Vascular capacitance responses to hypercapnia of the vascularly isolated head

1986 ◽  
Vol 251 (1) ◽  
pp. H164-H170 ◽  
Author(s):  
M. L. Gaddis ◽  
C. L. MacAnespie ◽  
C. F. Rothe
Keyword(s):  
Peripheral Resistance ◽  
Systemic Circulation ◽  
Systemic Arterial Pressure ◽  
Filling Pressure ◽  
Whole Body ◽  
Mean Circulatory Filling Pressure ◽  
Vascular Capacitance ◽  
Carotid Bodies ◽  
The Brain ◽  
Stimulation Of

Hypercapnic stimulation of the brain may account for some of the decrease in vascular capacitance (venoconstriction) seen with whole-body hypercapnia. Six mongrel dogs were anesthetized with alpha-chloralose and paralyzed with pancuronium bromide. The vagi were cut and the carotid bodies and sinuses were denervated. The head circulation was isolated and perfused with normoxic [arterial partial pressure of O2 (Pao2) = 112 mmHg], normocapnic (PaCO2 = 40 mmHg) blood, or one of three levels of normoxic, hypercapnic (PaCO2 = 56, 68, or 84 mmHg) blood. A membrane oxygenator was used to change gas tensions in the perfusate blood. The systemic circulation received normoxic, normocapnic blood (Pao2 = 107 mmHg; PaCO2 = 32 mmHg). Systemic arterial pressure increased from 111 to 134 mmHg, and heart rate decreased from 174 to 150 beats/min with a head blood PaCO2 of 84 mmHg. Central blood volume was not affected by head hypercapnia. Cardiac output significantly decreased only with a head blood PaCO2 of 84 mmHg. Mean circulatory filling pressure increased by 0.014 mmHg/1 mmHg increase in head PaCO2. The sensitivity of the total peripheral resistance to cephalic blood hypercapnia was 0.88%/mmHg, whereas that for the mean circulatory filling pressure was only 0.19%/mmHg. We conclude that stimulation of the brain, via perfusion of the head with hypercapnic blood, causes a small but significant increase in mean circulatory filling pressure, due to systemic venoconstriction.

Reflex control of vascular capacitance during hypoxia, hypercapnia, or hypoxic hypercapnia

1990 ◽  
Vol 68 (3) ◽  
pp. 384-391 ◽  
Author(s):  
Carl F. Rothe ◽  
A. Dean Flanagan ◽  
Roberto Maass-Moreno
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Systemic Arterial Pressure ◽  
Filling Pressure ◽  
Venous Tone ◽  
Mean Circulatory Filling Pressure ◽  
Vascular Capacitance ◽  
The Mean

We tested the hypothesis that the changes in venous tone induced by changes in arterial blood oxygen or carbon dioxide require intact cardiovascular reflexes. Mongrel dogs were anesthetized with sodium pentobarbital and paralyzed with veruronium bromide. Cardiac output and central blood volume were measured by indocyanine green dilution. Mean circulatory filling pressure, an index of venous tone at constant blood volume, was estimated from the central venous pressure during transient electrical fibrillation of the heart. With intact reflexes, hypoxia (arterial Pao2 = 38 mmHg), hypercapnia (Paco2 = 72 mmHg), or hypoxic hypercapnia (Pao2 = 41; Paco2 = 69 mmHg) (1 mmHg = 133.32 Pa) significantly increased the mean circulatory filling pressure and cardiac output. Hypoxia, but not normoxic hypercapnia, increased the mean systemic arterial pressure and maintained the control level of total peripheral resistance. With reflexes blocked with hexamethonium and atropine, systemic arterial pressure supported with a constant infusion of norepinephrine, and the mean circulatory filling pressure restored toward control with 5 mL/kg blood, each experimental gas mixture caused a decrease in total peripheral resistance and arterial pressure, while the mean circulatory filling pressure and cardiac output were unchanged or increased slightly. We conclude that hypoxia, hypercapnia, and hypoxic hypercapnia have little direct influence on vascular capacitance, but with reflexes intact, there is a significant reflex increase in mean circulatory filling pressure.Key words: cardiovascular reflex, vascular capacitance, hypoxia, hypercapnia, mean circulatory filling pressure, venoconstriction.

