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PubMed1983

Hind-limb vascular-capacitance responses in anaesthetized dogs.

In anaesthetized dogs a hind limb was vascularly isolated, perfused through the femoral artery at either constant flow or constant pressure and drained from the femoral vein at constant pressure. Inflow and outflow were recorded. Vascular-resistance changes were calculated from changes in pressure or flow and volume changes from the differences between inflow and outflow. During constant-flow perfusion, both changes in carotid sinus pressure and direct stimulation of efferent sympathetic nerves resulted in large resistance responses. However, changes in carotid sinus pressure did not result in changes in limb blood volume and only small decreases were obtained in response to direct stimulation. During constant-pressure perfusion, both reflex and direct stimulation resulted not only in significant changes in resistance but also in significant volume changes which were much larger than those obtained during constant-flow perfusion. Similar responses were obtained when the flow rate was changed by altering the pump speed. These results indicate that changes in pressure to carotid baroreceptors do not result in active capacitance responses in the limb circulation and that only very small responses are obtained even to electrical stimulation of sympathetic nerves. The larger responses occurring during constant-pressure perfusion are thought to be secondary to changes in blood flow.

Animals↗
PubMed1976

Responses of abdominal vascular capacitance in the anaesthetized dog to changes in carotid sinus pressure.

1. The abdominal circulation of anaesthetized dogs was vascularly isolated without opening the abdomen, by cutting or tying all structures immediately above the diaphragm and tying the proximal ends of the hind limbs. The region was perfused at constant flow through the aorta and drained at constant pressure from the inferior vena cava. 2. Vascular resistance responses were expressed as the changes in perfusion pressure and capacitance responses were determined by integrating changes in vena caval outflow. 3. Decreasing the pressure in the isolated carotid sinuses over the whole baroreceptor sensitivity range increased mean perfusion pressure from 91 to 149 mmHg (a 67% increase in resistance) and decreased mean capacitance by 111 ml. (5 ml. kg-1). 4. The range of carotid sinus pressures over which capacitance responses occurred was at a significantly higher level than the corresponding range for resistance responses. 5. Comparison of the reflex responses with the responses to direct stimulation of efferent sympathetic nerves shows that quantitatively similar responses of resistance and capacitance to those induced by a large step decrease in carotid pressure could be produced by stimulating maximally the efferent sympathetic nerves at 5 Hz. These results also suggest that at all levels of carotid sinus pressure there is no difference in the impulse traffic to resistance and capacitance vessels.

Abdomen↗
PubMed1976

Responses of abdominal vascular capacitance to stimulation of splachnic nerves.

In chloralose-anesthetized dogs the abdominal circulation was vascularly isolated without opening the abdominal cavity. The region was perfused at constant flow through the aorta and drained at constant pressure from the inferior vena cava. Changes in resistance were calculated from changes in perfusion pressure and changes in capacitance were calculated by integrating changes in venous outflow. Stimulation of both splanchnic nerves at 20 Hz increased resistance by 135% and reduced capacitance by 7.20 ml kg-1. The capacitance responses at 1 and 2 Hz (3.42 and 5.43 ml kg-1) were 48 and 67% of the responses at 20 Hz, However, the resistance responses at 1 and 2 Hz (14 and 31% increase) were only 12 and 26% of the responses at 20 Hz. After occlusion of the splenic pedicle, capacitance responses were reduced by about 40%. Although changes in inferior vena caval pressure changed the volume of blood in the abdomen by 0.92 ml kg-1 cmH2O-1, the responses to stimulation were relatively constant in any one animal at constant venous pressures between 5 and 15 cmH2O.

Abdomen↗
PubMed1991

Modifications by halothane of responses to acute hypoxia in systemic vascular capacitance, resistance, and sympathetic nerve activity in dogs.

