Mean Arterial Pressure Variability Research Articles

Prospective evaluation of autonomic dysfunction in aggressive management of diabetic microangiopathy

Twenty-six type I diabetic nephropathy patients in a rigorous schedule for glucose control to preserve kidney function were studied to determine autonomic functional changes during 18 months. Intercurrent and nonrelated acute illness, withdrawal from the study for personal reasons, or failure to undergo testing on schedule resulted in complete data at 1 year for 26 of the original 41 patients enrolled, 24 patients completing a further 6 months. Glycohemoglobin A1c dropped for the total group from 9.0 to 7.9 at 6 months, 8.0 at 12 months, and 8.1 at 18 months ( P < .01). Autonomic function tests revealed baseline results that were below the anticipated normals for age in 38% to 56% of patients. Timed ventilatory heart rate variations measured for the total group were 1.11, 1.13, 1.10, and 1.09 (normal ≥1.20). Valsalva heart rate variations for the total group were 1.27, 1.30, 1.255, and 1.35 (normal ≥1.50). Assumption of upright posture-related heart rate variations for the total group were 1.10, 1.07, 1.07, and 1.06 (normal ≥1.20). Mean arterial pressure day/night ratios for the total group were 1.04, 1.05, 1.05, and 1.08 (normal ≥1.10). Group analysis based on differences in insulin treatment programs, levels of blood pressure, and levels of renal function revealed no significant differences from the total group or companion groups during 18 months. Patients with a glycohemoglobin A1c of <8.0% were more likely to normalize mean arterial pressure day/night ratios than those with glycohemoglobin A1c ≥8.0%. We conclude that aggressive glucose control in diabetic patients with proteinuria for a period of 18 months resulted in a reproducible pattern of autonomic function tests during that period of time with neither worsening nor improvement. The restoration of day/night mean arterial pressure variation in a minority of patients should be studied with a larger cohort.

Effect of desipramine on spontaneous arterial pressure oscillations in the rat

There has been no previous report on the effect of the noradrenaline uptake inhibitor desipramine on short-term variability of arterial pressure. Mean arterial pressure was recorded in 9 conscious resting rats during 4 consecutive 30-min periods: (1) under baseline conditions, (2) after desipramine administration (2 mg/kg i.v., followed by 1 mg/kg every hour), then after (3) cardiac autonomic blockade with methylatropine and atenolol, and (4) α-adrenoceptor blockade with phentolamine. Fast Fourier transform analysis was applied to beat-to-beat data after resampling at 10 Hz of consecutive 205-s time series. Desipramine did not change the mean level and overall variability of mean arterial pressure. However, spectral power in the mid-frequency (0.3–0.5 Hz) band containing the Mayer waves was reduced by more than 80%, and power in the low-frequency (0.05–0.2 Hz) band was enhanced by approximately 50%, especially due to the appearance of a major oscillation centred at 0.095±0.005 Hz. This slow oscillation was further enhanced after cardiac autonomic blockade and was abolished after α-adrenoceptor blockade. In conclusion, desipramine profoundly alters short-term arterial pressure variability in resting rats, mainly by shifting vasomotor waves from 0.4 to 0.1 Hz. Desipramine may prove a valuable pharmacological tool to study the dynamic aspects of arterial pressure control.

Genetic determinants of blood pressure regulation.

Blood pressure homeostasis in humans reflects the coordinate interactions of cardiac output, peripheral vascular resistance, renal volume control, and CNS integration in response to short- and long-term environmental stimuli. Variations in mean arterial pressure within the population include a significant hereditary component. The clearest examples of this genetic contribution occur in rare forms of monogenic hypertension (glucocorticoid remediable aldosteronism, apparent mineralocoid excess, Liddle's syndrome) or hypotension (pseudohypoaldosteronism type I, Bartter's syndrome, Gitelman's syndrome). Primary hypertension, which comprises approximately 95% of hypertensives and is a major risk factor for coronary heart disease, stroke, and renal disease in the U.S., represents a multifactorial and polygenic disease with incremental contributions from genetic and environmental determinants. Efforts to date have identified several candidate genes involved in primary hypertension, including angiotensinogen (AGT), a vasoactive peptide; alpha-adducin, a protein that regulates sodium transport; and the G protein beta 3 subunit, a protein involved in intracellular signal transduction. Advances in knowledge and technology associated with the Human Genome Project, combined with continuing basic research on the physiologic and biochemical causes of hypertension, offer promise for improved diagnosis and therapy of this prevalent disease.

