Splanchnic vascular capacitance and positive end-expiratory pressure in dogs

1991 ◽  
Vol 70 (2) ◽  
pp. 818-824 ◽  
Author(s):  
C. Risoe ◽  
C. Hall ◽  
O. A. Smiseth
Keyword(s):  
Blood Volume ◽  
Venous Pressure ◽  
Portal Venous Pressure ◽  
Central Blood Volume ◽  
Positive End Expiratory Pressure ◽  
Splenic Volume ◽  
Vascular Volume ◽  
Vascular Capacitance ◽  
Anesthetized Dogs ◽  
Blood Volumes

We have investigated the effect of positive end-expiratory pressure ventilation (PEEP) on regional splanchnic vascular capacitance. In 12 anesthetized dogs hepatic and splenic blood volumes were assessed by sonomicrometry. Vascular pressure-diameter curves were defined by obstructing hepatic outflow. With 10 and 15 cmH2O PEEP portal venous pressure increased 3.1 +/- 0.3 and 5.1 +/- 0.4 mmHg (P less than 0.001) while hepatic venous pressure increased 4.9 +/- 0.4 and 7.3 +/- 0.4 mmHg (P less than 0.001), respectively. Hepatic blood volume increased (P less than 0.01) 3.8 +/- 0.9 and 6.3 +/- 1.4 ml/kg body wt while splenic volume decreased (P less than 0.01) 0.8 +/- 0.2 and 1.3 +/- 0.2 ml/kg body wt. The changes were similar with closed abdomen. The slope of the hepatic vascular pressure-diameter curves decreased with PEEP (P less than 0.01), possibly reflecting reduced vascular compliance. There was an increase (P less than 0.01) in unstressed hepatic vascular volume. The slope of the splenic pressure-diameter curves was unchanged, but there was a significant (P less than 0.05) decrease in unstressed diameter during PEEP. In conclusion, hepatic blood volume increased during PEEP. This was mainly a reflection of passive distension due to elevated venous pressures. The spleen expelled blood and thus prevented a further reduction in central blood volume.

Changes in regional vascular capacitance during prostacyclin-induced cardiac vagal reflex in pigs

1994 ◽  
Vol 267 (2) ◽  
pp. H535-H539
Author(s):  
Y. Wang ◽  
C. Drakonakis ◽  
J. L. Alderman ◽  
D. L. Rutlen
Keyword(s):  
Blood Volume ◽  
Diastolic Pressure ◽  
Venous Pressure ◽  
Blood Pool ◽  
Left Ventricular ◽  
Portal Venous Pressure ◽  
Vascular Capacitance ◽  
Blood Pool Scintigraphy ◽  
Vagal Reflex ◽  
Blood Volumes

The purpose of this study was to determine the effects of the prostaglandin I2 (prostacyclin; PGI2)-induced cardiac vagal reflex on intestinal and liver blood volumes and the intestinal vascular pressure-volume (P-V) relationship. In anesthetized pigs, blood volumes were measured by blood-pool scintigraphy. Portal venous pressure was varied by graded inflation of a portal vein constrictor to determine the intestinal vascular P-V relationship. Proximal right coronary infusion of PGI2 at a rate of 0.15 micrograms.kg-1.min-1 for 6 min increased intestinal blood volume by 7.0 +/- 1.2% (P < 0.01, means +/- SE) and shifted the intestinal vascular P-V relationship away from the pressure axis (i.e., a volume increase at a given venous pressure). This change was associated with decreases in liver blood volume and left ventricular end-diastolic pressure by 4.5 +/- 1.2 (P < 0.01) and 17 +/- 2% (P < 0.05), respectively. PGI2 also reduced central venous pressure by 16 +/- 2% from 3.2 +/- 0.5 mmHg (P < 0.05) and portal venous pressure by 7.0 +/- 0.6% from 7.6 +/- 0.6 mmHg (P < 0.05). These responses were abolished by bilateral vagotomy. The results demonstrate that intracoronary PGI2 infusion increases intestinal blood volume. This increase is mediated by a cardiac vagal reflex. The PGI2-induced shift in the intestinal vascular P-V relationship suggests that intestinal blood volume increases by an active change in vascular capacitance, whereas reductions in liver blood volume and left ventricular end-diastolic pressure appear to be due to passive mechanisms related to the shift of blood volume to the intestinal circulation.

