Effect of vasopressin on systemic capacity

1991 ◽  
Vol 261 (5) ◽  
pp. H1494-H1498 ◽  
Author(s):  
F. G. Welt ◽  
D. L. Rutlen
Keyword(s):  
Intact Animal ◽  
Venous Pressure ◽  
Portal Venous Pressure ◽  
Portal Flow ◽  
Compensatory Response ◽  
Venae Cavae ◽  
Subsequent Decrease ◽  
Constant Rate ◽  
Arterial Inflow ◽  
Ventricular Filling

To assess the effect of vasopressin (VP) on systemic capacity (SC), blood was drained from the venae cavae to an oxygenator and returned to the aorta at a constant rate so that changes in SC could be measured as the inverse of changes in oxygenator volume in 17 anesthetized pigs. After 10 min of VP administration (1.1 U/min ia), mean arterial pressure increased from 67 +/- 2 to 144 +/- 7 mmHg (P less than 0.001). SC decreased promptly and reached a nadir of 110 +/- 32 ml (P less than 0.02, 5.5 ml/kg) below control at 5 min but returned to 35 +/- 65 ml (P = not significant, 1.8 ml/kg) below control at 10 min. Portal venous pressure decreased from 19.3 +/- 2.6 to 16.6 +/- 2.7 mmHg (P less than 0.001), and portal flow decreased from 828 +/- 68 to 458 +/- 92 ml/min (P less than 0.001). Transhepatic venous resistance increased. After evisceration, VP caused only an increase in SC. Thus VP causes an initial SC decrement due entirely to a decrease in splanchnic capacity. The decrease in splanchnic capacity must be caused, at least in part, by the decrease in gastrointestinal arterial inflow and subsequent decrease in portal venous pressure. These initial effects of VP on SC would be expected to enhance ventricular filling and cardiac output in the intact animal and could be important in the acute compensatory response to hemorrhage.

Arginine vasopressin increases apparent whole body capacity in anesthetized cats

1990 ◽  
Vol 258 (3) ◽  
pp. H722-H728 ◽  
Author(s):  
D. S. Martin ◽  
J. R. McNeill
Keyword(s):  
Angiotensin Ii ◽  
Arginine Vasopressin ◽  
Venous Pressure ◽  
Whole Body ◽  
Passive Component ◽  
Reservoir Volume ◽  
Intravenous Infusions ◽  
Venae Cavae ◽  
Constant Rate ◽  
The Right

The effects of arginine vasopressin (AVP) on capacitance function were assessed in anesthetized cats by draining blood from the superior and inferior venae cavae into an external reservoir and then returning blood to the right atrium at a constant rate. Under these conditions, changes in reservoir volume were assumed to reflect reciprocal changes in whole body capacity. Intravenous infusions of AVP (1, 10, and 100 ng.kg-1.min-1) that elevated plasma AVP concentrations by approximately 30, 400, and 4,000 fmol/ml were associated with concentration-dependent increases in whole body capacity that ranged between 1.6 and 8 ml/kg. In contrast to AVP, intravenous infusions of angiotensin II (5, 10, and 50 ng.kg-1.min-1) had relatively little influence on capacity, whereas norepinephrine administration (300, 1,000, and 3,000 ng.kg-1.min-1) was associated with dose-dependent decreases in capacity of 4.5-10.3 ml/kg. Virtually the entire increase in whole body capacity to AVP can be accounted for by summation of the predicted contributions of an active reflex venodilatatory component and those of a passive component (arterial and cardiopulmonary compartments). Because systemic compliance (delta reservoir volume/delta venous pressure) was not changed by AVP administration, the contribution of a reflex venodilatatory component must be the result of increases in unstressed vascular volume (contained volume at 0 transmural pressure) as opposed to changes in compliance. These results may explain why AVP decreases cardiac output to a greater extent than either angiotensin II or sympathomimetics and, thus, why AVP is a weaker pressor agent in animals with intact autonomic function.

Portal venous pressure in “pipestem” fibrosis of the liver due to schistosomiasis

1959 ◽  
Vol 27 (5) ◽  
pp. 807-810 ◽  
Author(s):  
Arthur H. Aufses ◽  
Fenton Schaffner ◽  
William S. Rosenthal ◽  
Bernard E. Herman
Keyword(s):  
Venous Pressure ◽  
Portal Venous Pressure

scholarly journals Measurement of portal venous pressure prior to major liver resections: hospital based experience

HPB ◽  
2018 ◽  
Vol 20 ◽  
pp. S476
Author(s):  
H. Bari ◽  
F. Hanif ◽  
S.A. Akbar ◽  
U. Farooq
Keyword(s):  
Venous Pressure ◽  
Portal Venous Pressure ◽  
Liver Resections

Is Portal Venous Pressure Modulation Still Indicated for All Recipients in Living Donor Liver Transplantation?

