Mechanism of action of isoproterenol on venous return

1977 ◽  
Vol 232 (2) ◽  
pp. H152-H156 ◽  
Author(s):  
J. F. Green
Keyword(s):  
Venous Return ◽  
Venous Pressure ◽  
Portal Pressure ◽  
Vascular Effects ◽  
Right Heart ◽  
Control Value ◽  
Anesthetized Dogs ◽  
Venous Resistance ◽  
Right Heart Bypass ◽  
Transient And Steady State

The systemic vascular effects of isoproterenol infused in a dose of 1 mug-kg-1-min-1 was studied in 10 anesthetized dogs. A right heart bypass preparation allowed the separation of venous return into splanchnic and extrasplanchnic flows. Each channel was drained by gravity into an external reservoir. Venous return was then pumped into the pulmonary artery. During the infusion of isoproterenol, the pump was set at sufficient speed to maintain a constant level of blood in the external reservoir. Venous resistances and compliances of both channels were calculated from transient and steady-state volume shifts that occurred after rapid drops in splanchnic and then extrasplanchnic venous pressures. Isoproterenol affected both arterial and venous systems. Venous return increased from 1.62+/-0.11 to 2.40+/-0.19 liter/min (P less than 0.001) while arterial pressure fell from 97.5+/-3.8 to 70.2+/-5.9 mmHg (P less than 0.01). The compliances of the splanchnic and extrasplanchnic channels did not change significantly from their control values of 0.025+/-0.004 and 0.024+/-0.002 liter/mmHg. The venous resistance of the extrasplanchnic channel also did not change from its control value of 5.0 mmHg-liter-1-min-1; however, the splanchnic venous resistance decreased from 16.3+/-3.2 to 9.4+/-2.8 mmHg-liter-1-min-1 (P less than 0.001). The effective splanchnic back pressure, estimated by measuring the level to which hepatic venous pressure had to be raised to cause a change in portal pressure, decreased from 3.9 to 3.0 mmHg (P less than 0.01).

Interaction of interval-force relationship with aortic pressure and stroke volume

1976 ◽  
Vol 230 (4) ◽  
pp. 893-900 ◽  
Author(s):  
ER Powers ◽  
Foster ◽  
Powell WJ
Keyword(s):  
Heart Rate ◽  
Stroke Volume ◽  
Diastolic Pressure ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Cardiac Performance ◽  
Right Heart ◽  
Anesthetized Dogs ◽  
Right Heart Bypass ◽  
Force Relationship

The modification by aortic pressure and stroke volume of the response in cardiac performance to increases in heart rate (interval-force relationship) has not been previously studied. To investigate this interaction, 30 adrenergically blocked anesthetized dogs on right heart bypass were studied. At constant low aortic pressure and stroke volume, increasing heart rate (over the entire range 60-180) is associated with a continuously increasing stroke power, decreasing systolic ejection period, and an unchanging left ventricular end-diastolic pressure and circumference. At increased aortic pressure or stroke volume at low rates (60-120), increases in heart rate were associated with an increased performance. However, at increased aortic pressure or stroke volume at high rates (120-180), increases in heart rate were associated with a leveling or decrease in performance. Thus, an increase in aortic pressure or stroke volume results in an accentuation of the improvement in cardiac performance observed with increases in heart rate, but this response is limited to a low heart rate range. Therefore, the hemodynamic response to given increases in heart rate is critically dependent on aortic pressure and stroke volume.

