Systemic and hepatic hemodynamic changes in acute liver injury

1997 ◽  
Vol 272 (3) ◽  
pp. G617-G625 ◽  
Author(s):  
A. J. Makin ◽  
R. D. Hughes ◽  
R. Williams
Keyword(s):  
Blood Flow ◽  
Liver Injury ◽  
Hepatic Injury ◽  
Acute Liver Injury ◽  
Venous Blood ◽  
Marked Change ◽  
Arterial Blood Flow ◽  
Venous Flow ◽  
Subsequent Increase ◽  
Arterial Blood

Systemic and hepatic circulatory changes were studied in rats over the course of acute liver injury. Hepatic injury was induced by intraperitoneal injection of D-galactosamine (1.1 g/kg), and systemic and hepatic hemodynamics were measured over a 72-h period using a radioactive microsphere technique with direct measurement of arterial, portal venous, and hepatic venous blood oxygen content. Cardiac output increased to a maximum at 48 h, producing a marked increase (450%) in hepatic arterial blood flow so that it became the dominant supply of oxygen at the time of maximal hepatic injury. A subsequent increase in portal venous flow resulted in an overall increase in total hepatic blood flow of 500%. At this point the oxygen delivery by the hepatic arterial and portal venous systems was equal. These circulatory changes returned to control values by 72 h with recovery of liver function. These results demonstrate the development of a hyperdynamic circulation and a marked change in the normal relationship between portal venous and hepatic arterial blood flows that occur during hepatic injury.

Role of glucagon in splanchnic hyperemia of chronic portal hypertension

1986 ◽  
Vol 251 (5) ◽  
pp. G674-G677 ◽  
Author(s):  
J. N. Benoit ◽  
B. Zimmerman ◽  
A. J. Premen ◽  
V. L. Go ◽  
D. N. Granger
Keyword(s):  
Blood Flow ◽  
Portal Hypertension ◽  
Venous Blood ◽  
Reference Sample ◽  
Venous Hypertension ◽  
Arterial Blood Flow ◽  
Venous Blood Flow ◽  
Portal Vein Stenosis ◽  
Arterial Blood

The role of glucagon as a blood-borne mediator of the hyperdynamic circulation associated with chronic portal venous hypertension was assessed in the rat portal vein stenosis model. Selective removal of pancreatic glucagon from the circulation was achieved by intravenous infusion of a highly specific glucagon antiserum. Blood flow to splanchnic organs, kidneys, and testicles was measured with radioactive microspheres, and the reference-sample method. Glucagon antiserum had no effect on blood flow in the gastrointestinal tract of sham-operated (control) rats. However, the antiserum produced a significant reduction in hepatic arterial blood flow in the control rats, suggesting that glucagon contributes significantly to the basal tone of hepatic arterioles. In portal hypertensive rats glucagon antiserum significantly reduced blood flow to the stomach (22%), duodenum (25%), jejunum (24%), ileum (26%), cecum (27%), and colon (26%). Portal venous blood flow was reduced by approximately 30%. The results of this study support the hypothesis that glucagon mediates a portion of the splanchnic hyperemia associated with chronic portal hypertension.

Effects of systemic arterial hypoperfusion on splanchnic hemodynamics and hepatic arterial buffer response in pigs

2001 ◽  
Vol 280 (5) ◽  
pp. G819-G827 ◽  
Author(s):  
S. M. Jakob ◽  
J. J. Tenhunen ◽  
S. Laitinen ◽  
A. Heino ◽  
E. Alhava ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Tamponade ◽  
Venous Blood ◽  
Liver Blood Flow ◽  
Hepatic Function ◽  
Arterial Blood Flow ◽  
Cellular Damage ◽  
Aortic Blood Flow ◽  
Venous Blood Flow ◽  
Arterial Blood