To examine the effects of halothane on segmental vascular responses to hypoxia, we used cardiopulmonary bypass with venous outflow divided into three compartments (splanchnic, coronary, and "other") in dogs anesthetized with pentobarbital sodium. The reservoir volume changes represented the inverted changes in systemic blood volume (SBV). In addition, sympathetic efferent nerve activity (SENA) was simultaneously recorded from the ventral ansa subclavian nerve. Experiments were done in two groups: severe hypoxia (PO2 of 19 mm Hg) and moderate hypoxia (PO2 of 50 mm Hg). Hypoxia provoked a significant decrease in SBV of 22.3 +/- 3.1 mL/kg and 10.5 +/- 1.6 mL/kg during severe and moderate hypoxia, respectively. Two percent end-tidal halothane attenuated the decrease in SBV to 10.3 +/- 1.3 mL/kg during severe hypoxia, and 1% halothane attenuated the decrease to 3.7 +/- 1.4 mL/kg during moderate hypoxia. Subsequent chemoreceptor denervation in the presence of 1% halothane completely abolished the moderate hypoxia-induced decrease in SBV. In the presence of halothane, vascular resistance during hypoxia was significantly less than that during control conditions. Sympathetic efferent nerve activity increased significantly during severe and moderate hypoxia by about 180% and 55%, respectively. During severe hypoxia, halothane did not cause any change in the response of SENA, whereas during moderate hypoxia, halothane tended to decrease SENA, but not significantly, and subsequent chemoreceptor denervation completely abolished the increase in SENA. Coronary resistance showed a hypoxia-induced reduction that was not influenced by halothane. These results suggest that acute hypoxia causes a decrease in SBV dependent on the severity of hypoxia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Modulation of vascular capacitance by angiotensin and nitroprusside: a mechanism of changes in pericardial pressure.

The aim of the present study was to test the hypothesis that vasoactive drugs may modify left ventricular diastolic function by shifting blood between the systemic vascular bed and the heart, thereby changing pericardial and left ventricular pressure. The experiments were done in 10 open-chest, anesthetized, previously splenectomized dogs in which changes in pericardial surface pressure in response to intravenous sodium nitroprusside and angiotensin were related to changes in blood volume in the abdominal region. Blood volume was determined by blood pool scintigraphy (99mTc) and regions of interest were drawn in the liver and in the mesenteric area. Angiotensin was infused at rates that were adjusted to increase mean aortic pressure by 20 and 30 mm Hg, and nitroprusside was infused at rates to decrease mean aortic pressure by 30 and 50 mm Hg. Angiotensin increased pericardial pressure by 3 and 5 mm Hg at the respective doses and there were increments in left ventricular end-diastolic pressure (LVEDP) and left ventricular diameter (sonomicrometry). Angiotensin decreased blood volume in the mesenteric region by 14% and 17%, but did not significantly change blood volume in the liver region. Angiotensin increased portal venous pressure and decreased mesenteric blood volume, suggesting decreased mesenteric venous compliance. Nitroprusside had opposite effects: pericardial pressure was decreased by 5.5 and 6.5 mm Hg by the respective doses. The doses of nitroprusside increased blood volume in the mesenteric region by 14% and 20%, but did not significantly change blood volume in the liver region.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1990

Autoregulation of cardiac output by passive elastic characteristics of the vascular capacitance system.