Effects of nifedipine and captopril on vascular capacitance of ganglion-blocked anesthetized dogs

1990 ◽  
Vol 68 (3) ◽  
pp. 431-438 ◽  
Author(s):  
Richard I. Ogilvie ◽  
Danuta Zborowska-Sluis
Keyword(s):  
Cardiac Output ◽  
Pulmonary Artery ◽  
Arterial Pressure ◽  
Blood Volume ◽  
Filling Pressure ◽  
Right Atrial ◽  
Central Blood Volume ◽  
Mean Circulatory Filling Pressure ◽  
Vascular Capacitance ◽  
Blood Volumes

The hemodynamic effects of nifedipine and captopril at doses producing similar reductions in arterial pressure were studied in pentobarbital- anesthetized ventilated dogs after splenectomy during ganglion blockade with hexamethonium. Mean circulatory filling pressure (Pmcf) was determined during transient circulatory arrest induced by acetylcholine at baseline circulating blood volumes and after increases of 5 and 10 mL/kg. Central blood volumes (pulmonary artery to aortic root) were determined from transit times, and separately determined cardiac outputs (right atrium to pulmonary artery) were estimated by thermodilution. Nifedipine (n = 5) increased Pmcf at all circulating blood volumes and reduced total vascular capacitance without a change in total vascular compliance. Central blood volume, right atrial pressure, and cardiac output were increased with induced increases in circulating blood volume. In contrast, captopril (n = 5) did not alter total vascular capacitance, central blood volume, right atrial pressure, or cardiac output at baseline or with increased circulating volume. Thus, at doses producing similar reductions in arterial pressure, nifedipine but not captopril increased venous return and cardiac output in ganglion-blocked dogs.Key words: mean circulatory filling pressure, vascular compliance, vascular capacitance, nifedipine, captopril.

Contribution of abdomen and legs to central blood volume expansion in humans during immersion

1997 ◽  
Vol 83 (3) ◽  
pp. 695-699 ◽  
Author(s):  
Lars Bo Johansen ◽  
Thomas Ulrik Skram Jensen ◽  
Bettina Pump ◽  
Peter Norsk
Keyword(s):  
Blood Volume ◽  
Volume Expansion ◽  
Protein Concentration ◽  
Water Immersion ◽  
Venous Pressure ◽  
Cuff Inflation ◽  
Central Blood Volume ◽  
Central Venous ◽  
Plasma Protein Concentration ◽  
Blood Volume Expansion

Johansen, Lars Bo, Thomas Ulrik Skram Jensen, Bettina Pump, and Peter Norsk. Contribution of abdomen and legs to central blood volume expansion in humans during immersion. J. Appl. Physiol. 83(3): 695–699, 1997.—The hypothesis was tested that the abdominal area constitutes an important reservoir for central blood volume expansion (CBVE) during water immersion in humans. Six men underwent 1) water immersion for 30 min (WI), 2) water immersion for 30 min with thigh cuff inflation (250 mmHg) during initial 15 min to exclude legs from contributing to CBVE (WI+Occl), and 3) a seated nonimmersed control with 15 min of thigh cuff inflation (Occl). Plasma protein concentration and hematocrit decreased from 68 ± 1 to 64 ± 1 g/l and from 46.7 ± 0.3 to 45.5 ± 0.4% ( P < 0.05), respectively, during WI but were unchanged during WI+Occl. Left atrial diameter increased from 27 ± 2 to 36 ± 1 mm ( P < 0.05) during WI and increased similarly during WI+Occl from 27 ± 2 to 35 ± 1 mm ( P < 0.05). Central venous pressure increased from −3.7 ± 1.0 to 10.4 ± 0.8 mmHg during WI ( P < 0.05) but only increased to 7.0 ± 0.8 mmHg during WI+Occl ( P < 0.05). In conclusion, the dilution of blood induced by WI to the neck is caused by fluid from the legs, whereas the CBVE is caused mainly by blood from the abdomen.