Alexithymia: a facet of essential hypertension.

Two hundred thirty-seven newly diagnosed yet untreated hypertensive men and women, 35 to 54 years of age, were compared with an age- and gender-stratified random population sample of 146 normotensive men and women to find out whether psychological distress symptoms, anger expression, and alexithymia are associated with elevated blood pressure and whether the possible associations are independent of sodium and alcohol intake, body mass index, and physical fitness. The independent attributes of mean arterial pressure were studied by multivariate regression analyses after combining the subjects in the hypertensive and control groups. Three questionnaires were used: the Brief Symptom Inventory (BSI-37), a 31-item version of the Spielberger State-Trait Anger Expression Inventory (STAXI), and the Toronto Alexithymia Scale (TAS-26). Total scores of the TAS-26 were higher (P<0.001) in hypertensive men and women than in their normotensive control subjects (75.6+/-7.8 vs 64.1+/-9.8 in men and 72.9+/-7.1 vs 57.5+/-11.5 in women). There were no differences between the study and control groups in psychological distress symptoms, including anxiety, depression, and hostility, or in anger expression. In multivariate regression analyses, higher age, male gender, higher sodium intake, lower physical fitness, and alexithymia were independently and highly significantly (P<0.01 for male gender, P<0.0001 for other variables) associated with increased blood pressure, explaining altogether 39.5% of the cross-sectional variation in mean arterial pressure. We conclude that alexithymia, that is, poor ability to experience and express emotions, is associated with elevated blood pressure independent of sodium and alcohol intake, body mass index, and physical fitness.

The role of purinergic and adrenergic transmitters of the sympathetic system in the control of arterial blood pressure variability

Variability of mean arterial pressure (MAP) was examined in chronically instrumented, conscious, freely moving rats with pharmacologically altered efferent sympathetic influences on the cardiovascular system. MAP was recorded for 30 min beat-to-beat, using a computer under both control and experimental conditions: after administration of adrenoceptor antagonists (prazosin or phentolamine) or under P2X receptor inactivation produced either by desensitization with α, β-methylene ATP or by PPADS blockade. Inhibition of adrenergic sympathetic effects on the cardiovascular system produced long-lasting and stable decrease in MAP. Prazosin did not modify MAP variability whereas phentolamine enhanced it. Under P2X receptor desensitization MAP decreased, the hypotensive effect being accompanied by a significant increase in MAP variability. A similar increase in MAP variability was observed after PPADS administration, while MAP level was not changed. Administration of PPADS in combination with phentolamine increased MAP variability more significantly than each of the drugs given separately. Changes in MAP variability under the various experimental conditions were not consistently correlated with changes in heart rate variability. We propose that ATP, being a mediator of sympathetic vasoconstriction, participates in baroreceptor-induced stabilization of MAP level.

Changes of Renal Sympathetic Activity in Acute and Chronic Conscious Sinoaortic Denervated Rats

