Measurement of mean circulatory filling pressure and vascular capacitance in the rat.
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Spleen as an experimental model for the study of vascular capacitance.
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Acetylcholine↗
Reflex control of veins and vascular capacitance.
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Animals↗
Reflex control of vascular capacitance.
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Animals↗
Hyperosmolarity and pulmonary vascular capacitance.
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Animals↗
Autonomic nervous control of nasal vasculature and airflow resistance in the anaesthetized dog.
1. In pentobarbitone-anaesthetized dogs with constant-flow vascular perfusion of nasal mucosa on both sides, nasal airway resistance, vascular resistance, vascular capacitance (via changes in total venous outflow) and blood flow in the anterior and posterior venous systems were measured. 2. Electrical stimulation of the cut peripheral ends of the cervical sympathetic trunk, caudal nasal nerve, or major palatine nerve increased vascular resistance and decreased vascular capacitance and airway resistance. Propranolol and atropine had no effect on the responses while bretylium completely abolished them; phentolamine greatly lessened the vascular resistance response and partially decreased the vascular capacitance and airway responses. Hence, sympathetic stimulation causes constriction of the resistance vessels via alpha-adrenergic mechanism and constriction of capacitance vessels via alpha-adrenergic as well as some non-adrenergic and non-cholinergic mechanisms. 3. Denervation of the cervical sympathetic trunk, caudal nasal nerve and major palatine nerve decreased nasal vascular resistance and increased vascular capacitance and airway resistance, suggesting tonic sympathetic discharge to nasal mucosa via caudal nasal and major palatine nerves. 4. Electrical stimulation of the nerve of pterygoid canal decreased vascular resistance but increased vascular capacitance (in the posterior venous system) and airway resistance to low-voltage stimulation (below 10 V), and decreased vascular capacitance (in the anterior venous system) and airway resistance to high-voltage stimulation (above 10 V). Hexamethonium reversed the vascular resistance response as well as vascular capacitance and airway responses to high-voltage stimulation. Bretylium and phentolamine enhanced the vascular resistance response and reversed vascular capacitance and airway resistance responses to high-voltage stimulation. Hence, low-voltage stimulation results in parasympathetic dilatation of resistance and capacitance vessels whereas high-voltage stimulation results in parasympathetic dilatation of resistance vessels and sympathetic constriction of capacitance vessels. The parasympathetic vasodilatation was atropine resistance and the sympathetic vasoconstriction was partially via alpha-adrenergic mechanisms. 5. Denervation of the nerve of pterygoid canal did not affect vascular resistance, vascular capacitance or airway resistance suggesting negligible tonic parasympathetic and sympathetic discharges to nasal blood vessels via the nerve. 6. Simultaneous optimal stimulation of sympathetic and parasympathetic nerves resulted in vasoconstriction, especially in capacitance vessels, suggesting sympathetic predominance over parasympathetic control.
Airway Resistance↗
Effect of perindopril in pacing-induced canine models of acute and chronic heart failure.
OBJECTIVE: To examine the effects of perindopril, a nonsulfhydryl-containing angiotensin-converting enzyme inhibitor, on total vascular capacitance and hemodynamics in acute and chronic dog models of heart failure. METHODS: Acute heart failure was induced in anesthetized, splenectomized dogs by a volume load (dextran 70, 20 mL/kg) during rapid right ventricular pacing (RRVP) at 250 beats/min. Pretreatment with perindopril (0.3 mg/kg daily for six days, n = 7) was compared with no treatment (n = 7). Total vascular capacitance and compliance were measured from plots of mean circulatory filling pressure during acetylcholine-induced circulatory arrests at different blood volumes. Chronic heart failure was induced by continuous RRVP in splenectomized dogs treated with perindopril (0.3 mg/kg daily, n = 8), which were compared with untreated dogs (n = 8). Hemodynamics and total vascular capacitance and compliance were measured at baseline and after 33 days of RRVP. RESULTS: Perindopril treatment did not significantly modify the increased pulmonary capillary wedge and mean circulatory filling pressures, reduced total vascular compliance or total vascular capacitance associated with the volume load and acute RRVP. During chronic RRVP, perindopril reduced weight gain and the development of ascites, reduced right atrial pressure (6.3 +/- 1.3 versus 10.3 +/- 1.2 mmHg), mean circulatory filling pressure (9.3 +/- 1.0 versus 14.7 +/- 1.2 mmHg), stressed blood volume (22 +/- 3 versus 33 +/- 4 mL/kg) and central blood volume (10 +/- 1 versus 14 +/- 1 mL/kg) while increasing cardiac output (122 +/- 9 versus 98 +/- 7 mL/kg). However, the reduction in total vascular capacitance was not attenuated and pulmonary capillary wedge pressure was not lowered significantly (18.5 +/- 1.5 versus 21.4 +/- 1.3 mmHg). CONCLUSION: Perindopril failed to modify hemodynamics in the pacing-induced canine model of acute heart failure but had beneficial effects in the model of chronic heart failure.
