Circulatory responses to a CO2 buffer following lethal injections of endotoxin

1961 ◽  
Vol 200 (4) ◽  
pp. 751-754 ◽  
Author(s):  
Lerner B. Hinshaw ◽  
James A. Vick ◽  
David L. Nelson ◽  
Lorentz E. Wittmers ◽  
Orville P. Swenson
Keyword(s):  
Vascular Resistance ◽  
Total Peripheral Resistance ◽  
Venous Return ◽  
Intact Animal ◽  
Peripheral Resistance ◽  
Tissue Fluid ◽  
Vascular Effect ◽  
Arterial Inflow ◽  
Prolonged Hypotension ◽  
Total Body

The circulatory actions of a CO2 buffer (THAM) have been studied in the isolated perfused dog leg and kidney and in the intact dog. Techniques involving controlled arterial inflow were used in order that changes in vascular resistance could be calculated. Changes in organ weight were correlated with alterations in vascular resistance and hematocrit. Cardiac inflow was controlled and monitored in total body perfusion experiments in order that total peripheral resistance calculations and changes in venous return could be readily obtained. The infusion of THAM results in marked decreases in vascular resistance of leg, kidney and the totally perfused intact animal. Following the onset of THAM infusion there is a significant increase in venous return, brought about primarily by the reabsorption of tissue fluid. The vascular effect of THAM on the kidney may account for the profound diuretic action, although its use during prolonged hypotension appears to be detrimental. The findings of the present study indicate that the possible uses of THAM in hypertension and edema are worthy of investigation.

RSR-13, an allosteric effector of hemoglobin, increases systemic and iliac vascular resistance in rats

1996 ◽  
Vol 271 (2) ◽  
pp. H602-H613 ◽  
Author(s):  
M. P. Kunert ◽  
J. F. Liard ◽  
D. J. Abraham
Keyword(s):  
Cardiac Output ◽  
Vascular Resistance ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Experimental Models ◽  
Metabolic Demand ◽  
Flow Probe ◽  
Inositol Hexaphosphate ◽  
Control Value ◽  
Allosteric Effector

Tissue O2 delivery in excess of metabolic demand may be a factor in the development of high vascular resistance in experimental models of volume-expanded hypertension. This hypothesis was previously tested in rats with an exchange transfusion of red blood cells treated with inositol hexaphosphate or an intravenous infusion of RSR-4, allosteric effectors of hemoglobin. The binding of these drugs with hemoglobin effect a conformational change in the molecule, such that the affinity for O2 is reduced. However, in both preparations, the changes in vascular resistance could have been nonspecific. The present studies used intravenous infusions of RSR-13, which did not share some of the problematic characteristics of RSR-4 and inositol hexaphosphate. Conscious instrumented rats (an electromagnetic flow probe on ascending aorta or an iliac, mesenteric, or renal Doppler flow probe) were studied for 6 h after an RSR-13 infusion of 200 mg/kg in 15 min. This dose significantly increased arterial P50 (PO2 at which hemoglobin is 50% saturated) from 38 +/- 0.8 to 58 +/- 1.4 mmHg at 1 h after the start of the infusion. In the 3rd h cardiac output fell significantly from a control value of 358 +/- 33 to 243 +/- 24 ml.kg-1.min-1 and total peripheral resistance significantly increased from 0.31 +/- 0.03 to 0.43 +/- 0.04 mmHg.ml-1.kg.min. Cardiac output and P50 returned toward control over the next few hours. Neither cardiac output nor total peripheral resistance changed in the group of rats receiving vehicle alone. In a separate group of rats, iliac flow decreased significantly to 60% of control and iliac resistance increased to 160% of control. Iliac flow increased significantly in the group of rats that received vehicle only. Although the mechanism of these changes has not been established, these results suggest that a decreased O2 affinity leads to an increased total peripheral resistance and regional vascular resistance and support the hypothesis that O2 plays a role in the metabolic autoregulation of blood flow.

Atrial natriuretic peptide increases resistance to venous return in rats

1987 ◽  
Vol 252 (5) ◽  
pp. H894-H899 ◽  
Author(s):  
Y. W. Chien ◽  
E. D. Frohlich ◽  
N. C. Trippodo
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Total Peripheral Resistance ◽  
Venous Return ◽  
Venous Pressure ◽  
Peripheral Resistance ◽  
Atrial Natriuretic