The arterial pressure level attained in sinoaortic denervated rats depends on the net effect of eliminating excitatory and inhibitory influences (chemoreceptor and baroreceptor elimination, respectively). After sinoaortic denervation is completed, the hypertension usually observed within the first few days is followed by normotension at the chronic stages. In this work renal sympathetic nerve activity was measured in conscious, unrestrained rats 6 hours (acute) and 20 days (chronic) after sinoaortic denervation. Increased arterial pressure (154 +/- 10 versus 114 +/- 3 mm Hg in controls) and renal sympathetic nerve activity (32 +/- 5 versus 13 +/- 2 bars per cycle in controls) with no changes in heart rate (404 +/- 17 vs 380 +/- 26 beats per minute) were observed in rats with acute sinoaortic denervation. In rats with chronic sinoaortic denervation, arterial pressure (119 +/- 8 mm Hg) and renal sympathetic nerve activity (13 +/- 6 bars per cycle) returned to control levels. Bradycardiac and tachycardiac responses to changes in blood pressure were reduced to 88% and 89%, respectively, in rats with acute sinoaortic denervation and 76% and 74%, respectively, in rats with chronic sinoaortic denervation. The reflex control of renal sympathetic nerve activity after acute and chronic sinoaortic denervation showed an impairment of sympathoinhibition (0.13 +/- 0.02 and 0.25 +/- 0.1 bars per cycle, respectively, versus 0.9 +/- 0.17 bars per cycle in controls). Sympathoexcitatory responses also were impaired in rats with acute and chronic sinoaortic denervation (0.08 +/- 0.03 and 0.37 +/- 0.1 bars per cycle, respectively, compared with 0.98 +/- 0.2 bars per cycle in controls).(ABSTRACT TRUNCATED AT 250 WORDS)

Hypertension artérielle contrôlée et protection cérébrale

Among the techniques of cerebral protection, the use of controlled arterial hypertension is based on the following arguments : 1) Cerebral ischaemia is the final common pathway of any insult to the brain, particularly through secondary lesions. Causes of secondary cerebral lesions include pressure under the brain retractors, temporary clipping, arterial hypotension, hypoxaemia, anaemia and hypercapnia. 2) In the brain, the critical lower value for cerebral blood flow is around 25 mL · 100 g −1 · min −1, under which two types of ischaemic areas can be defined : the penlucida type where cerebral function is abolished, without permanent cerebral lesion and the penumbra type where cerebral tissue recovers only if flow is rapidly restored. In the latter case the duration of ischaemia is very important. 3) Cerebral blood flow is maintained stable within a large range of variations of mean arterial pressure through the autoregulation mechanisms, which is based on vasomotricity of the cerebral circulation, which implies major variations in cerebral blood volume. However, autoregulation needs several dozens of seconds to be achieved. Therefore, sudden variations in mean arterial pressure are associated with short lasting but major variations in cerebral blood volume. 4) In case of increased intracranial pressure, a decrease in cerebral perfusion pressure causes cerebral vasodilation through the autoregulation mechanism, with an increase in cerebral blood volume which will, in turn, increase intracranial pressure and thus decrease cerebral perfusion pressure, and so on. This is the vasodilatory cascade. The therapeutical increase in mean arterial pressure will correct this phenomenon and decrease intracranial pressure. This is called the vasoconstrictive cascade. 5) In case of vascular occlusion by vasospasm, extrinsic compression or during temporary clipping, cerebral protection may be based on the collateral vessels near the ischaemic area and also on vascular anastomoses inside the circle of Willis. Following Poiseuille's law, as vasodilation is already maximal distally to the stenosis, the major factor of vascular resistance is no longer the radius of the vessel, but its length. Accordingly, the increase in perfusion pressure will improve the local flow and participate in prevention or treatment of an ischaemic event. Indeed, the increase, although modest, of the local flow may be sufficient to switch from an ischaemia of penumbra type to a penlucida type. Finally, controlled arterial hypertension 1) implies to achieve the optimal cerebral perfusion pressure in order to create the vasoconstrictive cascade under cover of intracranial pressure monitoring and 2) helps to decrease the ischaemic risk secondary to vasospasm, for example by achieving a mean arterial pressure between 70 and 100 mmHg before clipping and between 100 and 120 mmHg after clipping. To obtain this level of pressure, phenylephrine, noradrenaline and dopamine are the agents of choice, as they are free of harmful effects on the cerebral circulation.

Diurnal blood pressure variation and dietary salt in spontaneously hypertensive rats.