The hepatic arterial buffer response (HABR) tends to maintain liver blood flow under conditions of low mesenteric perfusion. We hypothesized that systemic hypoperfusion impairs the HABR. In 12 pigs, aortic blood flow was reduced by cardiac tamponade to 50 ml · kg−1 · min−1 for 1 h (short-term tamponade) and further to 30 ml · kg−1 · min−1 for another hour (prolonged tamponade). Twelve pigs without tamponade served as controls. Portal venous blood flow decreased from 17 ± 3 (baseline) to 6 ± 4 ml · kg−1 · min−1 (prolonged tamponade; P = 0.012) and did not change in controls, whereas hepatic arterial blood flow decreased from 2 ± 1 (baseline) to 1 ± 1 ml · kg−1 · min−1 (prolonged tamponade; P = 0.050) and increased from 2 ± 1 to 4 ± 2 ml · kg−1 · min−1in controls ( P = 0.002). The change in hepatic arterial conductance (Δ C ha) during acute portal vein occlusion decreased from 0.1 ± 0.05 (baseline) to 0 ± 0.01 ml · kg−1 · min−1 · mmHg−1(prolonged tamponade; P = 0.043). In controls, Δ C ha did not change. Hepatic lactate extraction decreased, but hepatic release of glutathione S-transferase A did not change during cardiac tamponade. In conclusion, during low systemic perfusion, the HABR is exhausted and hepatic function is impaired without signs of cellular damage.

Splenic baroreceptors control splenic afferent nerve activity

2006 ◽  
Vol 290 (2) ◽  
pp. R352-R356 ◽  
Author(s):  
Karli Moncrief ◽  
Susan Kaufman
Keyword(s):  
Blood Flow ◽  
Venous Pressure ◽  
Venous Blood ◽  
Splenic Vein ◽  
Afferent Nerve ◽  
Arterial Blood Flow ◽  
Venous Blood Flow ◽  
Nerve Activity ◽  
Vein Occlusion ◽  
Arterial Blood

Stenosis of either the portal or splenic vein increases splenic afferent nerve activity (SANA), which, through the splenorenal reflex, reduces renal blood flow. Because these maneuvers not only raise splenic venous pressure but also reduce splenic venous outflow, the question remained as to whether it is increased intrasplenic postcapillary pressure and/or reduced intrasplenic blood flow, which stimulates SANA. In anesthetized rats, we measured the changes in SANA in response to partial occlusion of either the splenic artery or vein. Splenic venous and arterial pressures and flows were simultaneously monitored. Splenic vein occlusion increased splenic venous pressure (9.5 ± 0.5 to 22.9 ± 0.8 mmHg, n = 6), reduced splenic arterial blood flow (1.7 ± 0.1 to 0.9 ± 0.1 ml/min, n = 6) and splenic venous blood flow (1.3 ± 0.1 to 0.6 ± 0.1 ml/min, n = 6), and increased SANA (1.7 ± 0.4 to 2.2 ± 0.5 spikes/s, n = 6). During splenic artery occlusion, we matched the reduction in either splenic arterial blood flow (1.7 ± 0.1 to 0.7 ± 0.05, n = 6) or splenic venous blood flow (1.2 ± 0.1 to 0.5 ± 0.04, n = 5) with that seen during splenic vein occlusion. In neither case was there any change in either splenic venous pressure (−0.4 ± 0.9 mmHg, n = 6 and +0.1 ± 0.3 mmHg, n = 5) or SANA (−0.11 ± 0.15 spikes/s, n = 6 and −0.05 ± 0.08 spikes/s, n = 5), respectively. Furthermore, there was a linear relationship between SANA and splenic venous pressure ( r = 0.619, P = 0.008, n = 17). There was no such relationship with splenic venous ( r = 0.371, P = 0.236, n = 12) or arterial ( r = 0.275, P = 0.413, n = 11) blood flow. We conclude that it is splenic venous pressure, not flow, which stimulates splenic afferent nerve activity and activates the splenorenal reflex in portal and splenic venous hypertension.