Effect of a transient displacement of blood toward the heart on the pulse rate

1965 ◽  
Vol 20 (6) ◽  
pp. 1153-1156
Author(s):  
Roger L. Walker ◽  
Ian F. S. Mackay
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Pulse Rate ◽  
Venous Return ◽  
Human Subjects ◽  
Venous Pressure ◽  
Right Heart ◽  
Sudden Release

Sudden release of venous congesting cuffs in human subjects may cause a tachycardia. Among the factors that may be responsible for this increase in heart rate are a) a fall in arterial pressure, b) the hyperpnea that follows the cuff release, and c) an increase in “venous return.” A technique was designed which excluded the first two of these factors and, under the conditions of this technique, a demonstrable transient displacement of blood toward the heart with an associated rise in venous pressure but no change in arterial pressure did not cause cardiac acceleration. The presence of a “Bainbridge” type of reflex in man is questioned. Bainbridge reflex; cardiac reflexes in man; right heart filling Submitted on September 28, 1964

Hepatic venous resistance site in the dog: localization and validation of intrahepatic pressure measurements

1987 ◽  
Vol 65 (3) ◽  
pp. 352-359 ◽  
Author(s):  
Dallas J. Legare ◽  
W. Wayne Lautt
Keyword(s):  
Blood Volume ◽  
Nerve Stimulation ◽  
Venous Pressure ◽  
Portal Pressure ◽  
Vena Cava ◽  
Pressure Rise ◽  
Vascular Occlusion ◽  
Portal Venous Pressure ◽  
Hepatic Veins ◽  
Venous Resistance

Intrahepatic pressure (9.4 ± 0.3 mmHg; 1 mmHg = 133.32 Pa), measured proximal to a hepatic venous resistance site, was insignificantly different from portal venous pressure (9.6 ± 0.4 mmHg). This lobar venous pressure is not wedged hepatic venous pressure as it is measured from side holes in a catheter with a sealed tip. Validation of the lobar venous pressure measurement was done in a variety of ways and using different sizes and configurations of catheters. The site of hepatic venous resistance in the dog is localized to a narrow sphincterlike region about 0.5 cm in length and within 1–2 cm (usually within 1 cm) of the junction of the vena cava and hepatic veins. Sinusoidal and portal venous resistance appears insignificant in the basal state and large increases in liver blood volume (histamine infusion or passive vena caval occlusion) or large decreases in liver blood volume (passive vascular occlusion) do not alter the insignificant pressure gradient between portal and lobar venous pressures. Norepinephrine infusion (1.25 μg∙kg−1∙min−1 intraportal) and hepatic sympathetic nerve stimulation (10 Hz) led to a significantly greater rise in portal venous pressure than in lobar venous pressure, indicating some presinusoidal (and (or) sinusoidal) constriction and this indicates that lobar venous pressure cannot be assumed under all conditions to accurately reflect portal pressure. However, most of the rise in portal venous pressure induced by intraportal infusion of norepinephrine or nerve stimulation and virtually all of the pressure rise induced by histamine could be attributed to the postsinusoidal resistance site. This site was highly localized since 62% of the pressure drop from the portal vein to the inferior vena cava in the basal state occurred over a 0.5-cm length. However, the anatomical position of this site was different in the dog compared with the cat.

Quantitation of right-to-left shunting by double indicator and oxygen techniques

1976 ◽  
Vol 41 (3) ◽  
pp. 409-415 ◽  
Author(s):  
D. P. Copley ◽  
R. A. Klocke ◽  
F. J. Klocke
Keyword(s):  
Cardiac Output ◽  
Sulfur Hexafluoride ◽  
Venous Return ◽  
Right Heart ◽  
Indocyanine Green Dye ◽  
Arterial Blood ◽  
Vascular Space ◽  
Systemic Venous Return ◽  
Low Solubility ◽  
Right Heart Bypass

An improved double indicator technique for quantitating right-to-left shunting has been validated in a canine right-heart bypass shunt model and compared to standard O2 shunt measurements in the same preparation. A bolus of dissolved sulfur hexafluoride (SF6) and indocyanine green dye (ICG) is injected into systemic venous return and a single, time-averaged arterial blood sample is collected during the initial circulation of indicators. Because of its low solubility, SF6 is eliminated essentially quantitatively from blood traversing gas-filled alveoli; correction for volatile tracer in arterial blood derived from nonshunt pathways in therefore unnecessary. ICG remains confined to the vascular space and SF6 is not lost in shunt pathways. Ratios of SF6-ICG shunt to directly measured shunt averaged 0.99 +/- 0.27 (SD) in 55 comparisons of shunts ranging from 2 to 25% of cardiac output; differences between actual and measured shunt averaged 0.5 +/- 2.9% of cardiac output. Simultaneously determined ratios of O2 shunt to directly measured shunt averaged 0.98 +/- 0.48 in 34 comparisons; differences between actual and measured shunt were 0.7 +/- 3.4% of cardiac output.