We have previously reported that high dietary salt exposure significantly increases daytime mean arterial pressure in spontaneously hypertensive rats (SHR) but not in normotensive Wistar-Kyoto (WKY) controls. In the present study, we used a telemetry monitoring system to evaluate the effects of high dietary salt exposure on diurnal variation of mean arterial pressure and heart rate in SHR and WKY rats. After implantation of a radio frequency transducer, SHR and WKY rats were maintained on either high (8%) or basal (1%) salt diets. Hemodynamic values were then analyzed for diurnal variation with the use of a nonlinear data-fitting program. After 2 weeks of dietary exposure, high salt-fed SHR had significantly greater 24-hour mean arterial pressure (156 +/- 3 mmHg) than SHR receiving basal (135 +/- 2 mmHg) and WKY rats receiving high (100 +/- 2 mmHg) or basal (100 +/- 1 mmHg) salt diets. Rhythm analysis indicated significant increases in both daytime and nighttime mean arterial pressure during high salt exposure in SHR. In WKY rats, high salt exposure increased nighttime but not daytime mean arterial pressure, with no net effect on 24-hour mean arterial pressure. High dietary salt exposure significantly decreased heart rate in both SHR and WKY rats, and it did not significantly alter the pattern of diurnal blood pressure or heart rate variation. These results indicate that WKY rats manifest an acute sensitivity to salt ingestion but have compensatory mechanisms sufficient to prevent sustained increases in mean arterial pressure; such mechanisms are lacking in SHR.

Hemodynamic variability and circadian rhythm in rats with heart failure: role of locomotor activity

Heart rate variability is known to be decreased by heart failure; however, the influences of concomitant diseases, changes in activity level, evolution through time, and abnormalities in the circadian rhythm are unknown. This study evaluated the influence of these factors by assessing hemodynamic variability in rats with heart failure (n = 8) and sham-operated controls (n = 8) through telemetric monitoring of heart rate, blood pressure, and locomotor activity for 8 wk. Hemodynamic variability was assessed by the standard deviation as well as hourly standard deviations and coefficients of variation of these variables over 48 h at 2, 4, and 8 wk after myocardial infarction. The circadian rhythm was investigated through power spectral analysis. Heart failure was associated with marked decreases in heart rate and mean arterial pressure variability and circadian rhythm without any differences in activity and no change through time. Heart failure in rats due to myocardial infarction in the absence of any confounding diseases is associated with marked abnormalities in hemodynamic variability and circadian rhythm independent of locomotor activity.

Falling Intracranial Pressure: An Important Element in the Genesis of Intracranial Hemorrhage in the Beagle Puppy

To study the role of extravascular intracranial pressure (ICP) in the genesis of intracranial hemorrhage in the beagle puppy, we measured ICP in animals on the day of birth, untreated 3-day-old controls, and 3-day-old animals treated from birth with prolactin. Baseline ICP varied substantially in all 3 groups. Only 8% of this variability was attributable to variability in mean arterial pressure and central venous pressure. ICP was lower in the 3-day-old controls, animals at high risk for intracranial hemorrhage after a hypovolemic/hypotensive insult followed by rapid volume expansion, than in the other groups which are at lower risk. Administration of a hyperosmolar insult, intraperitoneal glycerol, to animals whose ICP was relatively high promptly lowered ICP. After this treatment, the risk of intracranial hemorrhage was markedly increased in these previously low-risk groups. We conclude that the normal neonatal decrease in brain water content and the consequent fall in ICP substantially increase the risk of intracranial hemorrhage in the beagle puppy, a model which appears similar in pathophysiology to hemorrhage in the preterm human infant.

Estrogen replacement in middle-aged women: thermoregulatory responses to exercise in the heat.