Nitric oxide increases hepatic arterial blood flow in rats with carbon tetrachloride–induced acute hepatic injury

1999 ◽  
Vol 117 (1) ◽  
pp. 173-180 ◽  
Author(s):  
Noriko Tanaka ◽  
Katsuaki Tanaka ◽  
Yoji Nagashima ◽  
Masaaki Kondo ◽  
Hisahiko Sekihara
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Carbon Tetrachloride ◽  
Hepatic Injury ◽  
Arterial Blood Flow ◽  
Hepatic Arterial Blood Flow ◽  
Arterial Blood ◽  
Acute Hepatic Injury

scholarly journals Venous flow velocity, venous volume and arterial blood flow.

Circulation ◽  
1975 ◽  
Vol 52 (1) ◽  
pp. 141-145 ◽  
Author(s):  
J D Coffman ◽  
J A Lempert
Keyword(s):  
Blood Flow ◽  
Flow Velocity ◽  
Arterial Blood Flow ◽  
Venous Flow ◽  
Arterial Blood ◽  
Venous Volume

scholarly journals Effect of Electrical Stimulation on Blood Flow in Calf Muscles in Different Body Positions

2018 ◽  
Vol 1 (96) ◽  
Author(s):  
Julius Dovydaitis ◽  
Albinas Grūnovas
Keyword(s):  
Blood Flow ◽  
Body Position ◽  
Venous Blood ◽  
The Body ◽  
Arterial Blood Flow ◽  
Reserve Capacity ◽  
Horizontal Position ◽  
Blood Flows ◽  
Arterial Blood ◽  
Electrical Muscle

Background.  In  most  studies  on  cardiovascular  system,  testing  of  subjects  was  performed  in  a  horizontal position. With the change of the body position, certain functional changes occur in the cardiovascular system. The aim of this study was to analyze the effect of electrical muscle stimulation (EMS) on arterial and venous blood flows.Methods. Eighteen athletes aged 19–23 performed two sessions of tests in horizontal and sitting positions. Changes in arterial and venous blood flows were recorded before and after EMS. In each session two occlusions were performed. In the horizontal position, the initial occlusion pressure of 20 mmHg was applied and as the balance in arterial and venous blood flow rates was reached, the additional pressure of 20 mmHg (40  mmHg in total). In the sitting position, the occlusion pressure of 40 and 20 mmHg was applied respectively (60 mmHg in total). In both sessions EMS was performed using the electrical stimulator Mioritm 021.Results. In both horizontal and vertical positions, the effect of EMS on arterial blood flow, venous reserve capacity and venous elasticity was insignificant. Arterial and venous blood flows was affected significantly by the change of the body position. In the sitting position, arterial blood flow was significantly (p < .05) lower compared to the horizontal position. Similar results were recorded in venous reserve capacity.Conclusion.  The  study  suggests  that  blood  flow  in  the  calf  muscles  is  affected  by  the  body  position  and hydrostatic pressure; arterial blood flow increases in the horizontal body position.Keywords:  electrical muscle stimulation (EMS), arterial blood flow, venous reserve capacity, venous elasticity

Pre-clinical pharmacology of zolmitriptan (Zomig™; formerly 311C90), a centrally and peripherally acting 5HT1B/1D agonist for migraine

Cephalalgia ◽  
1997 ◽  
Vol 17 (18_suppl) ◽  
pp. 4-14 ◽  
Author(s):  
Gr Martin
Keyword(s):  
Blood Flow ◽  
Nucleus Tractus Solitarius ◽  
Ex Vivo ◽  
Partial Agonist ◽  
Venous Blood ◽  
Arterial Blood Flow ◽  
Vascular Effects ◽  
Protein Extravasation ◽  
Trigeminal Stimulation ◽  
Arterial Blood