2018 ◽  
Vol 24 (11) ◽  
pp. 1578-1588 ◽  
Author(s):  
Siyuan Yao ◽  
Toshimi Kaido ◽  
Ryuji Uozumi ◽  
Shintaro Yagi ◽  
Yosuke Miyachi ◽  
...  
Keyword(s):  
Liver Transplantation ◽  
Living Donor ◽  
Living Donor Liver Transplantation ◽  
Venous Pressure ◽  
Portal Venous Pressure ◽  
Donor Liver ◽  
Donor Liver Transplantation ◽  
Pressure Modulation

Changes in the dimensions of the venae cavae

1959 ◽  
Vol 196 (4) ◽  
pp. 741-744 ◽  
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.

Effect of portal hypertension on splenic blood flow, intrasplenic extravasation and systemic blood pressure

2003 ◽  
Vol 284 (6) ◽  
pp. R1580-R1585 ◽  
Author(s):  
Susan Kaufman ◽  
Jody Levasseur
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Portal Hypertension ◽  
Portal Vein ◽  
Venous Pressure ◽  
Splenic Vein ◽  
Systemic Blood Pressure ◽  
Portal Venous Pressure ◽  
Systemic Blood ◽  
Fluid Extravasation

We have previously shown that intrasplenic fluid extravasation is important in controlling blood volume. We proposed that, because the splenic vein flows in the portal vein, portal hypertension would increase splenic venous pressure and thus increase intrasplenic microvascular pressure and fluid extravasation. Given that the rat spleen has no capacity to store/release blood, intrasplenic fluid extravasation can be estimated by measuring the difference between splenic arterial inflow and venous outflow. In anesthetized rats, partial ligation of the portal vein rostral to the junction with the splenic vein caused portal venous pressure to rise from 4.5 ± 0.5 to 12.0 ± 0.9 mmHg ( n = 6); there was no change in portal venous pressure downstream of the ligation, although blood flow in the liver fell. Splenic arterial flow did not change, but the arteriovenous flow differential increased from 0.8 ± 0.3 to 1.2 ± 0.1 ml/min ( n = 6), and splenic venous hematocrit rose. Mean arterial pressure fell (101 ± 5.5 to 95 ± 4 mmHg). Splenic afferent nerve activity increased (5.6 ± 0.9 to 16.2 ± 0.7 spikes/s, n = 5). Contrary to our hypothesis, partial ligation of the portal vein caudal to the junction with the splenic vein (same increase in portal venous pressure but no increase in splenic venous pressure) also caused the splenic arteriovenous flow differential to increase (0.6 ± 0.1 to 1.0 ± 0.2 ml/min; n = 8). The increase in intrasplenic fluid efflux and the fall in mean arterial pressure after rostral portal vein ligation were abolished by splenic denervation. We propose there to be an intestinal/hepatic/splenic reflex pathway, through which is mediated the changes in intrasplenic extravasation and systemic blood pressure observed during portal hypertension.

Microvascular control of capillary pressure during increases in local arterial and venous pressure

1988 ◽  
Vol 254 (4) ◽  
pp. H772-H784 ◽  
Author(s):  
M. J. Davis
Keyword(s):  
Hydrostatic Pressure ◽  
Capillary Pressure ◽  
Venous Pressure ◽  
The Body ◽  
Cell Velocity ◽  
Arterial Inflow ◽  
Tissue Act ◽  
Pallid Bats ◽  
Red Cell Velocity ◽  
Capillary Pressures

The extent to which capillary hydrostatic pressure might be protected from increases in local arterial and venous pressure was examined in the wing microcirculation of unanesthetized pallid bats (Antrozous pallidus). Arterial inflow and venous outflow pressures to the wing were elevated using a box technique to increase pressure around the body of the animal in steps of 12 mmHg between 0 and +60 mmHg for 3-min periods. During this time, hydrostatic pressure, diameter, and red cell velocity in single microvessels were continuously recorded. All branching orders of arterioles constricted significantly during increases in box pressure (Pb), while capillaries and venules dilated. First-order arteriole and venule pressures increased 1:1 with Pb. Capillary pressures increased by only a fraction of Pb up to +36 mmHg, but at higher Pb, the change in capillary pressure was equivalent to the change in Pb. Calculations of vascular resistance indicate that changes in both pre- and postcapillary resistance in this tissue act to prevent increases in capillary pressure during moderate, but not during large, increases in arterial and venous pressure.

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.

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