Thermoregulatory, cardiovascular, and body fluid responses during exercise in the heat were tested in five middle-aged (48 +/- 2 yr) women before and after 14-23 days of estrogen replacement therapy (ERT). The heat and exercise challenge consisted of a 40-min rest period followed by semirecumbent cycle exercise (approximately 40% maximal O2 uptake) for 60 min. At rest, the ambient temperature was elevated from a thermoneutral (dry bulb temperature 25 degrees C; wet bulb temperature 17.5 degrees C) to a warm humid (dry bulb temperature 36 degrees C; wet bulb temperature 27.5 degrees C) environment. Esophageal (Tes) and rectal (Tre) temperatures were measured to estimate body core temperature while arm blood flow and sweating rate were measured to assess the heat loss response. Mean arterial pressure and heart rate were measured to evaluate the cardiovascular response. Blood samples were analyzed for hematocrit (Hct), hemoglobin ([Hb]), plasma 17 beta-estradiol (E2), progesterone (P4), protein, and electrolyte concentrations. Plasma [E2] was significantly (P < 0.05) elevated by ERT without affecting the plasma [P4] levels. After ERT, Tes and Tre were significantly (P < 0.05) depressed by approximately 0.5 degrees C, and the Tes threshold for the onset of arm blood flow and sweating rate was significantly (P < 0.05) lower during exercise. After ERT, heart rate during exercise was significantly lower (P < 0.05) without notable variation in mean arterial pressure. Isotonic hemodilution occurred with ERT evident by significant (P < 0.05) reductions in Hct and [Hb], whereas plasma tonicity remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary artery bypass grafting using two different anesthetic techniques: Part 3: Adrenergic responses

Twenty patients were studied during and after coronary artery bypass grafting (CABG). The patients were randomly assigned to two groups. In 10 patients, intraoperative general anesthesia (GA) was based on a combination of intravenous (IV) sufentanil and midazolam. In 10 other patients, thoracic epidural analgesia (TEA) with 0.375% bupivacaine plus sufentanil, 1:200,000 (5 μ/mL), and intraoperative GA with midazolam/N 2O were used. During the prebypass period, lower heart rates (HR), less variability in mean arterial pressure (MAP), and systemic vascular resistance (SVR) was accompanied by less variability in plasma norepinephrine (NE) concentrations in the TEA group. Although no differences were observed between the groups in perfusion pressure and the amount of vasoactive drugs used during the bypass period, variability in SVR was less in the TEA group. This was accompanied by less increase in NE and less variability in epinephrine (E) plasma concentrations. However, cortisol (Co) release was higher during this period in the TEA group. Weaning from bypass was accompanied by higher MAP and SVR in the TEA group at a lower HR, whereas no differences were observed in the E, NE, and Co plasma concentrations between the groups. During the first and second postoperative days, better pain relief and lower E and Co plasma concentrations were found in the TEA group It can be concluded that better hemodynamic stability during the prebypass and bypass periods was accompanied by less E and NE release during these periods. Co release in the TEA group was higher during the bypass period. Weaning from bypass was characterized by better hemodynamics in the TEA group. Better postoperative pain relief was accompanied by less E and Co release in the TEA group.

Influence of infusion pumps on the pharmacologic response to nitroprusside

To compare the relationship between variability in nitroprusside delivery from five infusion pumps and the resulting variability in mean arterial pressure (MAP). Randomized, crossover study design. A pediatric ICU in a university hospital. Informed parental consent was obtained for six patients who were hemodynamically stable and receiving a continuous nitroprusside infusion for a clinical application. Subjects ranged in age from 11 months to 9 yr. All of the subjects were administered nitroprusside using selected infusion pumps, which included Abbott (Micro), 3M/AVI (210), IMED (965), IVAC (565), and Kendall McGaw (MicroRate). After an initial equilibration interval for each device, MAP was measured and recorded at 10-sec intervals for greater than or equal to 90-min intervals using a computerized data collection technique. Variation in nitroprusside administration (flow continuity) for each infusion pump was determined in vitro using a computerized gravimetric technique. Variation in both MAP and flow continuity was mathematically expressed as the coefficient of variance (CV) of the measured values for each of the respective infusion pumps. For the Abbott, IMED, 3M/AVI, IVAC, and Kendall McGaw, infusion pumps, mean +/- SD continuity CV values were 85 +/- 31%, 39 +/- 26%, 19 +/- 8%, 17 +/- 3%, and 12 +/- 3%, respectively, and MAP CV values were 18 +/- 21%, 15 +/- 11%, 8 +/- 2%, and 16 +/- 10%, respectively. An apparent direct relationship between MAP variability and flow continuity was observed. We speculate that variation in effect of potent short-acting drugs may, in part, be due to infusion pump operation.