Effect of pulmonary arterial PCO2 on slowly adapting pulmonary stretch receptors

1986 ◽  
Vol 60 (6) ◽  
pp. 2048-2055 ◽  
Author(s):  
J. F. Green ◽  
E. R. Schertel ◽  
H. M. Coleridge ◽  
J. C. Coleridge
Keyword(s):  
Lung Mechanics ◽  
Right Heart ◽  
Arterial Pco2 ◽  
Stretch Receptors ◽  
Pulmonary Stretch Receptors ◽  
Venous Pco2 ◽  
Anesthetized Dogs ◽  
Pulmonary Arterial ◽  
Right Heart Bypass ◽  
Pulmonary Stretch Receptor

We recorded pulmonary stretch receptor (PSR) activity in anesthetized dogs and examined the effect of varying pulmonary arterial PCO2 (PpCO2) in both the naturally perfused and vascularly isolated pulmonary circulations while ventilating the lungs with room air. Steady-state increases in PpCO2 from approximately 25 to 50 Torr and from 50 to 70 Torr decreased PSR activity (impulses/ventilatory cycle) by 15 and 9%, respectively (P less than 0.001). Rapid increases in PpCO2 from approximately 50 to 80 Torr in a right-heart bypass preparation (with pulmonary blood flow constant) decreased PSR activity by 27%. Depression of firing, which was proportionately greater in deflation, was not dependent on changes in lung mechanics. Results show that loading CO2 intravascularly depresses PSR activity, the effects extending above as well as below resting PpCO2. Rapidly increasing PpCO2 above the resting level markedly depresses PSR activity during the transient. We conclude that PSRs may contribute to altered breathing resulting from changes in mixed venous PCO2 over the physiological range.

Effect of the nitric oxide donor V-PYRRO/NO on portal pressure and sinusoidal dynamics in normal and cirrhotic mice

2008 ◽  
Vol 294 (6) ◽  
pp. G1311-G1317 ◽  
Author(s):  
Claire Edwards ◽  
Hong-Qiang Feng ◽  
Christopher Reynolds ◽  
Lan Mao ◽  
Don C. Rockey
Keyword(s):  
Nitric Oxide ◽  
Portal Hypertension ◽  
Mean Arterial Pressure ◽  
Liver Injury ◽  
Arterial Pressure ◽  
Venous Pressure ◽  
Portal Pressure ◽  
Nitric Oxide Donor ◽  
No Production ◽  
Vascular Effects

Reduced sinusoidal endothelial nitric oxide (NO) production contributes to increased intrahepatic resistance and portal hypertension after liver injury. We hypothesized that V-PYRRO/NO, an NO donor prodrug metabolized “specifically” in the liver, would reduce portal venous pressure (PVP) without affecting the systemic vasculature. Liver injury was induced in male BALB/c mice by weekly CCl4gavage. PVP and mean arterial pressure were recorded during intravenous administration of V-PYRRO/NO. In vivo microscopy was used to monitor sinusoidal diameter and flow during drug administration. Mean PVP was increased in CCl4-treated mice compared with sham-treated mice. In dose-response experiments, the minimum dose of PYRRO/NO required to acutely lower PVP by 20%, the amount believed to yield a clinically meaningful outcome, was 200 nmol/kg. This dose decreased portal pressure in cirrhotic (23.4 ± 2.0%, P < 0.001 vs. vehicle) and sham-treated (19.5 ± 2.3%, P < 0.001 vs. vehicle) animals by a similar magnitude. This concentration also led to dilation of hepatic sinusoids and an increase in sinusoidal volumetric flow, consistent with a reduction of intrahepatic resistance. The effect of V-PYRRO/NO on mean arterial pressure was significant at all concentrations tested, including the lowest, 30 nmol/kg ( P < 0.001 vs. vehicle for all doses). We conclude that V-PYRRO/NO had widespread vascular effects and, as such, is unlikely to be suitable for treatment of portal hypertension. As the potential of this or other similar compounds for treatment of portal hypertension is evaluated, effects on the systemic vasculature will also need to be considered.

