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PubMed2003

The effect of acute plasma volume expansion on venous capacitance.

AIM: The purpose of this study was to examine the effect of plasma volume (PV) expansion, induced by 1 single bout of high intensity exercise, on venous capacitance. METHODS: Fourteen active but untrained healthy young males were randomly assigned to an exercise (n=7) or control group (n=7). The exercise protocol consisted of 8 4-min bouts of exercise at 70-85% of maximal oxygen consumption (VO(2)max) with 5-min recovery periods between bouts. Resting and exercise HR and venous capacitance were assessed before and 24 hours after one bout of cycle exercise. Exercise HR was assessed during cycle exercise at 30, 45, and 60% of VO(2)max, whereas forearm and leg venous capacitance were examined by determining limb volume change after 2 min of venous occlusion at 50 mmHg. PV, plasma albumin, and sodium and potassium concentration were analysed pre and 24 hours post exercise. RESULTS: Twenty-four hours after one single bout of exercise, PV was increased by 7.7%. The increase in PV was accompanied by a decrease in exercise HR of 5.8% at the 2 higher intensities (45 and 60% of VO(2)max) but no change in venous capacitance was found. No significant changes in plasma albumin and sodium concentration occurred, although potassium concentration was significantly increased by 29%. CONCLUSION: An acute exercise-induced increase in plasma volume appears to be able to reduce exercise HR but has no effect on venous capacitance.

Adolescent↗
PubMed1998

Blood mobilization from the liver of the anaesthetized dog.

The abdominal circulation contains a high proportion of the total blood volume and this can change either passively in response to changes in vascular distending pressure or actively (termed a capacitance response) to changes in sympathetic nervous activity. The liver is the largest abdominal organ and this study was designed to evaluate its potential contribution to overall vascular capacitance and compliance. In chloralose anaesthetized dogs, the liver was vascularly isolated, perfused through the portal vein and hepatic artery at either constant pressures or constant flows and drained from the hepatic veins at constant pressure. Changes in vascular resistance were assessed from changes in inflow pressures or flows and hepatic blood volume was determined by differences between net inflow and outflow. During constant flow perfusion the change in hepatic volume (capacitance change) in response to supramaximal stimulation of sympathetic nerves at 16 Hz was (mean +/- S.E.M.) -2.40 +/- 0.61 ml (kg body weight)-1. This response was not significantly different during constant pressure perfusion. The changes in portal venous and hepatic arterial pressures during stimulation at constant flow perfusion were +0.67 +/- 0.13 and +4.92 +/- 0.67 kPa, respectively. The compliance of the liver, assessed as the change in volume to a change in hepatic venous pressure, was +5.44 +/- 0.18 ml kg-1 kPa-1. These results indicate that the liver has a major capacitance role, comparable to that of the canine spleen and, in addition, is highly compliant. No evidence was found to suggest that a sphincter on the hepatic outflow exists. Assuming similar responses occur in humans, who do not possess a large contractile spleen, the liver would be the most important controllable blood reservoir in the body.

Anesthesia↗
PubMed1996

Circuit factors in the high cardiac output of sepsis.