Acute Disease↗
Captopril and angiotensin II receptor antagonist therapy in a pacing model of heart failure.
Twenty-four splenectomized dogs were subjected to rapid right ventricular pacing (RRVP) at 250 beats/min for five weeks. During the final three weeks, four groups six dogs were untreated or treated with captopril alone, with the angiotensin II type 1 (AT1) receptor antagonist L158,809 alone or with the two drugs combined by constant intravenous infusion. Hemodynamic studies were carried out during light anesthesia at baseline, and after two and five weeks of pacing. Total vascular capacitance and stressed blood volume were calculated from the mean circulatory filling pressure during transient circulatory arrest after acetylcholine administration at three different circulating volumes. Central blood volume and cardiac output were measured by thermodilution. Severe heart failure was present in the untreated group after five weeks of RRVP, characterized by low cardiac output and total vascular capacitance, high right atrial and pulmonary capillary wedge and mean circulatory filling pressure, plus increased stressed and central blood volumes. While L158,809 had not effect, captopril alone or combined with L158,809 ameliorated the reduction in total vascular capacitance, and reduced right atrial and mean circulatory pressure and stressed blood volumes. Combined therapy reduced pulmonary capillary wedge pressure. Thus, angiotensin-converting enzyme inhibition with captopril was effective in this model of chronic low output heart failure, whereas AT1 receptor antagonism was not.
Angiotensin II↗
Vascular and cardiac effects of amlodipine in acute heart failure in dogs.
BACKGROUND: Amlodipine improves exercise capacity in patients with chronic congestive heart failure (HF), but the mechanisms of this effect are unknown. OBJECTIVE: To test the hypothesis, in a canine model of acute, ischemic HF, that amlodipine increases vascular capacitance and reduces cardiac filling pressures. METHODS: Amlodipine was given to 13 anesthetized, splenectomized dogs (six controls and seven with HF). Aortic, left ventricular end-diastolic (LVEDP) and portal venous (Pportal) pressures, cardiac output, portal flow (ultrasonic probe) and intestinal blood volume (IBV, 99mTc blood-pool scintigraphy) were measured. Intestinal vascular conductance (= 1/resistance) and vascular capacitance (CAP) were measured before and 15 mins after repetitive 150 micrograms/kg dosages of amlodipine (maximum cumulative dosage, 1000 micrograms/kg). Pportal-IBV curves were obtained by impeding portal flow (pneumatic cuff), and change in CAP was defined by the change in IBV at Pportal = 7.5 mmHg. HF was induced by microsphere embolization of the left coronary artery. RESULTS: CAP increased in the control group (+ 28%, P < 0.01) but decreased (-9%, P < 0.05) in the HF group. Left ventricular stroke work increased in the control group (P < 0.05), while it decreased (P < 0.05) in the HF group, suggesting a negative inotropic effect. In the control group, LVEDP increased after amlodipine was given (P < 0.05) but did not change significantly in the HF group. CONCLUSIONS: In the acute experimental HF model, amlodipine failed to increase intestinal vascular CAP or decrease filling pressures, and may have had a negative inotropic effect. The experiment failed to demonstrate a beneficial hemodynamic effect of amlodipine in acute HF, and the mechanism of benefit of this agent in chronic HF remains unclear.
Acute Disease↗
Effect of pregnancy on pressure-volume relationships in circulation of rabbits.
