head-up tilt-mediated presyncope.

In 28 healthy adults, we compared the dynamic interaction between respiration and cerebral autoregulation in 2 groups of subjects: those who did and did not develop presyncopal symptoms during 70 degrees passive head-up tilt (HUT), i.e., nonpresyncopal (23 subjects) and presyncopal (5 subjects). Airflow, CO2, cerebral blood flow velocity (CBF), ECG, and blood pressure (BP) were recorded. To determine whether influences of mean BP (MBP) and systolic SP (SBP) on CBF were altered in presyncopal subjects, coherencies and transfer functions between these variables and mean and peak CBF (CBFm and CBFp) were estimated. To determine the influence of end-tidal CO2 (ETco2) on CBF, the relative CO2 reactivity (%change in CBFm per mmHg change in ETco2) was calculated. We found that in presyncopal subjects before symptoms during HUT, coherence between SBP and CBFp was higher (P=0.02) and gains of transfer functions between BP (MBP and SBP) and CBFm were larger (MBP, P=0.01; SBP, P=0.01) in the respiratory frequency region. In the last 3 min before presyncope, presyncopals had a reduced relative CO2 reactivity (P=0.005), likely a consequence of the larger decrease in ETco2. We hypothesize that the CO2-mediated increase in resistance attenuates autoregulation such that the relationship between systemic and cerebral hemodynamics is enhanced. Our results suggest that an altered cardiorespiratory interaction involving cerebral hemodynamics may contribute in the cascade of events during tilt that culminate in unexplained syncope.

How does blood oxygen level-dependent (BOLD) contrast correlate with oxygen partial pressure (pO2) inside tumors?

Blood oxygen level-dependent (BOLD) contrast-based functional MRI (fMRI) has been reported as a method to assess the evolution of tumor oxygenation after hyperoxic treatments, because of its sensitivity to changes in blood flow and deoxyhemoglobin content. However a number of questions remain: 1) In view of tumor heterogeneity, how good is the correlation between the MR parameters in gradient-echo imaging (signal intensity (SI) or effective transverse relaxation time (T(*)(2))) and local tumor oxygen partial pressure (pO(2))? 2) Is the magnitude of the change in SI or T(*)(2) a quantitative marker for variation in pO(2)? 3) Is initial T(*)(2) a good marker for initial pO(2)? To address these questions, murine tumors were imaged during respiratory challenges at 4.7 Tesla, using fiber-optic microprobes to simultaneously acquire tumor pO(2) and erythrocyte flux. The BOLD signal response (SI and T(*)(2)) was temporally correlated with changes in pO(2). However, the magnitude of the signal bore no absolute relation to pO(2) across tumors, i.e., a given change in SI corresponded to a 25 mmHg pO(2) change in one tumor, but to a 100 mmHg change in another. The initial T(*)(2) value did not reliably predict tumor oxygenation at the beginning of the experiment. In conclusion, the major advantages of the technique include noninvasiveness, high spatial resolution, and real-time detection of pO(2) fluctuations. Information afforded by the BOLD imaging technique is qualitative in nature and may be combined with other techniques capable of providing an absolute measure of pO(2).

The effect of corneal thickness and corneal curvature on pneumatonometer measurements

Purpose. The purpose of this study was to investigate the influence of corneal topography and thickness on intraocular pressure (IOP) and pulse amplitude (PA) as measured using the Ocular Blood Flow Analyzer (OBFA) pneumatonometer (Paradigm Medical Industries, Utah, USA). Methods. 47 university students volunteered for this crosssectional study: mean age 20.4 yrs, range 18 to 28 yrs; 23 male, 24 female. Only the measurements from the right eye of each participant were used. Central corneal thickness and mean corneal radius were measured using Scheimpflug biometry and corneal topographic imaging respectively. IOP and PA measurements were made with the OBFA pneumatonometer. Axial length was measured using A-scan ultrasound, due to its known correlation with these corneal parameters. Stepwise multiple regression analysis was used to identify those components that contributed significant variance to the independent variables of IOP and PA. Results. The mean IOP and PA measurements were 13.1 (SD 3.3) mmHg and 3.0 (SD 1.2) mmHg respectively. IOP measurements made with the OBFA pneumatonometer correlated significantly with central corneal thickness (r = +0.374, p = 0.010), such that a 10 µm change in CCT was equivalent to a 0.30mmHg change in measured IOP. PA measurements correlated significantly with axial length (part correlate = –0.651, p < 0.001) and mean corneal radius (part correlate = +0.459, p < 0.001) but not corneal thickness. Conclusions. IOP measurements taken with the OBFA pneumatonometer are correlated with corneal thickness, but not axial length or corneal curvature. Conversely, PA measurements are unaffected by corneal thickness, but correlated with axial length and corneal radius. These parameters should be taken into consideration when interpreting IOP and PA measurements made with the OBFA pneumatonometer.

Carbon dioxide and the cerebral circulation.

Carbon dioxide and the cerebral circulation.