PURPOSE: The increase of cardiac output (CO) in sepsis must be matched by an increase in venous return. Our goal was to determine which of the determinants of venous return are responsible in volume-loaded and nonvolume-loaded pigs with endotoxemia. The determinants include stressed volume, venous compliance (Cv), venous resistance (RVR) and right atrial pressure (Pra). We also tested the effect of the nitric oxide (NO) synthase inhibitor, N omega-nitro-L-arginine-methyl ester (L-NAME) after the hemodynamics with endotoxin stabilized. METHODS: Pigs were anesthetized and mechanically ventilated. We measured CO by thermodilution, mean circulatory filling pressure (MCFP) by inflating a balloon in the right atrium, blood volume by dye dilution, and Cv by rapid blood infusions. RVR was calculated from MCFP-Pra/CO). After baseline measurements, we infused 10 micrograms/(kg x h-1) of Escherichia coli endotoxin. Eight animals also received 30 mL x kg-1 of dextran over the 2 hours (volume treated), and seven did not (no volume). After 2 hours we injected 25 mg x kg-1 of the NO synthase inhibitor, L-NAME, and repeated the measurements. RESULTS: In volume-treated animals, CO increased from 3.9 +/- 0.7 to 5.4 +/- 0.8 L x min-1 (P < .05), and blood pressure (BP) fell from 118 +/- 9 to 76 +/- 12 mmHg. MCFP rose, and there was no change in RVR or Cv, whereas capacitance increased (ie, right shift of pressure-volume curve). Cardiac function (ie, Starling curve) did not change. In no-volume animals, CO fell from 4.47 +/- 0.64 to 2.50 +/- 0.86 L x min-1, BP from 114 +/- 10 to 9 +/- 13 mmHg and MCFP fell. Systemic vascular resistance did not change. Cardiac function was markedly depressed, and the heart rate increased from 143 +/- 13 to 203 +/- 30 beats x min-1. L-NAME restored BP in both groups but also increased RVR and depressed cardiac function. CONCLUSION: Changes in vascular tone during endotoxemia are dependent on volume status. The increased cardiac output in volume-treated septic animals occurred because of an increase in stressed volume due to the volume given in combination with a dilated vasculature. L-NAME restored arterial tone but decreased CO because of a rise in RVR and decrease in cardiac function.

Analysis of Variance↗
PubMed1996

Ventricular interaction and venous capacitance modulate left ventricular preload.

The concept of left ventricular (LV) 'preload' has seemed simple and straightforward. Similarly, the capacitance function of the veins seemed to be defined, in spite of the fact that 'venous return' might be said to be increased in heart failure when it was obvious that cardiac output was substantially decreased. In studies during the past several years, we have demonstrated that pericardial pressure, as a major modulator of ventricular interaction, must be accounted for before preload, myocardial compliance or contractility can be assessed reliably. Also, using a new conceptual model based on venous pressure-volume relations that explains how changes in venous capacitance modulate ventricular preload, we have defined the comparative capacitance-conductance effects of various vasodilators in a model of heart failure. We conclude that left ventricular preload is significantly modulated by both changes in ventricular interaction and venous capacitance. To optimize the care of patients with heart disease, it is important to understand both these mechanisms.

Heart Failure↗
PubMed1998

Reduced venous compliance in lower limbs of aging humans and its importance for capacitance function.

Venous compliance in the calf of humans and its importance for capacitance function in relation to age were studied with the aid of 22, 44, and 59 mmHg lower body negative pressure (LBNP). Negative pressure transmission to the calf as well as changes in calf volume were studied, and venous compliance was calculated [change in volume with pressure change (dV/dP)]. The change in capacitance response of the calf with age (20-70 yr) was evaluated during LBNP 44 mmHg. Transmission of negative pressure to the subcutaneous tissue was almost full without any changes with age (92%). However, it was reduced to 80% in the underlying muscle tissue, irrespective of depth. Venous compliance in the young was 0.051 ml . 100 ml-1 . mmHg-1 and was reduced by 45% to 0.029 ml . 100 ml-1 . mmHg-1 in the old (P < 0.05). Accordingly, the capacitance response was reduced by 0.015 ml . 100 ml-1 . yr-1 (P < 0.005). Furthermore, the hemodynamic response to hypovolemic circulatory stress was attenuated with age. The reduced pressure transmission in muscle tissue is probably due to restriction of the muscle fascia envelope. The reduced venous compliance with age and the concomitant reduction in capacitance response during LBNP have implications for both the sympathetic reflex responses as well as the capacitance response during acute hypovolemic circulatory stress, which might be defected in aging humans.

Adult↗
PubMed2005

A subnormal plasma volume in formerly preeclamptic women is associated with a low venous capacitance.