Role of β-adrenergic agonists in the control of vascular capacitance

1990 ◽  
Vol 68 (5) ◽  
pp. 575-585 ◽  
Author(s):  
Carl F. Rothe ◽  
A. Dean Flanagan ◽  
Roberto Maass-Moreno
Keyword(s):  
Cardiac Output ◽  
Blood Volume ◽  
Peripheral Resistance ◽  
Filling Pressure ◽  
Adrenergic Agonists ◽  
Adrenergic Agonist ◽  
Central Venous ◽  
Mean Circulatory Filling Pressure ◽  
Vascular Capacitance

The role of β-adrenergic agonists, such as isoproterenol, on vascular capacitance is unclear. Some investigators have suggested that isoproterenol causes a net transfer of blood to the chest from the splanchnic bed. We tested this hypothesis in dogs by measuring liver thickness, cardiac output, cardiopulmonary blood volume, mean circulatory filling pressure, portal venous, central venous, pulmonary arterial, and systemic arterial pressures while infusing norepinephrine (2.6 μg∙min−1∙kg−1), or isoproterenol (2.0 μg∙min−1∙kg−1), or histamine (4 μg∙min−1∙kg−1), or a combination of histamine and isoproterenol. Norepinephrine (an α- and β1-adrenergic agonist) decreased hepatic thickness and increased mean circulatory filling pressure, cardiac output, cardiopulmonary blood volume, total peripheral resistance, and systemic arterial and portal pressures. Isoproterenol increased cardiac output and decreased total peripheral resistance, but it had little effect on liver thickness or mean circulatory filling pressure and did not increase the cardiopulmonary blood volume or central venous pressure. Histamine caused a marked increase in portal pressure and liver thickness and decreased cardiac output, but it had little effect on the estimated mean circulatory filling pressure. Isoproterenol during histamine infusions reduced histamine-induced portal hypertension, reduced liver size, and increased cardiac output. We conclude that the β-adrenergic agonist, isoproterenol, has little influence on vascular capacitance or liver volume of dogs, unless the hepatic outflow resistance is elevated by agents such as histamine.Key words: β-adrenergic agonists, vascular capacitance, mean circulatory filling pressure, isoproterenol, histamine, liver sphincters.

scholarly journals The spleen is required for 5-HT1A receptor agonist-mediated increases in mean circulatory filling pressure during hemorrhagic shock in the rat

2009 ◽  
Vol 296 (5) ◽  
pp. R1392-R1401 ◽  
Author(s):  
Ruslan Tiniakov ◽  
Karie E. Scrogin
Keyword(s):  
Metabolic Acidosis ◽  
Hemorrhagic Shock ◽  
Receptor Agonist ◽  
Blood Gases ◽  
Filling Pressure ◽  
Whole Body ◽  
Acid Base Balance ◽  
Acid Base ◽  
Mean Circulatory Filling Pressure ◽  
Base Balance

The 5-HT1A receptor agonist, 8- OH-DPAT, increases whole body venous tone (mean circulatory filling pressure; MCFP), and attenuates metabolic acidosis in a rat model of unresuscitated hemorrhagic shock. To determine whether improved acid-base balance was associated with sympathetic activation and venous constriction, MCFP, sympathetic activity (SA), and blood gases were compared in hemorrhaged rats following administration of 5-HT1A receptor agonist 8-OH-DPAT, the arterial vasoconstrictor arginine vasopressin (AVP), or saline. To further determine whether protection of acid-base balance was dependent on splenic contraction and blood mobilization, central venous pressure (CVP), MCFP, and blood gases were determined during hemorrhage and subsequent 8-OH-DPAT-administration in rats subjected to real or sham splenectomy. Subjects were hemorrhaged to an arterial pressure of 50 mmHg for 25 min and subsequently were treated with 8-OH-DPAT (30 nmol/kg iv), AVP titrated to match the pressor effect of 8-OH-DPAT (∼2 ng/min iv), or infusion of normal saline. 8-OH-DPAT increased MAP, CVP, MCFP, and SA, and decreased lactate accumulation. AVP did not affect CVP or SA, but raised MCFP slightly to a level intermediate between 8-OH-DPAT- and saline-treated rats. Infusion of AVP also produced a modest protection against metabolic acidosis. Splenectomy prevented the rise in CVP, MCFP, and protection against metabolic acidosis produced by 8-OH-DPAT but had no effect on the immediate pressor response to the drug. Together, the data indicate that 8-OH-DPAT produces a pattern of cardiovascular responses consistent with a sympathetic-mediated venoconstriction that is, in part, responsible for the drug's beneficial effect on acid-base balance. Moreover, blood mobilization stimulated by the spleen is required for the beneficial effects of 8-OH-DPAT.