Distributions of vascular volume and compliance in the lung

1988 ◽  
Vol 64 (1) ◽  
pp. 266-273 ◽  
Author(s):  
C. A. Dawson ◽  
D. A. Rickaby ◽  
J. H. Linehan ◽  
T. A. Bronikowski
Keyword(s):  
Arterial Pressure ◽  
Information Content ◽  
Blood Volume ◽  
Vascular Resistance ◽  
Venous Pressure ◽  
Upper Bounds ◽  
Lower And Upper Bounds ◽  
Vascular Volume ◽  
Capillary Bed ◽  
Lung Lobes

The ether- and dye-dilution methods were used to estimate the arterial, capillary, and venous volumes and compliances in isolated dog lung lobes. In the range of arterial pressure from approximately 7 to 14.5 Torr and venous pressure of 1.4 to 10.8 Torr, the total lobar blood volume ranged from approximately 2 to approximately 2.6 ml/kg body wt. About 19% of the lobar vascular volume was in the arteries, approximately 59% was in the capillaries, and approximately 22% was in the veins. The lobar vascular compliance was approximately 0.065 ml.Torr-1.kg body wt-1 with an arterial-capillary-venous distribution of approximately 30:49:21. These results suggest that the largest fractions of the intralobar blood volume and compliance are in the capillary bed. The segmental compliances along with outflow occlusion data were used to place lower and upper bounds on the arterial, capillary, and venous resistances. These bounds were 13.6 and 61.4% of the total vascular resistance for the arteries, 0 and 59.4% for the capillaries, and 5.5 and 64.9% for the veins, respectively. These bounds are rather broad, but they help to put the information content of the occlusion data under the conditions of these experiments into perspective.

Reflex mechanisms for changes in renal nerve activity during positive end-expiratory pressure

1988 ◽  
Vol 65 (1) ◽  
pp. 109-115 ◽  
Author(s):  
M. Aibiki ◽  
S. Koyama ◽  
K. Ogli ◽  
Y. Shirakawa
Keyword(s):  
Carotid Sinus ◽  
Venous Pressure ◽  
Control Level ◽  
Vagal Afferents ◽  
Positive End Expiratory Pressure ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Renal Nerve Activity ◽  
Anesthetized Dogs ◽  
Cardiopulmonary Receptors

This study was designed to investigate the interaction between carotid sinus baroreceptors and cardiopulmonary receptors in the reflex control of renal nerve activity (RNA) during positive end-expiratory pressure (PEEP) in anesthetized dogs. PEEP at two different levels (10 and 20 cmH2O) was applied to the following groups: animals with neuraxis intact (I group, n = 12); vagal and aortic nerve denervated animals with carotid sinus nerves intact (V group, n = 6); carotid sinus denervated animals with vagal and aortic nerves intact (SD group, n = 6); and carotid sinus denervated animals also having severed vagal and aortic nerves (SAV group, n = 12). Mean blood pressure (MBP), central venous pressure, and mean airway pressure were also simultaneously measured. In the I group, no significant alterations in RNA occurred during PEEP at both levels, even when MBP fell significantly. Although the drop in MBP in the SD group was similar to that in the I group, RNA decreased significantly 10 s after intervention at both PEEP levels, followed by a recovery of RNA toward the control level. In contrast, a significant increase in RNA, which continued until the end of PEEP, appeared in the V group immediately after each intervention. In the SAV group, RNA responses to PEEP, which were observed in the other groups, were abolished. These results provide evidence that during PEEP, renal nerve activity is modified by an interaction between carotid sinus baroreceptors and cardiopulmonary receptors; excitatory effects occur via carotid sinus nerves and inhibitory effects occur via vagal afferents.

Alpha- and beta-adrenergic mechanisms in the control of vascular capacitance by the carotid sinus baroreflex system

1994 ◽  
Vol 267 (1) ◽  
pp. H201-H210 ◽  
Author(s):  
K. Shigemi ◽  
M. J. Brunner ◽  
A. A. Shoukas
Keyword(s):  
Adrenergic Receptor ◽  
Carotid Sinus ◽  
Venous Pressure ◽  
Systemic Circulation ◽  
Adrenergic System ◽  
Beta Adrenergic ◽  
Vascular Volume ◽  
Adrenergic Mechanisms ◽  
Vascular Capacitance ◽  
Carotid Sinus Baroreflex