各月齢における意識下ウサギ血圧およびその変動性

Mean level and its variability of mean arterial pressure (MAP) were studied in 25 unanesthetized rabbits aged 6, 12, 18, 24 and 30 months. They were selected from the same large colony and bred with an ordinary rabbit food under a given environmental conditions. MAP in the aortic arch was continuously monitored with a catheter-transducer system for 3 hrs. Mean (M) and variance (V) of MAP for 3 hrs were not significantly altered with aging (p greater than 0.05, Kruskal-Wallis' multi-sample test). Intra-animal variations of the M and SD were small. Most of histograms of MAP for 3 hrs shows an exaggerated mode at any age. Distribution pattern of the histogram was not specific to age. These suggest that responsiveness of the baroreflex system should not be affected by aging from 6 to 30 months.

Pressor Responses to Laboratory Stresses and Daytime Blood Pressure Variability

We studied 56 patients with essential hypertension to determine whether responses to standardized laboratory mental and physical challenges accurately reflect blood pressure variability during routine daily activities. Four activities were performed in the laboratory: mental arithmetic, a reaction time test, isometric exercise, and submaximal bicycle exercise. Blood pressure was measured directly from a brachial artery catheter. We then recorded intra-arterial ambulatory blood pressure away from hospital over 24 h. A frequency histogram was constructed from all cardiac cycles when subjects were awake. Variability of ambulatory blood pressure was defined as the standard deviation about the mean waking value. The increase in mean arterial pressure (MAP) during each of these four challenges correlated significantly with the variability of mean arterial pressure (highest correlation: reaction time test, r = 0.53, P less than 0.00001; lowest correlation: mental arithmetic, r = 0.26, P less than 0.03), and five subjects who were highly reactive to all four challenges also demonstrated increased blood pressure variability. We therefore conclude that these commonly used laboratory tests can give some information about the behaviour of blood pressure in daily life in some subjects, but overall the variance in blood pressure variability that can be accounted for by the pressor response to these standardized challenges is low.

Leisure-time physical activity is inversely related to risk factors for coronary heart disease in middle-aged Finnish men.

Coronary risk factors and levels of physical activity at leisure were measured in a random sample of 3975 men 25-64 years of age residing in four areas of Finland. An index of leisure-time physical activity (LTPA) as the product of weekly exercise sessions times their usual intensity (expressed as metabolic equivalents) was computed. It showed a graded, inverse association with mean arterial blood pressure, smoking and serum thiocyanate, coronary heart disease risk estimate (combining blood pressure, total cholesterol and smoking), and a nonlinear favorable association with serum lipoproteins. In multiple regression analysis, LTPA contributed significantly and independently to the variation in mean arterial pressure; the standardized regression coefficients were -0.06 for LTPA, 0.09 for weekly alcohol consumption, 0.25 for body mass index, 0.25 for age. In the regression of coronary risk estimate, the standardized regression coefficients were -0.19 for LTPA, 0.22 for weekly alcohol consumption, 0.09 for body mass index, 0.15 for age. There was no evidence that LTPA above 2000 kcal of weekly energy expenditure was associated with further reduced coronary risk factor levels. These findings thus support the inverse direction of the association between exercise and coronary risk factors but they also point towards an independent, but modest, role of leisure-time physical activity as a determinant of coronary risk estimate and blood pressure.

The relative contribution of body fat and fat pattern to blood pressure level.

