Effect of stimulation of hepatic nerves on hepatic O2 uptake and blood flow

1977 ◽  
Vol 232 (6) ◽  
pp. H652-H656
Author(s):  
W. W. Lautt
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Oxygen Uptake ◽  
Portal Vein ◽  
Hepatic Artery ◽  
Venous Blood ◽  
Neurogenic Vasoconstriction ◽  
Pressure Changes ◽  
Hepatic Nerves ◽  
Stimulation Of

Acute denervation of the liver did not result in changes of oxygen uptake or hemodynamics in the intact liver of the cat. Stimulation of the hepatic nerves resulted in a marked reduction of vascular conductance of the hepatic artery and portal vein (intrahepatic) resulting in almost complete cessation of arterial flow and increased portal blood pressure. The hepatic artery showed a more complete escape from the neurogenic vasoconstriction than did the portal vein. During the stable "escape phase" oxygen delivery was 86% of control, but hepatic extraction of oxygen increased so that oxygen uptake was not altered from control values. The return of oxygen consumption to normal during nerve stimulation suggests that redistribution of hepatic blood flow did not occur. In spite of arterial and portal venous blood pressure changes and changes in gut conductance, oxygen extraction of the gut did not change.

H2S contributes to the hepatic arterial buffer response and mediates vasorelaxation of the hepatic artery via activation of KATP channels

2008 ◽  
Vol 295 (6) ◽  
pp. G1266-G1273 ◽  
Author(s):  
Nikolai Siebert ◽  
Daniel Cantré ◽  
Christian Eipel ◽  
Brigitte Vollmar
Keyword(s):  
Blood Flow ◽  
Portal Vein ◽  
Hepatic Artery ◽  
Buffer Capacity ◽  
Venous Blood ◽  
Control Level ◽  
Vena Cava ◽  
Arterial Blood Flow ◽  
Venous Blood Flow ◽  
Arterial Blood

Hepatic blood supply is uniquely regulated by the hepatic arterial buffer response (HABR), counteracting alterations of portal venous blood flow by flow changes of the hepatic artery. Hydrogen sulfide (H2S) has been recognized as a novel signaling molecule with vasoactive properties. However, the contribution of H2S in mediating the HABR is not yet studied. In pentobarbital-anesthetized and laparotomized rats, flow probes around the portal vein and hepatic artery allowed for assessment of the portal venous (PVBF) and hepatic arterial blood flow (HABF) under baseline conditions and stepwise reduction of PVBF for induction of HABR. Animals received either the H2S donor Na2S, DL-propargylglycine as inhibitor of the H2S synthesizing enzyme cystathionine-γ-lyase (CSE), or saline alone. Additionally, animals were treated with Na2S and the ATP-sensitive potassium channel (KATP) inhibitor glibenclamide or with glibenclamide alone. Na2S markedly increased the buffer capacity to 27.4 ± 3.0% ( P < 0.05 vs. controls: 15.5 ± 1.7%), whereas blockade of H2S formation by DL-propargylglycine significantly reduced the buffer capacity (8.5 ± 1.4%). Glibenclamide completely reversed the H2S-induced increase of buffer capacity to the control level. By means of RT-PCR, Western blot analysis, and immunohistochemistry, we observed the expression of both H2S synthesizing enzymes (CSE and cystathionine-β-synthase) in aorta, vena cava, hepatic artery, and portal vein, as well as in hepatic parenchymal tissue. Terminal branches of the hepatic afferent vessels expressed only CSE. We show for the first time that CSE-derived H2S contributes to HABR and partly mediates vasorelaxation of the hepatic artery via activation of KATP channels.

Influence of blood volume restoration and tissue trauma on corticosteroid secretion in dogs

1959 ◽  
Vol 197 (4) ◽  
pp. 781-785 ◽  
Author(s):  
William F. Walker ◽  
William C. Shoemaker ◽  
Aud J. Kaalstad ◽  
Francis D. Moore
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Blood Volume ◽  
Venous Blood ◽  
Total Output ◽  
Anesthetized Dogs ◽  
Adrenocortical Failure ◽  
Tissue Trauma ◽  
Pressure Changes ◽  
Corticosteroid Secretion

In this third paper the authors record the corticosteroid data derived from the animals reported in the previous studies. A total of 12 animals is described. Acute reduction in blood volume in dogs resulted in markedly increased concentrations of corticosteroids in the adrenal vein blood. In some instances, alteration in flow was so balanced that there was no increase in total secretion of corticosteroids; in others, the adrenal blood flow was such that the output total was increased. In dogs subjected to a more chronic shock challenge by prolonged bleeding, the concentration and output of corticosteroids varied considerably according to adrenal blood flow and the presence or absence of the ‘taking-up’ phenomena. Replacement of lost blood was accompanied by a reduction in concentration and, in some cases, total output of corticosteroids. Fracture of the femur in anesthetized dogs resulted in increased concentration of corticosteroids in the adrenal venous blood, seemingly unrelated to blood pressure changes. There was no sign of adrenocortical failure in any of these animals and in one case a low output of corticosteroids in response to hemorrhage did not appear to influence the resistance of the animal to hemorrhagic hypotension.