To examine mechanisms by which administration of atrial natriuretic peptide (ANP) decreases venous return, we compared the hemodynamic effects of ANP (0.5 microgram X min-1 X kg-1), furosemide (FU, 10 micrograms X min-1 X kg-1), and hexamethonium (HEX, 0.5 mg X min-1 X kg-1) with those of vehicle (VE) in anesthetized rats. Compared with VE, ANP reduced mean arterial pressure (106 +/- 4 vs. 92 +/- 3 mmHg; P less than 0.05), central venous pressure (0.3 +/- 0.3 vs. -0.7 +/- 0.2 mmHg; P less than 0.01), and cardiac index (215 +/- 12 vs. 174 +/- 10 ml X min-1 X kg-1; P less than 0.05) and increased calculated resistance to venous return (32 +/- 3 vs. 42 +/- 2 mmHg X ml-1 X min X g; P less than 0.01). Mean circulatory filling pressure, distribution of blood flow between splanchnic organs and skeletal muscles, and total peripheral resistance remained unchanged. FU increased urine output similar to that of ANP, yet produced no hemodynamic changes, dissociating diuresis, and decreased cardiac output. HEX lowered arterial pressure through a reduction in total peripheral resistance without altering cardiac output or resistance to venous return. The results confirm previous findings that ANP decreases cardiac output through a reduction in venous return and suggest that this results partly from increased resistance to venous return and not from venodilation or redistribution of blood flow.

Venous Pressure and Total Peripheral Resistance in the Dog

1958 ◽  
Vol 192 (3) ◽  
pp. 609-612 ◽  
Author(s):  
Raymond C. Read ◽  
Hiroshi Kuida ◽  
John A. Johnson
Keyword(s):  
Blood Flow ◽  
Total Peripheral Resistance ◽  
Venous Pressure ◽  
Peripheral Resistance ◽  
Classical View ◽  
Total Body

The techniques of total body perfusion have been applied to the problem of the influence of venous distension on resistance to blood flow. The results obtained support the classical view that a rise in venous pressure leads to a fall in total peripheral resistance. The possibility of a venivasomotor constrictor reflex occurring in certain parts of the circulation was not excluded by these studies.

Microvascular rarefaction and tissue vascular resistance in hypertension

1989 ◽  
Vol 256 (1) ◽  
pp. H126-H131 ◽  
Author(s):  
A. S. Greene ◽  
P. J. Tonellato ◽  
J. Lui ◽  
J. H. Lombard ◽  
A. W. Cowley
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Flow Distribution ◽  
Cheek Pouch ◽  
Tissue Blood Flow ◽  
Hamster Cheek Pouch ◽  
Relative Contribution ◽  
Microvascular Rarefaction

The purpose of this study was to quantitatively estimate the relative contribution of arteriolar rarefaction (disappearance of microvessels) and arteriolar constriction to the increases in total peripheral resistance and changes in the patterns of flow distribution observed in hypertension. A mathematical model of the hamster cheek pouch intraluminal microcirculation was constructed based on data from the literature and observations from our own laboratory. Separate rarefaction and constriction of third-order (3A) and fourth-order (4A) arterioles were performed on the model, and the results were quantified based on the changes of the computed vascular resistance. The degree of increase in resistance depended both on the number and the order of vessels rarefied or constricted and also on the position of those vessels in the network. The maximum increases in resistance obtained in the model runs were 21% for rarefaction and 75% for constriction. Rarefaction, but not constriction, produced large increases in the degree of heterogeneity of blood flow in the various vessel orders. These results demonstrate that vessel rarefaction significantly influences tissue blood flow resistance to a degree comparable with vessel constriction; however, unlike constriction, microvascular rarefaction markedly altered blood flow distribution in our model of the hamster cheek pouch vascular bed. These findings conform with the hypothesis that a significant component of the increase in total peripheral resistance in hypertension may be due to vessel rarefaction.

Dose–response effects of cardiac glycosides on pooling and systemic and pulmonary hemodynamics

1970 ◽  
Vol 48 (8) ◽  
pp. 533-541 ◽  
Author(s):  
Linda T. Archer ◽  
Lerner B. Hinshaw
Keyword(s):  
Cardiac Glycosides ◽  
Venous Return ◽  
Intact Animal ◽  
Peripheral Resistance ◽  
Major Site ◽  
Pulmonary Hemodynamics ◽  
Relationship Of ◽  
The Relationship ◽  
Major Emphasis ◽  
Vascular Region

The effects of ouabain and digoxin on systemic and cardiopulmonary circulations and the degree and site of vascular pooling were evaluated in this study. A major emphasis was placed on the relationship of dosage to responses observed. Experiments were performed on 32 adult mongrel dogs using a venous return (constant cardiac inflow) preparation. Animals were divided into two groups, intact and eviscerated. Mean cumulative doses were 27, 55, and 81 μg/kg for intact ouabain-injected dogs; 21, 42, 63, 84, and 105 μg/kg for intact digoxin-injected dogs; and 26, 52, and 77 μg/kg for eviscerated ouabain-injected dogs. There was a positive correlation between amount of blood pooled and dose of cardiac glycosides given in the intact animal. The statistical difference in pooling at each dose of ouabain between intact and eviscerated animals implicated the hepatosplanchnic vascular bed as a major site of pooling. Since there was a significant statistical increase in total peripheral resistance in intact ouabain-injected dogs but not in ouabain-treated eviscerated animals, the site of peripheral resistance changes appears to be the hepatosplanchnic vascular region. Left atrial pressures rose significantly in intact and eviscerated dogs at higher ouabain doses. These findings underscore the complexity of the mechanisms of action of cardiac glycosides and emphasize the critical importance of dosage, type of glycoside administered, and individual variation of response in the canine species.

