Compensatory mechanisms in response to an elevated hepatic oxygen consumption in chronically ethanol-fed rats

1985 ◽  
Vol 248 (5) ◽  
pp. G507-G511 ◽  
Author(s):  
J. E. Bredfeldt ◽  
E. M. Riley ◽  
R. J. Groszmann
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Hepatic Artery ◽  
Oxygen Delivery ◽  
Venous Blood ◽  
Venous Blood Flow ◽  
Compensatory Mechanisms ◽  
Hepatic Oxygen Consumption ◽  
Portal Venous Blood

During conditions that elevate hepatic oxygen consumption (VLO2), oxygen delivery, or oxygen extraction may also increase, acting as compensatory mechanisms. VLO2 was quantitated by an in vivo method in chronically ethanol-fed rats to establish whether VLO2 was increased and what compensatory mechanisms might ensue. VLO2 was increased 45% (0.32 +/- 0.02 ml O2 X min-1 X 100 g body wt-1; P less than 0.001) in rats chronically fed ethanol for 8 wk, while VLO2 (0.28 +/- 0.04; P = NS) was not increased in chronically ethanol-fed rats withdrawn from ethanol 20 h before study compared with control rats (0.22 +/- 0.01). Oxygen delivery was increased 31% (P less than 0.05) in ethanol-fed rats and adequately compensated for the increased VLO2. Hepatic artery blood flow did not increase in ethanol-fed rats, indicating a lack of hepatic artery vasodilation in response to the elevated VLO2. As a result, a greater percentage of oxygen delivery was supplied via portal venous blood flow that has a reduced oxygen content. These observations might suggest that ethanol-fed rats may have a decreased reserve for maintaining an adequate oxygen supply to the liver and may be at an increased liability for developing hepatic hypoxia if oxygen delivery and/or extraction were compromised.

Liver Blood Flow and Oxygen Consumption during Metabolic Acidosis and Alkalosis in the Greyhound

1981 ◽  
Vol 60 (4) ◽  
pp. 355-361 ◽  
Author(s):  
R. L. Hughes ◽  
R. T. Mathie ◽  
W. Fitch ◽  
D. Campbell
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Venous Blood ◽  
Liver Blood Flow ◽  
Arterial Blood Flow ◽  
Venous Blood Flow ◽  
Hepatic Arterial Blood Flow ◽  
Portal Venous Blood Flow ◽  
Arterial Blood ◽  
Portal Venous Blood

1. Hepatic arterial and portal venous blood flow and hepatic oxygen consumption were measured in two groups of greyhounds anaesthetized with pentobarbitone. Flows were measured with electromagnetic flowmeters. 2. In the first group the effects of metabolic acidosis produced by the infusion of a molar solution of lactic acid were studied. In the second group the effects of metabolic alkalosis produced by the infusion of a molar solution of sodium bicarbonate were studied. 3. In the acidotic group hepatic arterial blood flow decreased from 35.2 to 9.6 ml min− 100 g− of liver whereas portal venous blood flow increased from 94.2 to 126.1 ml min− 100 g− of liver. Total liver blood flow was unchanged. Hepatic oxygen consumption increased, but not significantly, while hepatic venous oxygen content decreased significantly. Hepatic arterial resistance increased from 1.18 to 2.77 mmHg min− ml− while peripheral resistance was virtually unchanged. Portal venous pressure increased from 7.08 to 11.6 mmHg. 4. In the alkalotic group portal venous blood flow increased from 112 to 137 ml min− 100 g− of liver. Hepatic arterial blood flow increased, but not significantly. Total liver blood flow increased from 151 to 185, ml min− 100 mg− of liver. There were no significant changes in hepatic oxygen consumption. 5. It is concluded that metabolic acidosis reduces the supply of oxygen to the liver owing to the reduction in hepatic arterial blood flow and is therefore potentially harmful, whereas metabolic alkalosis probably has no biologically significant effect on liver blood flow.

scholarly journals Testicular microvascular flow is altered in Klinefelter syndrome and predicts circulating testosterone

2021 ◽  
Author(s):  
Francesco Carlomagno ◽  
Carlotta Pozza ◽  
Marta Tenuta ◽  
Riccardo Pofi ◽  
Luigi Tarani ◽  
...  
Keyword(s):  
Blood Flow ◽  
Klinefelter Syndrome ◽  
Mean Transit Time ◽  
Venous Blood ◽  
Experimental Studies ◽  
Principal Component ◽  
Endocrine Function ◽  
Venous Blood Flow ◽  
Testicular Blood Flow

ABSTRACTContextExperimental studies on Klinefelter syndrome (KS) reported increased intratesticular testosterone (T) levels coexisting with reduced circulating levels. Abnormalities in testicular microcirculation have been claimed; however, no studies investigated in vivo testicular blood flow dynamics in humans with KS.ObjectiveTo analyze the testicular microcirculation in KS by contrast-enhanced ultrasonography (CEUS) and correlate vascular parameters with endocrine function.Design and SettingProspective study. University Settings.Patients51 testicular scans, 17 testes from 10 T-naïve subjects with KS and 34 testes from age-matched eugonadal men (CNT) who underwent CEUS for incidental nonpalpable testicular lesions.Main OutcomesCEUS kinetic parameters.ResultsCEUS revealed slower testicular perfusion kinetics in subjects with KS than in age-matched CNT. Specifically, the wash-in time (Tin, p = 0.008), mean transit time (MTT, p = 0.008), time to peak (TTP, p < 0.001), and washout time (Tout 50%, p = 0.008) were all prolonged. Faster testicular blood flow was associated with higher total T levels. Principal component analysis and multiple linear regression analyses confirmed the findings, and supported a role for reduced venous blood flow as independent predictor of total T levels.ConclusionsTesticular venous blood flow is altered in KS and independently predicts T peripheral release.