OBJECTIVE: Pregnancy induces a smaller rise in plasma volume in formerly preeclamptic women with a pre-existent subnormal plasma volume than in their counterparts with a normal plasma volume. These women also have a three times higher recurrence rate of pregnancy-induced hypertensive disorders. In this study we tested the hypothesis that a subnormal plasma volume in these women is related to a lower capacitance of their venous compartment. METHODS: In 31 nonpregnant formerly preeclamptic women with a subnormal plasma volume and eight parous controls, we infused intravenously 500 mL of a modified gelatin solution over 30 minutes. Before and after infusion we measured the circulating levels of alpha-atrial natriuretic peptide (alpha-ANP) and active plasma renin concentration (APRC). During volume loading, we recorded the change in heart rate, stroke volume, and cardiac output using pulse contour analysis. We measured the ratio of percent change in blood volume and percent change in cardiac output during volume loading as a marker for venous capacitance. RESULTS: During volume loading, patients differed from controls by a larger rise in alpha-ANP, pulse rate, and cardiac output, and by a lower estimated venous capacitance. The concomitant response of stroke volume and APRC did not differ appreciably between groups. CONCLUSION: Formerly preeclamptic women with a subnormal plasma volume differ from controls with a normal plasma volume by a reduced venous capacitance. These results support our hypothesis that, in these women, a subnormal plasma volume indicates the presence of a subnormal venous capacitance.

Adult↗
PubMed2002

Varicose veins of the lower limbs and venous capacitance in postmenopausal women: relationship with obesity.

OBJECTIVE: The purpose of this study was to examine the association between body mass index (BMI), venous capacitance, and clinical evidence of varicose veins after adjustment for sex hormones in postmenopausal women. METHODS: This study group of the DIANA (DIet and ANdrogens) project (a randomized controlled trial on the effect of some dietary changes on sex hormone pattern in women with elevated androgenic hormone levels in Italy) was comprised of 104 healthy volunteer postmenopausal women, aged 48 to 65 years. The main outcome measures were physical examination to determine the presence and severity of varicose veins and plethysmographic measurement of lower limb venous capacitance and outflow. RESULTS: Women in the upper quartile of BMI (>30 kg/m(2)) showed a positive association with clinical evidence of varicose veins (odds ration, 5.8; 95% CI, 1.2 to 28.2) after adjustment for age, estradiol, testosterone, and sex hormone binding globulin. No association was found between BMI and plethysmographic measurements of venous parameters. CONCLUSION: Obesity is associated with clinical evidence of varicose veins independently from the influence of sex hormones in postmenopausal women and is not associated with venous capacitance. Increased body weight increases the risk of varicose veins.

Aged↗
PubMed2000

Inverse relation between aldosterone and venous capacitance in chronically treated congestive heart failure.

The purpose of this study was to examine if there is a relation between the aldosterone escape phenomenon and venous capacitance of the upper and lower limbs in patients with long-term congestive heart failure (CHF) receiving chronic treatment with angiotensin-converting enzyme (ACE) inhibitors. The study group consisted of 16 subjects with ischemic CHF in New York Heart Association functional class II (age 59 +/-2 years, ejection fraction 24+/-4%), stabilized under a constant drug regimen comprising furosemide, captopril 50 mg 3 times daily, and digoxin for at least 3 months. Thirteen apparently healthy volunteers, aged 50+/-4 years acted as controls. Forearm and calf venous capacitances were measured simultaneously by venous occlusion plethysmography using mercury-in-silastic strain gauges. The equilibration technique was used to derive venous capacitance from the recorded pressure-volume curves. Active renin, angiotensin II, and aldosterone levels were determined on venous blood samples obtained in the supine position. Angiotensin II (p<0.05) and aldosterone (p<0.01) were statistically significantly higher in patients with CHF under long-term ACE inhibition than in controls (aldosterone escape phenomenon). In CHF, forearm venous capacitance was 2.19+/-0.18 ml/100 ml; calf venous capacitance was 2.83+/-0.27 ml/100 ml. Aldosterone significantly and inversely correlated with venous capacitance in both upper (r = -0.586; p = 0.017) and lower (r = -0.625; p = 0.01) limbs. No correlations were found between forearm or calf venous capacitance and renin or angiotensin II. In patients with heart failure chronically treated with diuretics and full ACE inhibition, venous capacitance is inversely correlated with aldosterone through the mechanism of aldosterone escape, creating the potential for further deterioration of the CHF process.