scholarly journals Hemodynamic variables in piglets anesthetized with isoflurane or propofol, kept under spontaneous ventilation and FIO2 of 0.5

2019 ◽  
Vol 71 (6) ◽  
pp. 1846-1852
Author(s):  
C.K. Ido ◽  
P.E.S. Silva ◽  
H.R.A. Silva ◽  
E.G.F. Biteli ◽  
R.L. Carneiro ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Total Peripheral Resistance ◽  
Venous Pressure ◽  
Peripheral Resistance ◽  
Resistance Index ◽  
Spontaneous Ventilation ◽  
Stroke Index ◽  
Hemodynamic Variables

ABSTRACT This study aimed to evaluate comparatively the effects of propofol or isoflurane on hemodynamic variables in piglets that received inspired oxygen fraction (FIO2) of 0.5 under spontaneous ventilation. Therefore, sixteen piglets weighing 16±1.1kg, were randomly divided into two groups: GI (Isoflurane and FIO2 of 0.5) and GP (Propofol and FIO2 of 0.5). Heart rate (HR), systolic, diastolic and mean arterial pressure (SAP, DAP and MAP), central venous pressure (CVP), cardiac output (CO), mean pulmonary arterial pressure (mPAP) and mean capillary pulmonary pressure (mCPP) were assessed 40 minutes after anesthetic induction (T0), followed by 15 minutes intervals (from T15 to T60). The variables cardiac index (CI), stroke volume (SV), stroke index (SI), total peripheral resistance (TPR), total peripheral resistance index (TPRI), pulmonary vascular resistance (PVR), and pulmonary vascular resistance index (PVRI) were calculated. SAP and TPRI were significantly different between groups at T30 and T60 (P< 0.05) with higher GP values being recorded. There were no differences in the other variables, however, GP presented mean closer to normality on most of the analyzed variables. Therefore, we conclude that total intravenous anesthesia with propofol presented greater stability of the hemodynamic variables evaluated.

Angiotensin II: nitric oxide interaction and the distribution of blood flow

1993 ◽  
Vol 265 (6) ◽  
pp. R1276-R1283 ◽  
Author(s):  
D. H. Sigmon ◽  
W. H. Beierwaltes
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Angiotensin Ii ◽  
Vascular Resistance ◽  
Total Peripheral Resistance ◽  
Pressor Response ◽  
Peripheral Resistance ◽  
Conscious Rats

Nitric oxide (NO) contributes to the regulation of regional blood flow. Inhibition of NO synthesis increases blood pressure and vascular resistance. Using radioactive microspheres and the substrate antagonist N omega-nitro-L-arginine methyl ester (L-NAME) (10 mg/kg) to block NO synthesis, we tested the hypothesis that there is a significant interaction between the vasodilator NO and the vasoconstrictor angiotensin II, which regulates regional hemodynamics. Further, we investigated the influence of anesthesia on this interaction. L-NAME increased blood pressure, decreased cardiac output, and increased total peripheral resistance in both anesthetized and conscious rats. In anesthetized rats, L-NAME decreased blood flow to visceral organs (i.e. kidney, intestine, and lung) but had little effect on blood flow to the brain, heart, or hindlimb. Treating anesthetized rats with the angiotensin II receptor antagonist losartan (10 mg/kg) attenuated the decrease in cardiac output and the increase in total peripheral resistance without affecting the pressor response to L-NAME. Losartan also attenuated the visceral hemodynamic responses to L-NAME. In conscious rats, L-NAME decreased blood flow to all organ beds. Treating these rats with losartan only marginally attenuated the increase in total peripheral resistance to L-NAME without significantly affecting the pressor response or the decrease in cardiac output. Losartan had no effect on the regional hemodynamic responses to L-NAME. These data suggest that NO-mediated vascular relaxation is an important regulator of total peripheral and organ vascular resistance. (ABSTRACT TRUNCATED AT 250 WORDS)