Insufflation profile and body position influence portal venous blood flow during pneumoperitoneum

2003 ◽  
Vol 17 (12) ◽  
pp. 1951-1957 ◽  
Author(s):  
C. -G. Schmedt ◽  
O. Heupel ◽  
V. Riemer ◽  
C. N. Gutt
Keyword(s):  
Blood Flow ◽  
Body Position ◽  
Venous Blood ◽  
Venous Blood Flow ◽  
Portal Venous Blood Flow ◽  
Portal Venous Blood

Fasting and post-prandial splanchnic blood flow is reduced by a somatostatin analogue (octreotide) in man

1991 ◽  
Vol 81 (2) ◽  
pp. 169-175 ◽  
Author(s):  
A. M. Cooper ◽  
G. D. Braatvedt ◽  
M. I. Qamar ◽  
H. Brown ◽  
D. M. Thomas ◽  
...  
Keyword(s):  
Blood Flow ◽  
Superior Mesenteric Artery ◽  
Mesenteric Artery ◽  
Venous Blood ◽  
Splanchnic Blood Flow ◽  
Somatostatin Analogue ◽  
Venous Blood Flow ◽  
Blood Flows ◽  
Portal Venous Blood ◽  
Mesenteric Artery Blood Flow

1. The effects of the subcutaneous administration of a long-acting somatostatin analogue (octreotide) or of placebo on the splanchnic blood flow response to a mixed solid meal has been examined in eight normal subjects by using a transcutaneous Doppler ultrasound technique. Each subject was studied on two occasions more than 1 week apart. 2. On the control day, feeding had a pronounced effect on both superior mesenteric artery and portal venous blood flows, causing a peak rise of 82% in superior mesenteric artery blood flow at 15 min and of 75% in portal venous blood flow at 30 min post-prandially (P < 0.001). Blood flows remained elevated 2 h after the meal. Pulse and blood pressure showed no significant changes from baseline. 3. Octreotide reduced fasting superior mesenteric artery blood flow by 59% (P < 0.05) and portal venous blood flow by 49% (P < 0.01) and blunted the normal post-prandial rise. Pulse and blood pressure did not change in response to either the injection or the ingestion of the meal. 4. Octreotide suppressed the release of insulin, glucagon and pancreatic polypeptide in response to feeding and resulted in post-prandial hyperglycaemia. 5. The mechanism of action of octreotide on splanchnic blood flow is uncertain. It may be mediated via a direct vascular effect or it may act via suppression of vasoactive intestinal hormones.

Portal and splanchnic haemodynamics in patients with advanced post-hepatitic cirrhosis and in healthy adults

1998 ◽  
Vol 39 (2) ◽  
pp. 152-156
Author(s):  
H. Dinç ◽  
A. Sari ◽  
H. Resit Gümele ◽  
N. Cihanyurdu ◽  
A. Baki
Keyword(s):  
Blood Flow ◽  
Portal Vein ◽  
Venous Blood ◽  
Resistive Index ◽  
Venous Blood Flow ◽  
Blood Flows ◽  
Portal Venous Blood Flow ◽  
Portal Venous Blood ◽  
The Mean ◽  
Duplex Doppler

Purpose: to assess portal and splanchnic haemodynamics, and splanchnic vascular resistance in patients with advanced post-hepatitic cirrhosis and in healthy volunteers, by means of duplex Doppler ultrasound (US) Material and Methods: the duplex Doppler US examination was performed in 16 patients with cirrhosis and in 24 healthy volunteers. We investigated vessel diameters, mean flow velocities, and mean blood flows in the portal vein, the superior mesenteric artery (SMA), and the splenic artery (SA), and measured the resistive index values of SMA and SA Results: the mean portal venous blood flow in patients with cirrhosis (829 ± 264 ml/min) was not statistically different from those in the volunteers (734 ± 194 ml/min). the ratio of the SMA and SA blood flows (621 ml/min) to the portal venous blood flow (734 ml/min) was 0.85 in the control subjects. the mean portal venous blood flow (1261 ml/min) and the portal venous velocity (14.6 cm/s) were higher in the patients with recanalized para-umbilical veins than in the volunteers and in the patients without recanalized para-umbilical veins. the SMA and SA blood flows were significantly increased in patients with cirrhosis compared with volunteers. Splanchnic inflow (the sum of the SMA and SA blood flows) was higher than the portal blood flow in patients with cirrhosis except in the subjects with recanalized para-umbilical veins. SMA and SA resistive index values were significantly higher in these patients than in the volunteers Conclusion: Splanchnic blood flow and splanchnic vascular impedance increased significantly in patients with advanced post-hepatitic cirrhosis. Splanchnic inflow must not exceed portal venous blood flow in patients with recanalized para-umbilical veins. Portal vein velocity and portal venous blood flow measurements alone are not useful parameters for discriminating patients with cirrhosis from healthy subjects

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