Peripheral vascular responses during acute anemia

1981 ◽  
Vol 59 (2) ◽  
pp. 102-107 ◽  
Author(s):  
C. K. Chapler ◽  
W. N. Stainsby ◽  
M. A. Lillie
Keyword(s):  
Venous Return ◽  
Venous Pressure ◽  
Peripheral Vascular ◽  
Vasomotor Tone ◽  
Vascular Responses ◽  
Acute Anemia ◽  
Blood Exchange ◽  
Anesthetized Dogs ◽  
Pressure Changes ◽  
Arteries And Veins

Peripheral vascular responses during acute anemia were studied in 19 anesthetized dogs. In one study (n = 9) hindlimb weight and venous pressures were measured prior to and during acute anemia produced by isovolemic dextran-for-blood exchange. In another series of five control and five anemic dogs (hematocrit = 14 ± 1% (mean ± SE)), flow to the limb was occluded and arterial and venous pressure changes in the occluded limb were measured as an index of neurally mediated alterations in limb vasomotor tone. Following reduction of the hematocrit to 14 ± 0.3%, hindlimb weight decreased by an average of 10.0 g (P < 0.01) at 15 min and 12.8 g (P < 0.01) at 30 min of anemia. The decrease in limb weight was associated with a rise (P < 0.01) in limb venous pressure. There was also a relatively greater degree of vasomotor tone in the occluded hindlimb of anemic dogs as compared with control animals. Although both arterial and venous pressures decreased in an occluded hindlimb following the production of anemia, the decreases in vascular pressures were significantly less than those observed in control experiments. It was not possible to distinguish between tone changes in arteries and veins because of the presence of arteriovenous anastomoses. The data show that a peripheral-to-central blood volume translocation occurred in acute anemia which would increase venous return. Further, the results strongly suggest that the volume translocation was a result of an increase in venomotor tone.

Effect of hepatic venous sphincter contraction on transmission of central venous pressure to lobar and portal pressure

1987 ◽  
Vol 65 (11) ◽  
pp. 2235-2243 ◽  
Author(s):  
W. Wayne Lautt ◽  
Dallas J. Legare ◽  
Clive V. Greenway
Keyword(s):  
Vascular Resistance ◽  
Venous Pressure ◽  
Portal Pressure ◽  
Vena Cava ◽  
Pressure Rise ◽  
Portal Venous Pressure ◽  
Small Rise ◽  
Venous Resistance ◽  
Small Increments ◽  
Control State