We examined the active and passive contributions of the alpha- and beta-adrenergic receptor mechanisms to the changes in systemic vascular capacitance caused by the carotid sinus baroreflex system in anesthetized, vagotomized dogs. The carotid sinuses were isolated from the systemic circulation and perfused with controlled pressures. To determine the changes in vascular capacitance, a constant flow, constant venous pressure cardiopulmonary bypass was used. The changes in unstressed vascular volume were calculated when carotid sinus pressure was reduced from 200 to 50 mmHg without any adrenergic receptor antagonist, with either an alpha- (phentolamine) or a beta- (propranolol) antagonist and then with both. The reflex change in unstressed vascular volume in the systemic circulation (22.6 +/- 9.0 ml/kg without any antagonist) was reduced by 72% with phentolamine, by 35% with propranolol, and by 73% with both antagonists. Our results suggest that the alpha-adrenergic mechanisms contribute significantly to active changes in systemic venous capacity. In addition, the beta-adrenergic system has very little effect on active changes in venous vessels but does contribute to the overall capacity changes by dilating the hepatic outflow resistance when the carotid sinus baroreflex system is activated.

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.

Sequential changes in intrarenal hemodynamics during saline infusion in the dog

1975 ◽  
Vol 228 (6) ◽  
pp. 1663-1668 ◽  
Author(s):  
MT Velasquez ◽  
AV Notargiacomo ◽  
JN Cohn
Keyword(s):  
Blood Flow ◽  
Blood Volume ◽  
Venous Pressure ◽  
Indicator Dilution ◽  
Saline Infusion ◽  
Kidney Volume ◽  
Dilution Technique ◽  
Filtration Fraction ◽  
Anesthetized Dogs ◽  
Intrarenal Blood Flow

Intrarenal blood flow and volume (indicator-dilution technique), kidney volume (mercury-in-rubber resistance gage), intr-renal venous pressure, filtration fraction, and sodium excretion were determined dequentially before and during a l-h infusion of isotonicsaline 80 ml/kg in anesthetized dogs. The cortical fraction of renal blood flow roseduring the first 20 min of infusion from an average of 70 to 77%, butreturned nearly to control levels during the last 20 min of infusion because ofa low rise in noncortical flow. During the first 20 min a 23% increase in cortical blood volume accounted for one-third of the 8.5% increase in kidney volume, whereasin the last 20 min cortical blood volume had fallen nearly to control values and kidneyvolume was increased by 17.2%. Intrarenal resistances calculated from intrarenalpressure and flow indicated persistent cortical prevenous dilatation, progressive cortical venous constriction, and only a slight late reduction in noncortical resistance.These data indicate that hemodynamics are shanging continuously during saline infusion and the natriuresis probably is multifactorial.

Nonlinear resistances in hepatic microcirculation

1995 ◽  
Vol 269 (6) ◽  
pp. H1922-H1930 ◽  
Author(s):  
R. Maass-Moreno ◽  
C. F. Rothe
Keyword(s):  
Portal Vein ◽  
Blood Volume ◽  
Venous Pressure ◽  
Vena Cava ◽  
Portal Venous Pressure ◽  
Hepatic Microcirculation ◽  
Nonlinear Characteristics ◽  
Nonlinear Mode ◽  
Pressure Transmission ◽  
Liver Surface

The liver provides a reservoir available for mobilizing large amounts of blood, but if a change in downstream (outflow) pressure below a certain magnitude (break pressure) does not change upstream pressures, blood volume redistribution may be limited. For downstream pressures larger than the break pressure, the upstream pressures change proportionately. We tested the hypothesis that this nonlinear mode of pressure transmission could be found from the abdominal vena cava to the hepatic microcirculation and from the hepatic microcirculation to the portal vein. Using a servo-null micropipette technique, we measured microvascular pressures at the liver surface of rabbits. In 16 of 30 measurements, increasing the pressure at the liver outflow, by partially occluding the caudal thoracic vena cava, caused an increase in hepatic venular pressure only after the abdominal vena caval pressure exceeded a break pressure of 2.85 +/- 0.92 mmHg. In 13 of 31 measurements, portal venous pressure was not changed until the hepatic venular pressure exceeded a break pressure of 3.36 +/- 0.54 mmHg. Similar behavior and values were obtained for sinusoids and portal venules. When present, the sharp inflection in the upstream-downstream pressure plots suggests that this may be caused by a Starling resistor-type mechanism. When the break was absent, the downstream pressure may have been larger than the break pressure. We conclude that significant hepatic resistances with nonlinear characteristics exist upstream and downstream to the central venules, sinusoids, and portal venules.

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