Coronary pressure-flow autoregulation protects myocardium from pressure-induced changes in oxygen consumption.

Pressure-flow autoregulation minimizes changes in coronary blood flow (CBF) when coronary perfusion pressure (CPP) is altered. This investigation determined if autoregulation also minimizes CPP-induced changes in coronary vascular volume (CVV) and CVV-dependent changes in myocardial oxygen consumption (MVO2). In 11 anesthetized dogs, the left anterior descending coronary artery was cannulated, and responses to 20-mmHg changes in CPP were examined over a range of CPP from 60 to 180 mmHg. Changes in CPP had no significant effect on systemic hemodynamics or on left ventricular end-diastolic segment length, end-systolic segment length, or percent segment shortening. In hearts with effective pressure-flow autoregulation [closed-loop gain (GC) > 0.4], CVV increased 0.06%/mmHg change in CPP. For the same hearts, MVO2 increased 0.04%/mmHg change in CPP. In hearts with ineffective autoregulation (GC < 0.4), CVV increased 0.97%/mmHg (P < 0.001 vs. autoregulating hearts), and MVO2 increased 0.41%/mmHg (P < 0.001 vs. autoregulating hearts). MVO2 and CVV were correlated (r = 0.69, P < 0.0001) independently of autoregulatory capability, but only when autoregulation was poor and capacitance was elevated did CPP significantly affect MVO2. We conclude that pressure-flow autoregulation protects myocardium from CPP-induced changes in CVV, which in turn produces changes in oxygen consumption.

Autoregulation of intravascular pressure in preglomerular juxtamedullary vessels.

To quantify the functional significance of autoregulatory responses in preglomerular juxtamedullary (JM) vessels, intravascular pressures (P chi) were measured with a servonull instrument in blood-perfused arcuate (ArcA) and interlobular arteries (ILA), afferent arterioles (AA), and glomerular capillaries (GC) in vitro. P chi was determined at perfusion pressures (Pp) between approximately 60 and 150 mmHg, and the slope of the relationship between Px and Pp was estimated by linear regression. From the regression, Px was 98 +/- 1, 96 +/- 2, 64 +/- 9, and 48 +/- 2 mmHg for ArcA, ILA, AA, and GC, respectively, at the reference perfusion pressure of 100 mmHg. The results show good autoregulation of GC pressure (Pg), with a response slope of 0.10 +/- 0.07 mmHg per mmHg change in Pp, corresponding to an autoregulation index of 0.20 +/- 0.15. The slopes of the Px vs. Pp relationships in ArcA, ILA, and AA were 0.96 +/- 0.02, 0.79 +/- 0.08, and 0.32 +/- 0.11, respectively. To determine whether these observed relationships in preglomerular vessels reflect significant upstream resistance changes, we derived a new autoregulation index for Px measured at an arbitrary preglomerular location. This analysis takes into account the extent to which outflow pressure, Pg, is autoregulated by the ensemble action of the entire preglomerular vasculature. The analysis indicates that 20% autoregulatory compensation occurs upstream from the late ILA, 65% upstream from the late AA, and 80% for the entire preglomerular vascular tree. Hence, in the JM preglomerular circulation, the AA is the major site of autoregulatory resistances adjustment, with a smaller but significant contribution by the ILA.

Reactividad vascular cerebral al CO2 en la fase aguda de los traumatismos craneoencefálicos severos. Estudio preliminar de 20 casos

We report a preliminary study on 20 severe head injury patients admitted to our hospital, in whom cerebrovascular reactivity to arterial CO2 was evaluated. Entry criteria were the following: 1) time from accident to admission less than 24 hours, 2) continuous intracranial pressure monitoring, 3) no significant thoracic or lung lesions, 4) hemodynamic stability at the moment of study. In each patient, we evaluated CO2 reactivity by measuring the changes in mean intracranial pressure (ICP) that followed when manipulating the ventilator setting to reduce the arterial pCO2. The cerebrovascular reactivity index to hyperventilation (CVRIHR) was determined by measuring the change in mean ICP per mmHg change in pCO2. These tests, were done at 24 hour intervals during the first 48 hours after the accident. We considered that the CO2 reactivity was abolished when CVRIHR was inferior or equal to 0.10mmHg/mmHg pCO2 (5 cases). Patients with a measured CVRIHR above 0.10 and below 1 were considered as hyporeactive (6 cases). A CVRIHR above or equal to 1 was evaluated as normal CO2 reactivity (9 patients). All the patients with abolition of CO2 reactivity had abnormal motor responses on admission, obliterated basal cisterns and third ventricle in the CT scan and all had a fatal outcome. In all patients with preservation of CO2 reactivity, CVRIHR was 1.32±1.01 in the first 24 hours after the accident. In the same group, CVRIHR increased to 2.39±1.43 when measured over the next 48 hours (p<0.05). Our study suggests that CO2 responsivity is markedly impaired during the first 24 hours after the impact. We discuss our results and the importance that measuring CO2 reactivity could have in the management of severely head injured patients.