Aldosterone↗
PubMed2001

Preservation of venous endothelial function in the forearm venous capacitance bed of patients with chronic heart failure despite arterial endothelial dysfunction.

OBJECTIVES: The goal of this study was to assess whether endothelial dysfunction occurs in the forearm venous capacitance bed of patients with chronic heart failure (CHF) and to determine the role of nitric oxide (NO) in modulating venous tone. BACKGROUND: Control of venous tone is crucially important in CHF. More than 70% of blood volume lies in the venous capacitance beds. Therefore, small changes in venous tone may markedly affect cardiac filling pressures and cardiac output. METHODS: Venous tone was measured using radionuclide forearm venous plethysmography in 24 patients with CHF and 16 age-matched controls. The effect of basal NO activity on venous tone was assessed by infusing N-monomethyl-L-arginine 12 mg/min and stimulated NO using carbachol 15 microg/min. Brachial artery flow-mediated dilation was assessed by ultrasonic wall-tracking. RESULTS: Blockade of basal NO release caused a significant and similar venoconstriction in patients (9.6 +/- 1.8%, p < 0.01) and controls (6.6 +/- 1.7%, p < 0.01). Carbachol-induced venodilation was significant and similar in patients (36.8 +/- 3.9%, p < 0.001) and controls (40.7 +/- 3.9%, p < 0.001). Brachial artery flow-mediated dilation was impaired in patients compared with controls (2.0 +/- 0.6% vs. 7.5 +/- 2.5%, p < 0.01). CONCLUSIONS: Our data indicate that, despite marked impairment of the function of the arterial endothelium, there is preservation of both basal and stimulated NO release in the forearm venous capacitance bed. This may provide important insights into mechanisms of endothelial dysfunction in CHF and the potential for novel therapy.

Aged↗
PubMed2002

Age-related changes in vasomotor reflex control of calf venous capacitance response to lower body negative pressure in humans.

The present study was performed to test the hypothesis that calf venous capacitance would be reduced by mild gravitational stress through a vasomotor reflex in humans, and this response could be diminished with advancing age. Nine young (31 +/- 1 years, mean +/- SE) and 9 elderly (69 +/- 1 years) healthy males were exposed to a lower body negative pressure (LBNP) of 15 mmHg. Venous occlusion plethysmography was used to measure calf venous capacitance and calf blood flow. Muscle sympathetic nerve activity (MSNA) was recorded microneurographically from the tibial nerve along with cardiovascular variables. It was found that baseline MSNA was higher [21 +/- 4 (mean +/- SE) vs. 37 +/- 5 bursts x min(-1), young vs. elderly; p < 0.05] and calf venous capacitance was lower (1.71 +/- 0.12 vs. 1.44 +/- 0.10, ml x 100 ml(-1), young vs. elderly; p < 0.05) in the elderly group. At 15 mmHg-LBNP, heart rate and mean arterial pressure both remained unchanged, MSNA was enhanced, and calf blood flow was reduced in all subjects. Calf venous capacitance during LBNP decreased in the young, but did not change in the elderly. A significant negative correlation between percent changes in MSNA and percent changes in calf venous capacitance existed in the young group (y = 20.171x-11.863, r = 20.682; p = 0.0432), but disappeared in the elderly group. The ratio of percent changes in calf venous capacitance to percent changes in MSNA was markedly lower in the elderly (p < 0.01). In conclusion, these results substantiate our hypothesis that calf venous capacitance is reduced by mild LBNP through the vasomotor reflex, and this response is diminished in the elderly.

