Further Evidence that the Pulmonary Capillary Venous Pressure Pulse in Man Reflects Cyclic Pressure Changes in the Left Atrium

To test the hypothesis that acute changes in plasma volume affect the stimulus-response relations of high- and low-pressure baroreflexes, eight men (27-44 yr old) underwent measurements for carotid-cardiac and cardiopulmonary baroreflex responses under the following three volemic conditions: hypovolemic, normovolemic, and hypervolemic. The stimulus-response relation of the carotid-cardiac response curve was generated using a neck cuff device, which delivered pressure changes between +40 and -65 mmHg in continuous steps of 15 mmHg. The stimulus-response relationships of the cardiopulmonary baroreflex were studied by measurements of forearm vascular resistance (FVR) and peripheral venous pressure (PVP) during low levels of lower body negative pressure (0 to -20 mmHg). Altered vascular volume had no effect on response relations of the carotid-cardiac baroreflex but did alter the gain of the cardiopulmonary baroreflex (-7.93 +/- 1.73, -4.36 +/- 1.38, and -2.56 +/- 1.59 peripheral resistance units/mmHg for hypovolemic, normovolemic, and hypervolemic, respectively) independent of shifts in baseline FVR and PVP. These results indicate greater demand for vasoconstriction for equal reductions in venous pressure during progressive hypovolemia; this condition may compromise the capacity to provide adequate peripheral resistance during severe orthostatic stress. Fluid loading before reentry after spaceflight may act to restore vasoconstrictive capacity of the cardiopulmonary baroreflex but may not be an effective countermeasure against potential post-flight impairment of the carotid-cardiac baroreflex.

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Arterial, Atrial and Venous Pressure Changes in the Presence of an Arteriovenous Fistula

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1951.167.2.426 ◽

1951 ◽

Vol 167 (2) ◽

pp. 426-434 ◽

Cited By ~ 4

Author(s):

J. L. Nickerson ◽

F. W. Cooper ◽

R. Robertson ◽

J. V. Warren

Keyword(s):

Arteriovenous Fistula ◽

Venous Pressure ◽

Pressure Changes

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Localization of intrahepatic portal vascular resistance

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1986.251.3.g375 ◽

1986 ◽

Vol 251 (3) ◽

pp. G375-G381 ◽

Cited By ~ 4

Author(s):

W. W. Lautt ◽

C. V. Greenway ◽

D. J. Legare ◽

H. Weisman

Keyword(s):

Pressure Drop ◽

Portal Vein ◽

Vascular Resistance ◽

Venous Pressure ◽

Vena Cava ◽

Sympathetic Nerves ◽

Hepatic Veins ◽

Pressure Changes ◽

Stimulation Of ◽

Anesthetized Cat

The pressure drop from the portal vein to the vena cava occurs primarily across a postsinusoidal site localized to a narrow segment (less than 0.5 cm) of hepatic veins (roughly 1.5 mm diam) in the anesthetized cat. Portal venous pressure (PVP = 8.9 +/- 0.3 mmHg) and lobar hepatic venous pressure (LVP = 8.7 +/- 0.4 mmHg) are insignificantly different, and pressure changes imposed from the presinusoidal or postsinusoidal side are equally transmitted to both pressure sites. Several types of experiments were done to validate the LVP measurement. The portal vein, hepatic sinusoids, and hepatic veins proximal to the resistance site are all under a similar pressure. Previously reported calculations of hepatic vascular resistance are in error because of incorrect assumptions of sinusoidal pressure and localization of the portal resistance site as presinusoidal. Stimulation of hepatic sympathetic nerves for 3 min caused LVP and PVP to increase equally, showing that the increased "portal" resistance is postsinusoidal across the same region of the hepatic veins that was previously localized as the site of resistance in the basal state.

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Alteration in heart rate response to hemorrhage in conscious dogs with volume overload

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1978.235.4.h422 ◽

1978 ◽

Vol 235 (4) ◽

pp. H422-H428

Author(s):

M. M. LeWinter ◽

J. S. Karliner ◽

J. W. Covell

Keyword(s):

Heart Rate ◽

Central Venous Pressure ◽

Pulse Pressure ◽

Pressure Pulse ◽

Heart Rate Response ◽

Parasympathetic Nervous System ◽

Venous Pressure ◽

Volume Overload ◽

Conscious Dogs ◽

Central Venous

The heart rate response to hemorrhage was studied in conscious dogs before and up to 2 mo after the establishment of volume overload due to systemic arteriovenous (a-v) fistulas. Before a-v fistula, heart rate increased markedly during hemorrhage. When hemorrhage was preceded by dextran infusion, bleeding resulted in a gradual reduction in heart rate. The a-v fistula caused marked increases in resting heart rate, central venous pressure, pulse pressure, and blood volume. During hemorrhage, heart rate initially remained constant, but then declined abruptly from the resting value of 121 +/- 3.7 beats/min to a nadir of 89 +/- 6.5 beats/min (P less than 0.01). Although mean arterial pressure decreased markedly, there was no significant change in pulse pressure, and central venous pressure tended to stabilize with the heart rate decline. The abrupt heart rate decline was prevented by atropine but unaltered by propranolol. The response was observed as early as 5 days after a-v fistula. We conclude that an alteration in the heart rate response to hemorrhage appears early during volume overload. This alteration appears to be reflex in nature and to be mediated by the parasympathetic nervous system.