Mean circulatory filling pressure (MCFP) has been measured after vagally induced cardiac arrest in 11 nonpregnant and 10 near-term pregnant rabbits, anesthetized with pentobarbital sodium. MCFP was 6.1 +/- 0.4 (SD) mmHg in the nonpregnant and 7.2 +/- 0.4 mmHg in the pregnant animals. The difference of 1.1 mmHg was significant (P < 0.001). Sympathetic blockade with bretylium tosylate (10 mg/kg) reduced MCFP by 0.4 mmHg in both nonpregnant and pregnant rabbits. Vascular capacitance was examined in the two groups. Unstressed vascular volume and vascular compliance were derived from measurements of MCFP after increasing blood volume by 8 and 16% or reducing it by 8%. The unstressed vascular volumes, 33.9 +/- 3.9 (SD) ml/kg in the nonpregnant and 35.1 +/- 3.2 ml/kg in the pregnant group, were not significantly different, but compliance in the pregnant group (4.0 +/- 0.6 ml.kg-1.mmHg-1) was significantly greater than in the nonpregnant rabbits (3.4 +/- 0.6 ml.kg-1.mmHg-1) (P < 0.05). We conclude that there are changes in vascular capacitance in rabbit pregnancy, probably not related to alterations in vasomotor activity, but these are insufficient to fully compensate for the increase in blood volume, thus leading to the rise in MCFP.
Animals↗
Beta adrenergic dilator component of the sympathetic vascular response in skeletal muscle. Influence on the micro-circulation and on transcapillary exchange.
A neurogenic beta-adrenergic vasodilatation in skeletal muscle has been indicated by some recent investigations. The present study describes the extent to which this neurogenic beta-dilator mechanism contributes to the integrated vascular response in consecutive sections of the muscle vascular bed during sympathetic nerve activation. This was done by studying the vascular reactions to graded sympathetic stimulation (1-16 Hz) before and after beta-adrenoceptor blockade. Beta-blockade did not influence significantly the sympathetically induced changes of total muscle vascular resistance or capacitance. Vascular tone in the "micro-vessels" during stimulation was, however, clearly more pronounced in the beta-blocked than in the non-blocked region, as revealed by segmental resistance analysis and by determination of precapillary sphincter tone (CFC). In addition, beta-blockade markedly reduced the net transcapillary absorption of extravascular fluid evoked by nerve activation. This effect could be ascribed to the mentioned influence on the precapillary sphincters, leading to a decrease of the number of capillaries available for transcapillary exchange, and to a limitation of the nerve induced fall of capillary hydrostatic pressure. The described effects of alpha-blockade were observed at all rates of sympathetic stimulation.--The conclusion was reached that the beta-adrenergic dilator component of the sympathetic vascular response in skeletal muscle significantly modifies the alpha-adrenergic constriction in the micro-vessels. It is suggested that, in the intact organism, this neurogenic beta-dilator mechanism is primarily aimed at improving the transcapillary exchange.
Adrenergic beta-Antagonists↗
Mean circulatory filling pressure: its meaning and measurement.
The volume-pressure relationship of the vasculature of the body as a whole, its vascular capacitance, requires a measurement of the mean circulatory filling pressure (Pmcf). A change in vascular capacitance induced by reflexes, hormones, or drugs has physiological consequences similar to a rapid change in blood volume and thus strongly influences cardiac output. The Pmcf is defined as the mean vascular pressure that exists after a stop in cardiac output and redistribution of blood, so that all pressures are the same throughout the system. The Pmcf is thus related to the fullness of the circulatory system. A change in Pmcf provides a uniquely useful index of a change in overall venous smooth muscle tone if the blood volume is not concomitantly changed. The Pmcf also provides an estimate of the distending pressure in the small veins and venules, which contain most of the blood in the body and comprise most of the vascular compliance. Thus the Pmcf, which is normally independent of the magnitude of the cardiac output, provides an estimate of the upstream pressure that determines the rate of flow returning to the heart.
Animals↗
Theoretically optimal duty cycles for chest and abdominal compression during external cardiopulmonary resuscitation.
OBJECTIVE: To use an electronic model of human circulation to compare the hemodynamic effects of different durations of chest compression during external CPR, both with and without interposed abdominal compression (IAC). METHODS: An electrical analog model of human circulation was studied on digital computer workstations using SPICE, a general-purpose circuit simulation program. In the model the heart and blood vessels were represented as resistive-capacitive networks, pressures as voltages, blood flow as electric current, blood inertia as inductance, and cardiac and venous valves as diodes. External pressurization of the heart and great vessels, as would occur in IAC-CPR, was simulated by the alternate application of damped rectangular voltage pulses, first between intrathoracic vascular capacitances and ground, and then between intra-abdominal vascular capacitances and ground. With this model compression frequencies of 60, 80, and 100 cycles/min and duty cycles ranging from 10% to 90%, both with and without IAC, were compared. RESULTS: There was little difference in hemodynamics when the overall compression frequency was varied between 60 and 100 cycles/min, but the effects of duty cycle were substantial. During both standard CPR and IAC-CPR, total flow and coronary flow were greatest at chest compression durations equal to 30% of cycle time. Interposed abdominal compression substantially improved simulated systemic blood flow and perfusion pressure at all duty cycles, compared with standard CPR without abdominal compression. Mean arterial pressure > 75 mm Hg and artificial cardiac output > 2.0 L/min could be generated by 30% duty cycle compression with IAC. Coronary perfusion in the model is clearly optimized at 30% chest compression (i.e., high-impulse chest compression technique). CONCLUSION: Combined high-impulse chest compressions and IACs maximize blood flow during CPR in the electrical analog model of human circulation.