Adult↗
PubMed2000

Endotoxemia alters splanchnic capacitance.

The splanchnic circulation constitutes a major portion of the total capacitance vasculature and may affect venous return and subsequently cardiac output during low output states. This study assessed the effects of rapid (10 microg/kg over 5 min) and slow (10 microg/kg over 60 min) induction of endotoxin (Escherichia coli) shock on splanchnic blood volume in 8 farm swine. Blood volume was measured by using Tc99m-labeled erythrocytes and radionuclide imaging. Baseline arterial pressure (MAP), central venous pressure (CVP), and liver, splenic, mesenteric and total splanchnic volumes were stable during the 30-min baseline. Approximately 30 min after the rapid endotoxin infusion, splenic volume decreased by 45%, whereas liver volume increased by 40% and MAP decreased by 60% (P < 0.01). The reduction in splenic volume occurred within 10 min of the endotoxin infusion, whereas liver volume changes occurred after MAP reduction. The slow endotoxin infusion also reduced splenic volume by approximately 50% (P = 0.05), whereas MAP declined by 30% (P < 0.05). However, the slow endotoxin infusion lowered liver volume (P < 0.05). Mesenteric volume was unaffected by the fast or slow endotoxin infusion. Total splanchnic volume was unaffected by the fast infusion but decreased by 37% in the slow infusion group (P < 0.05). In summary, E. coli endotoxin reduces splenic blood volume and increases liver blood volume after acute hypotension ensues. Endotoxin does not increase total splanchnic blood volume and may actually decrease total splanchnic volume in the absence of circulatory collapse. This endotoxin shock model is not associated with blood volume pooling in the splanchnic capacitance circulation.

Animals↗
PubMed2000

Cardiovascular responses of perimenopausal women to hormonal replacement therapy.

OBJECTIVE: This study was undertake to test the hypothesis that hormone replacement therapy alters cardiovascular function during the first several months of therapy. STUDY DESIGN: Serial estimates of blood pressure, heart rate, stroke volume, and venous capacitance were obtained before and at 1, 5, 9, and 21 weeks after the beginning of hormone replacement therapy with daily estradiol and intermittent norethindrone. Measurements were performed by means of electrocardiography, automated blood pressure measurement (Dynamap; Critikon Company LLC, Tampa, Fla), echocardiography, and plethysmography. RESULTS: Hormone replacement therapy did not alter heart rate, blood pressure, or venous capacitance. End-diastolic volume and stroke volume were unchanged after 1 week of hormone replacement therapy but rose thereafter. After 5 weeks of hormone replacement end-diastolic volume and stroke volume were increased by 13 +/- 5 mL and 9 +/- 2 mL, respectively, and after 9 weeks the increases totaled 23 +/- 5 mL and 17 +/- 3 mL, respectively. As a result cardiac output rose progressively to a level 1.1 +/- 0.3 L/min (18%) greater than pretreatment values and systemic vascular resistance fell 15%. These changes were associated with a 3-fold increase in serum estradiol levels. CONCLUSION: The studied regimen of hormone replacement therapy produces progressive cardiac remodeling and peripheral vasodilatation during the first 2 months of therapy.

Blood Pressure↗
PubMed2006

Altered venous capacitance as a cause of postprandial hypotension in multiple system atrophy.

