Portal venous infusions of L-glutamine in anaesthetized dogs do not influence renal function

1992 ◽  
Vol 70 (10) ◽  
pp. 1432-1435
Author(s):  
Mortimer Levy
Keyword(s):  
Wistar Rats ◽  
Femoral Vein ◽  
Venous Pressure ◽  
Renal Perfusion ◽  
Portal Venous Pressure ◽  
Portal System ◽  
Similar Data ◽  
Free Base ◽  
Hepatorenal Reflex ◽  
Intraportal Infusion

It has been reported that the intraportal infusion of glutamine in Munich–Wistar rats will cause depression of renal perfusion and the urinary excretion of salt and water. We have attempted to reproduce these findings in anaesthetized dogs. L-Glutamine was infused at doses between 120 and 150 μmol/min into the portal vein and femoral vein of anaesthetized dogs. No effect was observed on portal venous pressure, blood pressure, or kidney function. Similar data were obtained with D-glutamine. Liver biopsy revealed no abnormalities. When 1.5–3 μg histamine (free base) was infused into the portal system, portal venous pressure rose from 15.2 ± 0.33 to 24.8 ± 0.40 cmH2O (p < 0.05) (1 cmH2O = 98.1 Pa). Glutamine infusions do not appear to initiate hepatorenal reflexes in dogs as they have been reported to do in rats.Key words: liver, portal hypertension, hepatorenal reflex.

Effect of histamine, norepinephrine, and nerves on vascular pressures in dog liver

1987 ◽  
Vol 252 (4) ◽  
pp. G472-G478 ◽  
Author(s):  
W. W. Lautt ◽  
D. J. Legare
Keyword(s):  
Pressure Drop ◽  
Hepatic Artery ◽  
Venous Pressure ◽  
Portal Venous Pressure ◽  
Hepatic Veins ◽  
Small Doses ◽  
Hepatic Nerves ◽  
Dog Liver ◽  
Control State ◽  
Intraportal Infusion

In the control state, lobar venous pressure (LVP) measured proximal to a hepatic venous sphincter in dog liver (9.9 +/- 0.3 mmHg) is insignificantly different from portal venous pressure (PVP = 9.9 +/- 0.3 mmHg). Essentially all of the pressure drop occurs across the hepatic veins. Intraportal infusion of histamine constricts the hepatic venous sphincter and leads to similar elevations of LVP and PVP, indicating that all of the rise in PVP (except at small doses = 1 microgram X kg-1. min-1) can be accounted for by hepatic venous sphincter constriction. Norepinephrine at doses from 0.25 to 1.25 micrograms X kg-1. min-1 (intraportal) caused both hepatic venous sphincter constriction and constriction proximal to hepatic venous sphincters to roughly equal proportions, with approximately 44% of the rise in PVP due to hepatic sphincter constriction. Hepatic nerves activated both resistance sites, with 90% of the rise in PVP due to hepatic venous constriction at 2 Hz stimulation. By 4 Hz stimulation, the postsinusoidal sphincters were nearly maximally activated, but the “presinusoidal” resistance continued to increase until, at 10 Hz, the hepatic venous sphincter component accounted for only 59% of the rise in PVP. The proportion of PVP rise accounted for by hepatic venous sphincter resistance was not significantly altered by prior occlusion of the hepatic artery.

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

Cardiovascular reflexes during abdominal ischemia in cats

1994 ◽  
Vol 267 (1) ◽  
pp. R97-R106 ◽  
Author(s):  
H. S. Huang ◽  
J. C. Longhurst
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Femoral Vein ◽  
Venous Pressure ◽  
Vena Cava ◽  
Left Ventricular ◽  
Mesenteric Arteries ◽  
Cardiovascular Reflexes ◽  
Group 3

The cardiovascular effects of regional abdominal ischemia and reperfusion were studied in cats anesthetized with alpha-chloralose. In group 1 (n = 9), central venous pressure was kept constant by a servo-controller while the celiac and superior mesenteric arteries were occluded by loop snares for 10 min. In group 2 (n = 9), a constant-perfusion circuit to the celiac and superior mesenteric arteries that could divert flow to the femoral vein was used to induce abdominal ischemia. In group 3 (n = 7), venous return from the inferior vena cava was controlled, and a constant-perfusion circuit was used to induce abdominal ischemia. Abdominal ischemia significantly (P < 0.05) increased portal venous blood lactate from 4.3 +/- 0.6 to 6.0 +/- 0.6 mM in group 3. The early increases in blood pressure caused by passive volume shifts in groups 1 and 2 were abolished in group 3. The late, i.e., 10 min, response to abdominal ischemia consisted of significant (P < 0.05) increases in mean arterial pressure (29 +/- 7, 24 +/- 7, and 33 +/- 8 mmHg in groups 1, 2, and 3, respectively). Abdominal ischemia also significantly (P < 0.05) increased the first derivative of left ventricular pressure at 40 mmHg developed pressure from 4,355 +/- 377 to 4,839 +/- 407 mmHg/s in group 3. Celiac and superior mesenteric ganglionectomy abolished the late but not the early hemodynamic changes. Ganglionectomy also significantly (P < 0.05) enhanced the decrease in mean arterial pressure during reperfusion in all groups. We conclude that the pressor and contractile responses during 10 min of abdominal ischemia and the relative maintenance of blood pressure during reperfusion after ischemia are reflex in nature.

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.

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.

Plication of the Sapheno–Femoral Junction: Effects on Incompetence after Two Years

1991 ◽  
Vol 6 (3) ◽  
pp. 159-165 ◽  
Author(s):  
Giovanni V. Belcaro
Keyword(s):  
Coronary Artery ◽  
Saphenous Vein ◽  
Femoral Vein ◽  
Venous Pressure ◽  
Signs And Symptoms ◽  
Long Term Results ◽  
Pressure Measurements ◽  
Venous Reflux ◽  
Long Saphenous Vein

Plication of the long saphenous vein at the sapheno–femoral junction (SFJ) is an alternative to flush ligation and stripping. This technique abolishes reflux at the SFJ without altering the vein; this may then be used for arterial surgery or coronary artery grafting. Candidates for plication were selected on the basis of ambulatory venous pressure measurements and duplex scanning. These tests indicate and quantify the degree of superficial venous incompetence. Plication of the SFJ reduces the calibre of the vein to 60–70% for a length of 1.5 cm, allowing the value cusps to close when flow in the femoral vein is reversed. In this study 20 limbs were evaluated (in 20 patients) 6, 12 and 24 months after plication. Venous reflux was significantly reduced and there was an improvement in signs and symptoms. Thus, SFJ plication seems to be an effective physiological alternative to flush ligation in some subjects. However, long-term results (> 5 years) must be still evaluated.

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