After a change in cardiac output, the magnitude of potential blood volume redistribution was investigated in 10 dogs anesthetized with chloralose. All of the venous return was pumped into a reservoir, using servocontrolled pumps to maintain fixed superior and inferior vena cava pressures. The cardiac output was set at various levels by pumping from the reservoir into the right atrium. Changes in reservoir volume were assumed to reflect the changes in vascular blood volume. After measuring the control responses, cardiovascular reflexes were blocked with hexamethonium. Reducing the cardiac output, for example, from 110 to 80 ml/(min.kg) with reflexes intact, caused a 9.2-ml/kg transfer of blood from the dog to the reservoir. With reflexes blocked, the same change in cardiac output caused 6.8 ml/kg of the blood to be transferred. Under the control conditions, throughout the range of 50-140 ml/(min.kg), an increase or decrease of cardiac output of 1 ml/(min.kg) elicited a 0.304 +/- 0.086 (mean +/- SD) ml/kg change in dog blood volume; with reflexes blocked, the flow sensitivity was 0.239 +/- 0.062 ml/kg. Thus, only 21% of the total blood volume redistribution was attributable to active reflex responses. Deterioration of the preparation may have attenuated the magnitude of active reflex activity. Neither the systemic vascular compliance of 1.80 +/- 0.35 ml/mm Hg.kg nor the fraction of venous return from the superior vena cava of 26.5 +/- 4.6% was significantly changed by reflex blockade.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Effects of heat stress on vascular capacitance.

In dogs and humans, heat stress is associated with an increase in cardiac output that sustains blood flow to heat-dissipating organs. Because cardiac output and venous return are equal in the steady state, the circulation must also adjust in heat stress to allow the venous return to increase. To analyze these adjustments, we measured blood volumes, unstressed volumes, blood flow distribution, venous compliance, venous resistance, and the time constant of venous drainage of the splanchnic and extrasplanchnic vascular beds in dogs anesthetized with alpha-chloralose at normal and at high core temperatures. We repeated the measurements at high core temperatures with ganglionic blockade, alpha-adrenergic receptor blockade, or beta-adrenergic receptor blockade to determine the efferent neurohumoral pathway. When core temperature was increased from 37.8 +/- 0.2 to 41.9 +/- 0.1 degrees C, total splanchnic blood volume decreased 23% (4.6 +/- 1.4 ml/kg) and splanchnic unstressed volume decreased 38.5%. None of the other determinants of venous return changed. Ganglionic blockade shifted the total and unstressed splanchnic blood volume during heat stress back to normothermic values. However, beta- and alpha-blockade did not affect splanchnic volumes. We conclude that a decrease in splanchnic unstressed volume is an important factor for the increased venous return during heat stress. Although mediated through sympathetic ganglions, this decrease is not abolished by alpha- or beta-receptor blockade.

Animals↗
PubMed1976

Vascular capacitance and fluid shifts in dogs during prolonged hemorrhagic hypotension.

The mean circulatory pressure (Pmc) in dogs anesthetized with chloralose-urethane was estimated from 0.5 to 150 minutes after hemorrhages of 0, 17, or 34 ml/kg, or that volume giving an arterial pressure (Pa) of 40 mm Hg. The Pmc was determined by fibrillating the heart and then rapidly pumping blood from aorta to vena cava until Pa=venous pressure (Pv)=Pmc. Within about 10 seconds, the heart was defibrillated. Vascular compliance was estimated as the ratio of a test blood volume change (0, +/- 8.5, or 17 ml/kg) to the change in Pmc, determined 0.5 minute after the start of the test volume change. Erythrocyte and plasma volumes were measured by 51Cr-erythrocyte and 125I-albumin dilution. In response to prolonged hemorrhage: (1) the total vascular compliance apparently decreased; (2) most of the changes in capacity vessels occurred within 5 minutes, and indeed a large part of the response probably had occurred by the time of the first measurement at 30 seconds; (3) the progressive recovery in Pmc after 5 minutes was primarily from fluid shifting into the vasculature; (4) even after 2 hours of severe hemorrhagic hypotension, the venoconstriction was not lost; but (5) after an hour of severe hemorrhagic hypotension (arterial pressure of 40 mm Hg) there was water loss from the vasculature, because plasma protein and erythrocyte concentrations and plasma oncotic pressure increased.

Animals↗
PubMed1983

Total body vascular capacitance changes during high intracranial pressure in dogs.