Central Vasomotor Stimulation by Angiotensin

1970 ◽  
Vol 39 (2) ◽  
pp. 239-245 ◽  
Author(s):  
C. M. Ferrario ◽  
C. J. Dickinson ◽  
J. W. McCubbin
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Internal Carotid ◽  
Peripheral Resistance ◽  
Systemic Arterial Pressure ◽  
Direct Stimulation ◽  
Vertebral Arteries ◽  
Reflex Bradycardia ◽  
The Difference ◽  
Stimulation Of

1. When angiotensin was infused at low rates into the vertebral arteries of anaesthetized dogs, it raised the blood pressure. When infused at similar rates intravenously or into the internal carotid artery it either did not change blood pressure, or raised it only very slightly. The difference in response was highly significant over the range of 1–50 ng kg−1 min−1. 2. During intravenous infusion at higher rates, angiotensin usually produced the well-known reflex bradycardia and fall of cardiac output, but on infusion into the vertebral arteries it rapidly raised systemic arterial pressure, often increased heart rate, and usually produced a transient increase of cardiac output. 3. Angiotensin by both routes raised peripheral resistance, but noradrenaline, by contrast, produced the same response whether it was given into the vertebral arteries or into a vein. 4. These observations suggest that part of the pressor effect of intravenous angiotensin may be mediated by a direct stimulation of some part of the hind brain.

Evaluation of whole body autoregulation in conscious dogs

1988 ◽  
Vol 255 (1) ◽  
pp. H44-H52 ◽  
Author(s):  
P. J. Metting ◽  
J. R. Strader ◽  
S. L. Britton
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Peripheral Resistance ◽  
Systemic Circulation ◽  
Aortic Pressure ◽  
Conscious Dogs ◽  
Whole Body ◽  
Pharmacological Blockade ◽  
The Relationship

The ability of the systemic circulation to maintain cardiac output during decreases in arterial pressure was evaluated in conscious dogs with intact reflexes (n = 8) and during pharmacological blockade of the autonomic nervous system, angiotensin II formation, and arginine vasopressin (n = 6). Cardiac output was measured electromagnetically, and aortic pressure was controlled via a gravity reservoir connected to a carotid artery. When aortic pressure was decreased in either small steps to approximately 60% of control, or decreased in a single square-wave step to 75% of control and maintained for 2 h, cardiac output decreased to the same or a greater extent in both control and areflexic dogs. Thus total peripheral resistance did not decrease, and autoregulation of the cardiac output did not occur in response to short-term (less than or equal to 2 h) decreases in arterial pressure, even in the absence of the major pressor systems. After long-term (greater than 8 h) decreases in arterial pressure to 75% of control in five dogs with all reflexes intact, significant autoregulation of the cardiac output occurred. The relationship between the gain of blood flow autoregulation and the corresponding values of mixed venous oxygen tension suggests that whole body autoregulation results when oxygen extraction reserve becomes limited.

Vascular compliance and mean circulatory filling pressure in trout: effects of ACE inhibition

1995 ◽  
Vol 268 (5) ◽  
pp. H1814-H1820 ◽  
Author(s):  
Y. Zhang ◽  
E. Jenkinson ◽  
K. R. Olson
Keyword(s):  
Blood Volume ◽  
Ace Inhibition ◽  
Filling Pressure ◽  
Whole Body ◽  
Mean Circulatory Filling Pressure ◽  
Vascular Compliance ◽  
Cardiac Fibrillation ◽  
Arterial Blood ◽  
Zero Flow