Although the association between body weight and blood pressure is irrefutable, body fat mass and blood pressure level may not necessarily be directly related. To clarify the relative contribution of fat mass to blood pressure level, we analyzed data on 399 adults consecutively entering a weight control program. Although most subjects were notably overweight (mean ideal body weight 177%), the population represented a wide spectrum of body weights and blood pressure levels. Study parameters included body fat mass (by total body water, 40K, and Steinkamp formula), lean body mass, body build (chest to height ratio), fat cell number and size from bilateral buttock biopsy specimens, upper fat pattern by arm to thigh circumference ratio, and central fat pattern by subscapular to triceps skinfold ratio. Our results concurred with previously noted correlations between obesity and blood pressure (as mean arterial pressure): weight (r = 0.44), percentage of body fat (r = 0.19), and absolute fat mass (r = 0.38; all p less than 0.01); however, lean body mass, age, and body build correlated highly with both fat mass and mean arterial pressure, thereby confounding this relationship. Multivariate analysis was performed to evaluate the relative contribution of fat mass to mean arterial pressure in the presence of these and other potentially confounding variables. Lean body mass, age, body build, and an upper body fat pattern were found to contribute significantly to the variation in mean arterial pressure (p less than 0.01). In their presence, percentage of body fat, absolute fat mass, central fat pattern, fat cell characteristics, and age of onset of obesity did not significantly improve the predictability of mean arterial pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Increased arterial pressure variability after arterial baroreceptor denervation in fetal lambs.

Baroreceptor reflexes can be demonstrated during fetal life, but whether baroreceptors normally regulate fetal arterial pressure is unknown. This problem was addressed directly by measuring arterial pressure and analyzing its variation in eight unanesthetized fetal lambs throughout the last third of gestation, and comparing these data with similar measurements made in seven fetal lambs with denervated arterial baroreceptors. Measurements were made at 5-minute intervals over 24 hours in a total of thirty-three experiments. The coefficient of variation of mean arterial pressure (standard deviation of mean arterial pressure/mean value of mean arterial pressure) expressed as a percentage was used as an index of blood pressure variability. Coefficients averaged 7.0% in intact lambs and 12.1% in barodenervated lambs (P less than 0.001), signifying considerably increased variability of mean arterial pressure after barodenervation. Mean arterial pressure averaged over 24 hours was not different between the two groups prior to 120 days (0.8) of gestation. Between 120 days and term, mean pressure was significantly greater in the denervated fetuses (65 cm H2O) than in the sham-operated controls (60 cm H2O, P less than 0.025). These data demonstrate that a baroreceptor-blood pressure reflex functions during late gestational development in lambs and signify an important role of arterial baroreceptors in regulating fetal arterial pressure. Failure to regulate arterial pressure in the barodenervated fetus could result in significant alterations in placental perfusion and exchange, and in the regional delivery of oxygen and substrates to developing organs in these animals.

Minute-to-minute covariations in cardiovascular activity of conscious dogs

Cardiovascular activity of chronically instrumented conscious dogs was monitored continuously during daily sessions of rest or of intermittent aversive stimulation. Data analysis of minute-to-minute averages revealed that cardiovascular variables changed in patterns, rather than as isolated independent events. Variations in cardiac output were highly positively correlated with concurrent variations in heart rate in all subjects under both conditions (mean r = +0.93). Variations in heart rate were two to five times as great as stroke volume, which was remarkably constant (coefficient of variation averaged only 4.6%). Variations in mean arterial pressure were consistently correlated with the variations in cardiac output (mean r = + 0.66) and heart rate (mean r = +0.68), but were poorly correlated with the small changes in stroke volume (mean r = -0.17) and total peripheral resistance (mean r = -0.16).

Autoregulation of capillary hydrostatic pressure in skeletal muscle during regional arterial hypo- and hypertension.

AbstractNet transcapillary fluid movements in the sympathectomized cat skeletal muscle were observed in response to regional mean arterial pressure variations in the range from 30 to 170 mm Hg. The transcapillary Starling fluid equilibrium prevailing at normal perfusion pressure was found to be roughly maintained over the entire range of arterial hypo‐ and hypertensions, indicating an approximate constancy of capillary hydrostatic pressure (pc). This “autoregulation of pe” was mainly due to active changes of vascular tone in the precapillary resistance vessels causing a resetting of the pre‐ to postcapillary resistance ratio (ra/rv), but disappeared after abolition of vascular tone by papaverine. In the lowest pressure range, a passive rise of postcapillary resistance contributed to the resetting of ra/rv. By this autoregulation of pc the muscle tissue is protected against undue redistributions of fluid between the intra‐ and extravascular spaces when arterial pressure per se is changed.