Abdomen↗
Endothelin in the splanchnic vascular bed of DOCA-salt hypertensive rats.
Vascular capacitance is reduced by endothelin-1 (ET-1) in deoxycorticosterone (DOCA)-salt hypertensive rats. This may contribute to hypertension development. Because the splanchnic blood vessels (especially veins) are important in determining vascular capacitance, we tested the hypothesis that ET-1 levels in the splanchnic vasculature are elevated in hypertensive DOCA-salt compared with normotensive rats. Tissue ET-1 content was measured by ELISA in aorta, vena cava, superior mesenteric artery and vein, and small mesenteric arteries and veins from normotensive sham-operated (sham) and 4-wk DOCA-salt rats. We also determined ET-1 concentration in aortic and portal venous blood (draining the nonhepatic splanchnic organs) in anesthetized and conscious sham and DOCA-salt rats before and after acute blockade of ETB receptor-mediated plasma clearance of ET-1. Results showed a higher ET-1 content in veins than in arteries of similar size. However, ET-1 content was similar in vessels from sham and DOCA-salt rats, except in aorta and superior mesenteric artery, where ET-1 content was greater in DOCA-salt rats. ET-1 concentration was significantly higher in portal venous than in aortic blood, indicating net nonhepatic splanchnic release (nNHSR) of ET-1. However, nNHSR of ET-1 was similar in sham and DOCA-salt rats. Although nNHSR of ET-1 increased significantly after ETB receptor blockade in sham rats, it was completely unchanged in DOCA-salt rats. These data suggest that, despite the absence of ETB receptor-mediated plasma clearance of ET-1, neither the venous peptide content nor the net release of ET-1 is increased in the splanchnic vasculature of DOCA-salt rats. These results argue against the hypothesis that increased venomotor tone in DOCA-salt hypertension is caused by increased ET-1 concentration around splanchnic venous smooth muscle cells.
Anesthesia↗
Catecholaminergic regulation of venous function in the rainbow trout.
The significance of the sympathetic nervous system (SNS) in regulating peripheral vascular resistance and cardiac function in fish has been well established, whereas its effect on venous function in vivo is unknown. Two protocols were employed in the present study to evaluate SNS effects on the venous system in intact, unanesthetized trout. In the first, trout were instrumented with pressure cannulas in the ventral (PVA) and dorsal (PDA) aortas and ductus Cuvier (PVEN), and cardiac output (CO) was measured with a flow probe around the ventral aorta. Heart rate, stroke volume, and gill and systemic resistances were calculated from the measured parameters. In the second group, vascular capacitance curves were obtained by monitoring mean circulatory filling pressure (PVEN) during transient interruption of CO and while blood volume was adjusted between 80 and 120% of normal. Unstressed blood volume (USBV) and vascular compliance (C) were derived from the capacitance curves. Infusion of epinephrine (Epi; 3.3 nmol.min-1.kg body wt-1) increased PVA, PDA, and PVEN, whereas norepinephrine (NE) infusion (3.3 nmol.min-1.kg body wt-1) increased PVA and PDA but did not affect PVEN. Epi (1.0 nmol.min-1.kg body wt-1), but not NE (2.6 or 10.4 nmol.min-1.kg body wt-1), displaced the capacitance curve to the right and significantly decreased USBV. Inhibition of alpha 1-adrenoceptors with prazosin, or ganglionic nicotinic receptor blockade with hexamethonium, produced a left shift in the capacitance curve, and both treatments increased USBV and C. Conversely, the alpha-adrenoceptor antagonist phentolamine did not effect vascular capacitance. These results show that Epi has potent effects on trout veins in vivo and that it mobilizes blood from the unstressed into the stressed vascular compartment and augments central venous pressure by decreasing venous compliance. These results also show that the SNS is an active effector of venous tone and compliance in trout; this is the first demonstration of tonic regulation of vascular capacitance in any fish.