Changes in Blood Pressure, Heart Rate and Breathing Rate During Moderate Swimming Activity in Rainbow Trout

1967 ◽  
Vol 46 (2) ◽  
pp. 307-315 ◽  
Author(s):  
E. DON STEVENS ◽  
D. J. RANDALL
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Rainbow Trout ◽  
Venous Blood ◽  
The Body ◽  
Swimming Activity ◽  
Breathing Rate ◽  
Blood Pressures ◽  
Ventral Aorta ◽  
Pressure Changes

1. Changes in blood pressure in the dorsal aorta, ventral aorta and subintestinal vein, as well as changes in heart rate and breathing rate during moderate swimming activity in the rainbow trout are reported. 2. Blood pressures both afferent and efferent to the gills increased during swimming and then returned to normal levels within 30 min. after exercise. 3. Venous blood pressure was characterized by periodic increases during swimming. The pressure changes were not in phase with the body movements. 4. Although total venous return to the heart increased during swimming, a decreased blood flow was recorded in the subintestinal vein. 5. Heart rate and breathing rate increased during swimming and then decreased when swimming ceased. 6. Some possible mechanisms regulating heart and breathing rates are discussed.

Maximal vascular leg conductance in trained and untrained men

1987 ◽  
Vol 62 (2) ◽  
pp. 606-610 ◽  
Author(s):  
P. G. Snell ◽  
W. H. Martin ◽  
J. C. Buckey ◽  
C. G. Blomqvist
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Oxygen Uptake ◽  
Maximal Oxygen Uptake ◽  
Reactive Hyperemia ◽  
Venous Occlusion ◽  
Vascular Conductance ◽  
Blood Flows ◽  
Arterial Blood ◽  
Sedentary Subjects

Lower leg blood flow and vascular conductance were studied and related to maximal oxygen uptake in 15 sedentary men (28.5 +/- 1.2 yr, mean +/- SE) and 11 endurance-trained men (30.5 +/- 2.0 yr). Blood flows were obtained at rest and during reactive hyperemia produced by ischemic exercise to fatigue. Vascular conductance was computed from blood flow measured by venous occlusion plethysmography, and mean arterial blood pressure was determined by auscultation of the brachial artery. Resting blood flow and mean arterial pressure were similar in both groups (combined mean, 3.0 ml X min-1 X 100 ml-1 and 88.2 mmHg). After ischemic exercise, blood flows were 29- and 19-fold higher (P less than 0.001) than rest in trained (83.3 +/- 3.8 ml X min-1 X 100 ml-1) and sedentary subjects (61.5 +/- 2.3 ml X min-1 X 100 ml-1), respectively. Blood pressure and heart rate were only slightly elevated in both groups. Maximal vascular conductance was significantly higher (P less than 0.001) in the trained compared with the sedentary subjects. The correlation coefficients for maximal oxygen uptake vs. vascular conductance were 0.81 (trained) and 0.45 (sedentary). These data suggest that physical training increases the capacity for vasodilation in active limbs and also enables the trained individual to utilize a larger fraction of maximal vascular conductance than the sedentary subject.

Localization of intrahepatic portal vascular resistance

1986 ◽  
Vol 251 (3) ◽  
pp. G375-G381 ◽  
Author(s):  
W. W. Lautt ◽  
C. V. Greenway ◽  
D. J. Legare ◽  
H. Weisman
Keyword(s):  
Pressure Drop ◽  
Portal Vein ◽  
Vascular Resistance ◽  
Venous Pressure ◽  
Vena Cava ◽  
Sympathetic Nerves ◽  
Hepatic Veins ◽  
Pressure Changes ◽  
Stimulation Of ◽  
Anesthetized Cat

The pressure drop from the portal vein to the vena cava occurs primarily across a postsinusoidal site localized to a narrow segment (less than 0.5 cm) of hepatic veins (roughly 1.5 mm diam) in the anesthetized cat. Portal venous pressure (PVP = 8.9 +/- 0.3 mmHg) and lobar hepatic venous pressure (LVP = 8.7 +/- 0.4 mmHg) are insignificantly different, and pressure changes imposed from the presinusoidal or postsinusoidal side are equally transmitted to both pressure sites. Several types of experiments were done to validate the LVP measurement. The portal vein, hepatic sinusoids, and hepatic veins proximal to the resistance site are all under a similar pressure. Previously reported calculations of hepatic vascular resistance are in error because of incorrect assumptions of sinusoidal pressure and localization of the portal resistance site as presinusoidal. Stimulation of hepatic sympathetic nerves for 3 min caused LVP and PVP to increase equally, showing that the increased "portal" resistance is postsinusoidal across the same region of the hepatic veins that was previously localized as the site of resistance in the basal state.

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.

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