Patients with multiple system atrophy (MSA) often have clinically significant postprandial hypotension (PPH). To elucidate the cause of insufficient cardiac preload augmentation that underlies PPH, we recorded calf venous capacitance (CVC) by strain-gauge plethysmography, in 17 MSA patients and eight healthy controls before and after oral glucose ingestion. Among 17 MSA patients, nine who showed a decrease in systolic blood pressure exceeding 20 mmHg and were diagnosed with PPH. MSA patients without PPH showed a significant decrease in CVC and a significant increase in cardiac output after oral glucose ingestion, as did controls; those with MSA exhibiting PPH showed a significant increase in CVC and no significant change in cardiac output. The change in CVC correlated positively with the decrease in systolic and diastolic blood pressure after glucose ingestion, and also correlated negatively with the increase in cardiac output. Physiologically, PPH is prevented by a decrease in venous capacitance, which increases circulating blood volume and cardiac output. In some MSA patients, failure of venous capacitance to decrease may induce PPH.

Aged↗
PubMed2006

Central venous pressure and mean circulatory filling pressure in the dogfish Squalus acanthias: adrenergic control and role of the pericardium.

Subambient central venous pressure (Pven) and modulation of venous return through cardiac suction (vis a fronte) characterizes the venous circulation in sharks. Venous capacitance was estimated in the dogfish Squalus acanthias by measuring the mean circulatory filling pressure (MCFP) during transient occlusion of cardiac outflow. We tested the hypothesis that venous return and cardiac preload can be altered additionally through adrenergic changes of venous capacitance. The experiments involved the surgical opening of the pericardium to place a perivascular occluder around the conus arteriosus. Another control group was identically instrumented, but lacked the occluder, and was subjected to the same pharmacological protocol to evaluate how pericardioectomy affected cardiovascular status. Routine Pven was negative (-0.08+/-0.02 kPa) in control fish but positive (0.09+/-0.01 kPa) in the pericardioectomized group. Injections of 5 microg/kg body mass (Mb) of epinephrine and phenylephrine (100 microg/kg Mb) increased Pven and MCFP, whereas isoproterenol (1 microg/kg Mb) decreased both variables. Thus, constriction and relaxation of the venous vasculature were mediated through the respective stimulation of alpha- and beta-adrenergic receptors. Alpha-adrenergic blockade with prazosin (1 mg/kg Mb) attenuated the responses to phenylephrine and decreased resting Pven in pericardioectomized animals. Our results provide convincing evidence for adrenergic control of the venous vasculature in elasmobranchs, although the pericardium is clearly an important component in the modulation of venous function. Thus active changes in venous capacitance have previously been underestimated as an important means of modulating venous return and cardiac performance in this group.

Adrenergic Agonists↗
PubMed1999

Biophysical characterization of skin damage and recovery after exposure to different surfactants.

The majority of adverse skin reactions to personal-care products are presumed to be caused by irritant substances, like surfactants. In this study, different aspects of the irritant reaction after a single exposure to 8 surfactants were characterized during 2 weeks. Solutions of 2% sodium lauryl sulfate, 5% sodium C12-15 pareth sulfate, 5% sodium cocoyl isethionate, 10% disodium laureth sulfosuccinate, 10% sodium cocoamphoacetate, 10% cocamide DEA, 10% cocamidopropyl betaine and 10% lauryl glucoside, respectively, were applied to the forearm of 12 volunteers. Clinical assessment, an evaporimeter, a laser Doppler flowmeter and a corneometer were used for evaluation. The surfactants induced different degrees of irritation. Erythema, transepidermal water loss and skin blood flow exhibited a similar time course, which seemed to be inversely related to the delayed scaling and reduced skin capacitance. The mechanism of the damaging effect of the surfactants seems to be similar, although some minor differences were noted.

Adult↗
PubMed2005

Reduced capacitative calcium entry in the mesenteric vascular bed of bile duct-ligated rats.