Zolmitriptan (Zomig™ formerly 311C90) is a novel 5-hydroxytryptamine (5HT)1B/1D receptor agonist with proven efficacy in the acute treatment of migraine with or without preceding aura. The drug differs from presently available members of this drug class in that it combines 5HT1B/1D receptor partial agonist activity with robust oral pharmacokinetics and an ability to inhibit trigeminovascular activation centrally as well as peripherally in preclinical studies. Consistent with its selectivity for 5HT1B/1D receptors, zolmitriptan produces constriction of various isolated blood vessels, most notably cranial arteries. In anaesthetized animals, these vascular effects manifest as a selective constriction of cranial arterio-venous anastomoses resulting in a redistribution of carotid arterial blood flow. This effect is produced without significant effects on heart rate, blood pressure or blood flow to the brain, heart or lungs. Zolmitriptan also inhibits trigeminal-evoked increases in cerebral blood flow in anaesthetized cats and blocks trigeminal-evoked plasma protein extravasation in the dura of guinea-pigs. These actions are consistent with a pre-junctional inhibition of neuropeptide release from perivascular afferents of the trigeminal nerve, as confirmed by independent studies showing that zolmitriptan blocks elevations of calcitonin-gene-related peptide in jugular venous blood during electrical stimulation of the trigeminal ganglion. In all of these effects, zolmitriptan is three to four times more potent than sumatriptan, but produces the same maximum response. Zolmitriptan crosses the intact blood-brain barrier to inhibit trigeminovascular activation in the brainstem. This was shown initially by the ability of the drug to block a brainstem reflex provoking vasoactive intestinal peptide release from the VIIth cranial (facial) nerve during trigeminal stimulation. Subsequent ex vivo autoradiography confirmed that intravenously injected [3H]zolmitriptan labels a discrete population of cells in the trigeminal nucleus caudalis (TNC) and nucleus tractus solitarius. Direct evidence for a central neuromodulatory effect of zolmitriptan was provided by electrophysiological experiments which clearly demonstrated that the drug inhibits the excitability of cells in the TNC after systemic administration. This novel preclinical profile not only distinguishes zolmitriptan from sumatriptan, but raises intriguing questions about the clinical relevance of a dual action. Studies to date show that zolmitriptan indeed modulates cranial sensory processing in humans, yet central side-effects are no different from sumatriptan. This property may account for the remarkable consistency in clinical efficacy observed in clinical trials.

Liver blood flow and oxygen consumption during hypocapnia and IPPV in the greyhound

1979 ◽  
Vol 47 (2) ◽  
pp. 290-295 ◽  
Author(s):  
R. L. Hughes ◽  
R. T. Mathie ◽  
W. Fitch ◽  
D. Campbell
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Airway Pressure ◽  
Venous Blood ◽  
Liver Blood Flow ◽  
Arterial Blood Flow ◽  
Venous Blood Flow ◽  
Hepatic Arterial Blood Flow ◽  
Arterial Blood ◽  
Intermittent Positive Pressure Breathing

Pentobarbital-anesthetized greyhounds were passively hyperventilated using intermittent positive-pressure breathing (IPPV) and the effects of raised airway pressure, accompanied by hypocapnia and then by normocapnia, on liver blood flow and oxygen consumption were studied. Electromagnetic flowmeters were used to measure hepatic arterial, portal venous, and splenic venous blood flow. Studies were carried out at three levels of raised airway pressure, both at normocapnia and hypocapnia. It was found that hypocapnic hyperventilation produced a decrease in portal venous and hepatic arterial blood flow. Normocapnic hyperventilation resulted in a restoration of portal venous blood flow but with a further decrease in hepatic arterial blood flow. A decrease in oxygen consumption with hypocapnia, returning to control values with normocapnia, was seen. It is suggested that the reduction in liver blood flow and oxygen consumption seen with passive hyperventilation is chiefly an effect of hypocapnia and is largely reversed by restoration of normocapnia.

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