The active capacitance response to increased intracranial pressure (Pic) was studied in nine chloralose-anesthetized dogs. The vena cavae were cannulated and drained into a reservoir as blood was pumped at a constant flow (Q) into the right atrium. Central blood volume was determined as Q times the mean transit time of dye from the right atrium to the aortic root. Arterial compliance (Ca) was determined from the monoexponential decay of systemic arterial pressure (SAP) during vagal cardiac arrest to compute changes in arterial volume (delta SAP X Ca). Atropine was administered to prevent bradycardia and dangerous, constant cardiac output-induced increases in pulmonary arterial (PAP) and right and left atrial pressures. Blood volume shifts indicative of active venoconstriction, included changes in reservoir, central, and arterial volumes during Pic of 100-200 mmHg. Raised Pic, after atropine, induced a tachycardia, increased systemic and pulmonary resistances, and increased SAP and PAP. Venoconstriction caused marked blood shifts between 125 and 200 mmHg Pic. The extrapolated response threshold was about 112 mmHg. In the most sensitive range, venoconstriction amounted to 3.9 ml X kg-1 per 25-mmHg change in Pic. These results indicate that intense active capacitance vessel constriction is an important part of cardiovascular hemostasis during rapidly increased intracranial pressure.

Animals↗
PubMed1976

The critical relationship of intravascular blood volume and vascular capacitance in sepsis.

The present article represents a more detailed study of the septic leg models used in our previous work on sepsis and septic shock. An improvement in this model is described, and the period of maximum hyperdynamic response is delineated. An attempt was made to measure changes in the rate of swelling of the septic leg in responding and nonresponding dogs. The exquisitely sensitive response of the dog with sepsis to minor reductions in blood volume was demonstrated. Results of our previous studies concerning the redistribution of blood flow in sepsis were extended using radioactively labeled microspheres.

Animals↗
PubMedDate not supplied

Regional vascular capacitance in rabbit one-kidney, one clip hypertension.

One-kidney Goldblatt hypertensive rabbits (New Zealand White) were studied after durations of renal artery clipping that varied from 6 to 17 days. Measurements included arterial pressure (ABP), iliac venous pressure (IVP), left atrial pressure (LAP), cardiac output (CO) (by thermodilution), blood volume (BV), cardiopulmonary volume (CPV), and hindleg thermodilution volume (HLV). These were determined at steady-state as well as during acute blood volume expansion. In sham-clipped animals, ABP was 74 +/- 1 mm Hg. This increased to 92 +/- 3 mm Hg by 6 to 9 days post-clipping, to 96 +/- 3 mm Hg by 10 to 13 days, to 89 +/- 4 mm Hg by 14 to 17 days. CO remained near 150 ml/min . kg until Day 13 and fell to 127 +/- 8 ml/min . kg at 14 to 17 days because of a fall in heart rate. Blood volume and stroke volume did not change significantly from 62 +/- 1 ml/kg and 0.60 +/- 0.04 ml/kg, respectively. The development of hypertension was due entirely to changes in peripheral resistance. CPV was 8.5 ml/kg initially and increased significantly as hypertension developed. HLV did not change significantly from about 10 ml/kg. During acute blood volume expansion, hypertensive animals showed smaller transient increases in CO than did sham-clipped normotensives, but the associated blood pressure rise was greater. This reduced vasodilator capacity was accompanied by reduced distensibility of the cardiopulmonary bed. In sham-clipped animals, the cardiopulmonary pressure/volume slope was between 0.05 and 0.07 mm Hg per ml/kg. This increased to 0.44 mm Hg per ml/kg by 14--17 days of clipping. The corresponding value for the hindleg region did not change significantly from 0.2 mm Hg per ml/kg. Cardiac output and stroke volume were directly correlated with cardiopulmonary volume. The slope of this correlation decreased significantly during hypertension. The data suggest that decreased cardiopulmonary compliance in hypertension minimizes transient changes in cardiac output. This is especially important for arterial blood pressure control in view of the impaired vasodilator capacity of the hypertensive circulation.

Animals↗