In this work, we analyzed the interaction of nitric oxide (NO) with some of the mechanisms known to regulate intracellular calcium levels in order to gain insight into the mechanisms responsible for the reduced vascular pressor response to vasoconstrictors observed in an experimental model of liver cirrhosis. Specifically, we hypothesized that the entry of calcium through capacitative channels is defective in this model. The experiments were performed with isolated, Krebs-perfused and de-endothelialized mesenteric arterial bed of rats with bile duct ligation (4 weeks) and their controls. Pretreatment with thapsigargin to inhibit calcium uptake into sarcoplasmic reticulum potentiated the pressor responses to methoxamine, but the response of the cirrhotic vessels was significantly lower than that of the controls. Under the same conditions, perfusion of the mesenteries with zero calcium-Krebs resulted in lower pressor responses to methoxamine, especially in the mesenteries of the bile duct-ligated rats. To specifically analyze the entry of calcium through store-operated calcium channels, the pressor response to the addition of calcium was studied in mesenteries perfused with zero calcium-Krebs and in the presence of thapsigargin. Again, the response of the cirrhotic mesenteric beds was significantly lower than that of the control vessels. Under all these experimental conditions, the differences between control and cirrhotic responses were abolished by pretreatment with the NO synthesis inhibitor N(w)-nitro-L-arginine (NNA). These results indicate that, in the mesenteric bed of bile duct-ligated rats, an excess of nitric oxide interferes with the release of calcium from thapsigargin-sensitive internal stores and also reduces the capacitative entry of calcium into vascular muscular cells induced by the depletion of calcium from internal stores. This mechanism may have an important role in the reduced pressor response observed in the mesenteric vascular bed in cirrhosis.

Adrenergic alpha-Agonists↗
PubMed1996

Effect of arterial compliance on carotid sinus baroreceptor reflex control of the circulation.

Capacitive properties of the arterial and venous segments of the peripheral circulation are important in the regulation of cardiac output and arterial blood pressure. We examined whether an acute increase in arterial compliance C(a) would alter carotid sinus baroreflex control of the circulation. Eight mongrel dogs were anesthetized with pentobarbital sodium, and the carotid sinus regions were isolated and perfused with nonpulsatile pressures. Open-loop baroreflex response curves for systemic arterial pressure (SAP), heart rate (HR), aortic blood flow (ABF), peripheral vascular resistance (PVR), and left ventricular (LV) contractility were obtained when carotid sinus pressure (CSP) was changed in 25-mmHg steps between 50 and 200 mmHg under a control condition and when C(a) was increased by including two hydraulic compliant chambers to the arterial circulation (CS 1.72 ml/mmHg and CL 5.05 ml/mmHg). The compliant chambers significantly increased C(a) and altered the ratio of arterial to venous compliance C(a)/Cv). Changes in C(a)/Cv significantly decreased the maximal open-loop baroreflex gain (Gmax) for SAP (-2.3 +/- 0.5, -1.6 +/- 0.3, and -1.1 +/- 0.2 mmHg/mmHg, control vs. CS vs. CL, P < 0.05). Gmax for ABF was decreased by CS (-0.9 +/- 0.2 vs. -0.3 +/- 0.1 ml.kg-1.min-1, control vs. CS, P < 0.05), and CL reversed the reflex changes in ABF (Gmax: +0.6 +/- 0.3 ml.kg-1.min-1). Gmax for HR, PVR, and LV contractility was not altered when C(a) was increased (P > 0.05). These findings indicate that an increase in C(a) changes C(a)/Cv and alters carotid baroreflex control of SAP by modifying the ABF response. We conclude that a change in C(a)/Cv affects the reflex control of the circulation by altering the distribution of blood volume between the arterial and venous circulations.

Animals↗
PubMed1977

Reactivity of the cerebral resistance and capacitance vessels and blood-brain water exchange in the experimental brain injury.

In conclusion, an estimate of the intracranial volumetric effects produced in anesthetized dogs by histamine, acetylcholine and CO2 shows that, on a basis of equiactivity on CBF, the effects of histamine on the intracranial content are twice greater than those produced by acetylcholine and CO2. This difference may be explained by a greater activity of histamine on the intracranial capacitance vessels and/or by an increase in the fluid escape from blood to the brain produced by histamine. Data obtained after the production of an acute, cold induced brain lesion support the second possibility.

Acetylcholine↗