Mean circulatory filling pressure (MCFP), whole body vascular compliance (C), and unstressed blood volume (USV) are important indexes of cardiovascular function in mammals, but they have not been measured in fish. In the present experiments, dorsal aortic (PDA) and sinus venosus (PSV) pressures were measured in unanesthetized trout before and during electrical cardiac fibrillation, while blood volume (BV) was manipulated between 50 and 150% of normal. Measurements were repeated after angiotensin-converting enzyme (ACE) inhibition with lisinopril. Cardiac fibrillation (zero-flow condition) rapidly (approximately 5 s) dropped PDA and increased PSV (equals MCFP). MCFP in normovolemic trout (4.8 +/- 0.3 mmHg) varied directly with BV. C determined from in vivo capacitance curves was similar to that obtained gravimetrically, in vitro (3.4 and 3.5 ml.mmHg-1.kg body wt-1, respectively). USV was 13.3 ml/kg body wt (approximately 45% of BV). ACE inhibition reduced PDA in unfibrillated trout at all BV and reduced PDA in fibrillated fish at BV > or = 80%. ACE inhibition did not affect PSV, MCFP, C, or USV. The systemic arteriovenous pressure gradient at zero flow (delta PF0) was greatest at 100% BV (8.2 +/- 0.5 mmHg) and was reduced by ACE inhibition at 80-120% BV. These results show that key indexes of venous function are readily measured in fish and that the trout venous system is not an effector of angiotensin-mediated regulation of arterial blood pressure. Thus angiotensin acts solely on arterial resistance vessels. Furthermore, the drop in delta PF0 during ACE inhibition is due to a decrease in arteriolar resistance.

Correlation between ventilatory and cerebrovascular responses to inhalation of CO

1977 ◽  
Vol 43 (3) ◽  
pp. 455-462 ◽  
Author(s):  
D. D. Doblar ◽  
T. V. Santiago ◽  
N. H. Edelman
Keyword(s):  
Statistical Significance ◽  
Venous Blood ◽  
O2 Consumption ◽  
Arterial Blood ◽  
Simultaneous Measurements ◽  
Carotid Bodies ◽  
Rate Of Decline ◽  
O2 Delivery ◽  
The Brain ◽  
Stimulation Of

To study the determinants of carbon monoxide (CO) induced hyperpnea simultaneous measurements were made of carboxyhemoglobin level in arterial blood (HbCO), ventilation (VE), cerebral blood flow (CBF), O2 delivery to the brain (CBF X O2 content of arterial blood), O2 consumption of the brain (CMRO2), and O2 tension in cerebral venous blood (PVO2) during inhalation of 1% CO in 40% O2 by six unanesthetized goats. HbCO increased to 65% in 10 min; VE remained constant until a HbCO level of approximately 50% was reached and then increased abruptly; CBF increased progressively; O2 delivery to the brain and CMRO2 decreased somewhat with CO inhalation; these decreases reached statistical significance at a HbCO level of 30–40% whereupon the rate of decline with respect to HbCO level increased substantially; and PVO2 decreased progressively from an average of from 31 to 14.6 Torr and averaged 19.2 Torr when hyperpnea was manifest. When considered in the light of previous studies which indicate that CO-induced hyperpnea is not caused by stimulation of the carotid bodies, these data suggest that this phenomenon is related to brain hypoxia. Calculations of brain tissue O2 tension with the Krogh equation support this contention.

Graphic format for teaching long-term control of systemic arterial pressure.

1996 ◽  
Vol 270 (6) ◽  
pp. S40
Author(s):  
J J Faber
Keyword(s):  
Cardiac Output ◽  
Steady State ◽  
Arterial Pressure ◽  
Peripheral Resistance ◽  
Systemic Arterial Pressure ◽  
Filling Pressure ◽  
Arterial Blood ◽  
Ventricular Filling Pressure ◽  
Ventricular Filling

Circulatory homeostasis is a difficult notion. The graphic format presented here facilitates the teaching of long-term control of systemic arterial blood pressure and cardiac output. It is based on the view that the following four "function curves" cooperate in long-term regulation: the relation between blood volume and ventricular filling pressure, the relation between ventricular filling pressure and cardiac output, the relation between cardiac output and peripheral resistance, and the relation between arterial pressure and natriuresis. Positioning the function curves in the format presented here clarifies their cooperativity. The distinction between a nonsteady state and a steady state deserves emphasis. Long-term pathophysiology of the circulation is most easily taught on the basis of the assumption that, generally, there will be a steady state. The format clarifies why some known physiological relations are almost impossible to demonstrate in the intact organism, and it discourages explanations of pathophysiology that are not firmly based on physiology.

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