In dogs anesthetized with pentobarbital, central vena caval pressure (CVP), portal venous pressure (PVP), and intrahepatic lobar venous pressure (proximal to the hepatic venous sphincters) were measured. The objective was to determine some characteristics of the intrahepatic vascular resistance sites (proximal and distal to the hepatic venous sphincters) including testing predictions made using a recent mathematical model of distensible hepatic venous resistance. The stimulus used was a brief rise in CVP produced by transient occlusion of the thoracic vena cava in control state and when vascular resistance was elevated by infusions of norepinephrine or histamine, or by nerve stimulation. The percent transmission of the downstream pressure rise to upstream sites past areas of vascular resistance was elevated. Even small increments in CVP are partially transmitted upstream. The data are incompatible with the vascular waterfall phenomenon which predicts that venous pressure increments are not transmitted upstream until a critical pressure is overcome and then further increments would be 100% transmitted. The hepatic sphincters show the following characteristics. First, small rises in CVP are transmitted less than large elevations; as the CVP rises, the sphincters passively distend and allow a greater percent transmission upstream, thus a large rise in CVP is more fully transmitted than a small rise in CVP. Second, the amount of pressure transmission upstream is determined by the vascular resistance across which the pressure is transmitted. As nerves, norepinephrine, or histamine cause the hepatic sphincters to contract, the percent transmission becomes less and the distensibility of the sphincters is reduced. Similar characteristics are shown for the "presinusoidal" vascular resistance and the hepatic venous sphincter resistance. Finally, a unit of pressure rise in downstream pressure will be more completely transmitted upstream as the basal starting downstream pressure is increased. These data fulfill the predictions of the distensible hepatic venous sphincter model developed for the cat liver and are incompatible with the Starling resistor – vascular waterfall theory. The distensible hepatic venous resistance allows the splanchnic blood volume to most efficiently buffer the largest changes in CVP by transmitting proportionately more pressure to the highly compliant splanchnic vessels. In addition the distensible sphincters serve to autoregulate portal venous pressure. As portal flow changes, the passively distensible sphincters minimize changes in PVP.

Gastrointestinal hemodynamics during compensation for hemorrhage and measurement of Pmcf

1994 ◽  
Vol 266 (3) ◽  
pp. H1242-H1250
Author(s):  
C. F. Rothe ◽  
R. Maass-Moreno
Keyword(s):  
Vascular Resistance ◽  
Venous Pressure ◽  
Portal Pressure ◽  
Peripheral Resistance ◽  
Portal Flow ◽  
Total Blood ◽  
Flow Measurements ◽  
Control Value ◽  
Vascular Compliance ◽  
Autonomic Blockade

To quantify the degree of autonomic reflex control of the gastrointestinal vasculature, we studied the responses to a 10-ml/kg hemorrhage or transfusion and autonomic blockade in fentanyl- and pentobarbital-anesthetized dogs. The active total blood volume was estimated by indocyanine green dilution. Transfusion and hemorrhage did not significantly change gastrointestinal vascular compliance [1.82 +/- 0.68 (SD) ml/mmHg], but autonomic blockade with hexamethonium and atropine increased it by 0.57 +/- 0.37 ml/mmHg. Neither hemorrhage nor autonomic blockade significantly changed gastrointestinal vascular resistance from its control value of 10.8 +/- 4 mmHg.ml-1.min.kg body wt, but transfusion reduced it by 3.0 +/- 1.2 mmHg.ml-1.min.kg body wt. The ratio of gastrointestinal vascular resistance to total peripheral resistance was not significantly changed, however. We conclude that vascular compliance and resistance of the gastrointestinal bed are minimally influenced by the autonomic nervous system under the conditions studied. Portal pressure and flow measurements (transit-time ultrasound) during the above maneuvers were also combined with estimations of mean circulatory filling pressure (Pmcf) to test the hypothesis that, when the heart is stopped to measure Pmcf, portal pressure equals central venous pressure (Pcv) and hence that portal flow is zero. Seven seconds after the heart was stopped, portal venous pressure (Ppv) remained 0.83 +/- 0.78 mmHg higher than Pcv and portal flow decreased to only 25% of its control value. However, gastrointestinal compliance times (Ppv-Pcv), an estimate of the extra distending volume, was only 0.07 +/- 0.07 ml/kg body wt. Thus we conclude that the error in estimating Pmcf, given this (Ppv-Pcv) difference, is physiologically insignificant.

Right Heart Pressure Transients and Pulmonary Venous Pressure

Cardiology ◽  
2016 ◽  
Vol 135 (2) ◽  
pp. 77-80
Author(s):  
William H. Gaasch
Keyword(s):  
Venous Pressure ◽  
Right Heart ◽  
Pressure Transients
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