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Changes in intestinal volume with hemorrhage

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1960.199.3.589 ◽

1960 ◽

Vol 199 (3) ◽

pp. 589-592 ◽

Cited By ~ 3

Author(s):

Paul C. Johnson

Keyword(s):

Small Intestine ◽

Blood Volume ◽

Sympathetic Nerve Activity ◽

Venous Pressure ◽

Volume Changes ◽

Local Pressure ◽

Local Reduction ◽

Pressure Changes ◽

Sympathetic Discharge ◽

Intestinal Weight

The purpose of these experiments was to study the changes in intestinal volume occurring with hemorrhage, utilizing a gravimetric technique which permitted a study of small segments of the intestine. It had been observed previously that intestinal weight often increased in the upper small intestine during hemorrhage, while in the lower small intestine it usually decreased. In studying the latter effect it was found that sympathetic nerve activity and reduction of venous pressure were both important in decreasing intestinal volume. Changes in tonus and local reduction in arterial pressure did not appear to be important. The increase in volume with hemorrhage appeared due to epinephrine discharge from the adrenal medulla since it was eliminated by adrenalectomy. Local pressure changes and alteration of tonus were eliminated as causal factors. It appears that systemic hypotension induces sympathetic discharge which in turn may cause either an increase or a decrease in intestinal blood volume. Sympathetic discharge over the vasoconstrictor fibers reduces blood volume while adrenal medullary secretion increases it. The observed response is apparently a resultant of these two antagonistic effects.

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Changes in the dimensions of the venae cavae

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1959.196.4.741 ◽

1959 ◽

Vol 196 (4) ◽

pp. 741-744 ◽

Cited By ~ 16

Author(s):

Hiroshi Irisawa ◽

Alexander P. Greer ◽

Robert F. Rushmer

Keyword(s):

Venous Pressure ◽

Dimensional Change ◽

Venous Flow ◽

Dimensional Changes ◽

Cyclic Patterns ◽

Venae Cavae ◽

Surgical Conditions ◽

Two Phases ◽

Pressure Changes ◽

Clockwise Hysteresis

In 11 dogs a variable resistance gauge, a bonded strain gauge, or mutual inductance coils were installed on the venae cavae under aseptic surgical conditions so that dimensional changes in unexposed veins could be measured directly. The cyclic patterns of dimensional change resembled inverted images of venous flow records obtained by others. Since some changes in the venous dimensions apparently were not related to pressure, active contraction of the walls may have been responsible. Studies involving infusion and hemorrhage confirmed the existence of two phases in the pressure-diameter relationship correlated with the level of venous pressure. The pattern of diameter and venous pressure changes during transfusion and withdrawal of blood tended to be a clockwise hysteresis loop.

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Differential hemodynamic effects of L-NMMA in endotoxemic and normal dogs

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1995.268.4.h1634 ◽

1995 ◽

Vol 268 (4) ◽

pp. H1634-H1642 ◽

Cited By ~ 4

Author(s):

J. P. Cobb ◽

C. Natanson ◽

Z. M. Quezado ◽

W. D. Hoffman ◽

C. A. Koev ◽

...

Keyword(s):

Arterial Pressure ◽

Venous Pressure ◽

Survival Rates ◽

No Production ◽

Hemodynamic Effects ◽

Survival Times ◽

Endotoxin Challenge ◽

Arterial Circulation ◽

Mean Pulmonary Arterial Pressure ◽

Pulmonary Capillary

We studied the differential hemodynamic effects of N omega-monomethyl-L-arginine (L-NMMA), an inhibitor of nitric oxide (NO) synthesis, in normal and endotoxemic dogs and examined its activity across the venous, pulmonary, and systemic circulations. Survival was used to determine therapeutic efficacy. In both normal and endotoxemic animals, L-NMMA similarly increased systemic (P = 0.01) and pulmonary (P = 0.047) vascular resistance, marginally increased mean arterial pressure (P = 0.07), and decreased oxygen delivery (P = 0.01) compared with normal saline. In contrast, the effect of L-NMMA on mean pulmonary arterial pressure, central venous pressure, and pulmonary capillary wedge pressure was different in endotoxemic than in normal animals (P < 0.05), but this differential effect occurred > 6 h after endotoxin challenge. L-NMMA (1–10 mg.kg-1.h-1) did not significantly increase survival rates or times in endotoxemic animals, but the highest dose decreased survival times (P < 0.05). Thus the effect of L-NMMA was similar on the systemic arterial circulation in endotoxemic dogs compared with normal dogs but was increased in the venous and pulmonary vascular beds after endotoxin, suggesting that the induction of NO production was greater in low-resistance vessels. We were unable to show that nonselective inhibition of NO production was beneficial in endotoxemic dogs.

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