Hemodynamics of obesity: influence of pattern of adipose tissue cellularity

1986 ◽  
Vol 251 (2) ◽  
pp. R314-R319
Author(s):  
D. L. Crandall ◽  
B. M. Goldstein ◽  
F. H. Lizzo ◽  
R. A. Gabel ◽  
P. Cervoni
Keyword(s):  
Blood Flow ◽  
Adipose Tissue ◽  
Vascular Resistance ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Tissue Expansion ◽  
Cellular Hypertrophy ◽  
Obese Rats ◽  
Hemodynamic Profile ◽  
Regional Vascular Resistance

Direct quantitation of blood flow with radioactive microspheres in conscious spontaneously obese rats indicated that the development of obesity was associated with an elevated cardiac output and stroke volume, a normotensive blood pressure, and a reduced total peripheral resistance when directly comparing obese rats with their lean counterparts. Obesity was also associated with increased blood flow and decreased regional vascular resistance in a variety of vascular beds, whereas cardiac index and total peripheral resistance per unit of body weight were similar between groups. When corrected for tissue weight, unique alterations in flow and resistance were observed in the adipose tissue. When expressed as resistance per organ, the greatest relative alterations in vascular resistance with the development of obesity also occurred in the adipose tissue. Furthermore, localized adipose tissue expansion through cellular hypertrophy was consistently associated with a different pattern of blood flow and vascular resistance than adipose tissue that expanded through both cellular hypertrophy and hyperplasia, implying an association between depot cellularity and its hemodynamic profile.

scholarly journals Effects of postural changes and removal of vestibular inputs on blood flow to and from the hindlimb of conscious felines

2009 ◽  
Vol 297 (6) ◽  
pp. R1777-R1784 ◽  
Author(s):  
K. J. Yavorcik ◽  
D. A. Reighard ◽  
S. P. Misra ◽  
L. A. Cotter ◽  
S. P. Cass ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Femoral Artery ◽  
Venous Return ◽  
Peripheral Resistance ◽  
Postural Changes ◽  
Femoral Artery Blood Flow ◽  
Before And After ◽  
Arterial Inflow ◽  
Regulation Of Blood Pressure

Considerable data show that the vestibular system contributes to blood pressure regulation. Prior studies reported that lesions that eliminate inputs from the inner ears attenuate the vasoconstriction that ordinarily occurs in the hindlimbs of conscious cats during head-up rotations. These data led to the hypothesis that labyrinthine-deficient animals would experience considerable lower body blood pooling during head-up postural alterations. The present study tested this hypothesis by comparing blood flow though the femoral artery and vein of conscious cats during 20–60° head-up tilts from the prone position before and after removal of vestibular inputs. In vestibular-intact animals, venous return from the hindlimb dropped considerably at the onset of head-up tilts and, at 5 s after the initiation of 60° rotations, was 66% lower than when the animals were prone. However, after the animals were maintained in the head-up position for another 15 s, venous return was just 33% lower than before the tilt commenced. At the same time point, arterial inflow to the limb had decreased 32% from baseline, such that the decrease in blood flow out of the limb due to the force of gravity was precisely matched by a reduction in blood reaching the limb. After vestibular lesions, the decline in femoral artery blood flow that ordinarily occurs during head-up tilts was attenuated, such that more blood flowed into the leg. Contrary to expectations, in most animals, venous return was facilitated, such that no more blood accumulated in the hindlimb than when labyrinthine signals were present. These data show that peripheral blood pooling is unlikely to account for the fluctuations in blood pressure that can occur during postural changes of animals lacking inputs from the inner ear. Instead, alterations in total peripheral resistance following vestibular dysfunction could affect the regulation of blood pressure.

Relative importance of venous and arterial resistances in controlling venous return and cardiac output

1959 ◽  
Vol 196 (5) ◽  
pp. 1008-1014 ◽  
Author(s):  
Arthur C. Guyton ◽  
Berry Abernathy ◽  
Jimmy B. Langston ◽  
Berwind N. Kaufmann ◽  
Hilton M. Fairchild
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Total Peripheral Resistance ◽  
Venous Return ◽  
Peripheral Resistance ◽  
Systemic Arterial Pressure ◽  
Cardiovascular Reflexes ◽  
Marked Rise ◽  
Arterial Resistance ◽  
Venous Resistance

In dogs with cardiovascular reflexes completely blocked by total spinal anesthesia, the total peripheral resistance was increased five- or more fold in two ways: first, by injecting small plastic microspheres into the arteries, thereby increasing the arterial resistance, and, second, by inflating pneumatic cuffs around the major veins, thereby increasing venous resistance. A small increase in venous resistance decreased cardiac output eight times as much as an increase in arterial resistance of similar magnitude. This difference was caused principally by a) a marked rise in systemic arterial pressure when arterial resistance was increased; this maintained the cardiac output at almost normal levels and b) a fall in systemic arterial pressure when venous resistance was increased; this promoted even more fall in cardiac output than increased total peripheral resistance alone would have caused.

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