Animals↗
Adaptations of the peripheral circulation to PEEP.
The purpose of this study was to determine the role of changes in the parameters of venous return on the homeostatic adaption to the application of PEEP. We studied 13 dogs anesthetized with alpha-chloralose, intubated, and ventilated. We measured central venous pressure (CVP), arterial pressure (Pao) and cardiac output by thermal dilution. The cardiac output was transiently stopped by inflating a balloon in the right atrium, and the subsequent plateau in the CVP was used to obtain mean circulatory filling pressure (MCFP). Total blood volume was measured with Evans blue. To measure vascular capacitance and compliance, we rapidly infused 4 ml/kg or 8 ml/kg of blood and repeated the MCFP measurement. The same volume was withdrawn after the measurement. The volume and MCFP were used to construct pressure-volume (P-V) lines, and the unstressed volume was calculated by extrapolating the P-V to zero pressure. The P-V appeared linear in the range studied. PEEP produced a left shift of the curves and, thus, a decrease in unstressed volume. The shift with 20 cm H2O of PEEP was greater than with 10 cm H2O of PEEP. The rise in MCFP matched the rise in CVP so that the pressure gradient for venous return did not change. However, there was also an increase in the resistance to venous return, which resulted in a lower cardiac output than expected for the rise in MCFP. In conclusion, homeostatic adjustments to PEEP included a decrease in vascular capacitance, which is partially offset by a rise in the resistance to venous return.
Adaptation, Physiological↗
Protective effect of physical training on cardiovascular responses to hemorrhagic hypotension and shock.
The primary objective of this study was to determine if a measurable degree of protective cardiovascular adaptation to hypovolemic shock is developed in response to aerobic training. Twelve rats were trained (T) by running on a rodent treadmill 60 min/day, 5 days/wk at 30 m/min on a 5 degree incline for a period of 13-17 weeks. Elevated levels of SDH activity in the vastus intermedius muscles of the trained group (T) verified physiological training. Each T rat was weight matched with a sedentary untrained (UT) control, anesthetized with sodium pentobarbital, and subjected to a modified Wiggers hemorrhagic shock protocol. The parameters monitored were the maximum reduction in vascular capacitance (ie, maximum blood shed) when MAP was lowered to 30 mm Hg by hemorrhage; the time necessary to achieve maximum blood loss at 30 mm Hg (compensation time); and the time between maximum and 20% uptake of the shed volume from the reservoir (decompensation time). The data show that the initial MAPs for the UT group were significantly higher than the T group (133 +/- 3 mm Hg vs 121 +/- 4 mm Hg). The maximum blood loss normalized to body weight and pressure drop was .268 +/- .012 ml/kg/mm Hg for UT and .343 +/- .02 ml/kg/mm Hg for T (P less than .001), suggesting that T had a better ability to reduce total vascular capacitance. Also, both the compensation and decompensation times were greater in the T than UT groups. These data suggest that treadmill exercise-conditioned rats have a greater inherent cardiovascular compensatory ability than untrained rats.
Animals↗
Carotid sinus baroreceptor reflex control of venular pressure-diameter relations in rat intestine.
We tested the hypothesis that the venules of the small intestinal muscle are responsible for decreases in vascular capacitance during bilateral carotid artery occlusion. We measured microvascular venular pressure and diameter relations in 135 vessels during both control and baroreflexive conditions (bilateral carotid occlusion). Microvascular pressure was measured using a servo-null pressure system, and diameters were obtained from a video-monitoring system with a total magnification of X1,000. First-, second-, and fourth-order microvenules were studied in rat small intestinal muscle. The vessels showed an average diameter decrease of 11-12% and an increased stiffness or pressure-diameter slope of 31-53% during bilateral occlusion. We also tested whether the observed constriction during bilateral occlusion was caused by an increase in the sympathetic nerve activity to the venules and/or increased hormonal release via the baroreflex system. We studied an additional 22 microvenules before and after denervation of the preparation. Denervation eliminated any significant change in diameter or stiffness during bilateral occlusion. Based on our data, we conclude that the changes in the venular properties observed during bilateral occlusion are due to the increased sympathetic nerve activity resulting from decreased carotid sinus pressure. Intestinal venules can actively constrict to change vascular capacitance during bilateral carotid occlusion.
Animals↗