Regulation of hepatic blood flow during resuscitation from hemorrhagic shock: role of NO and endothelins

1997 ◽  
Vol 272 (6) ◽  
pp. H2736-H2745 ◽  
Author(s):  
B. H. Pannen ◽  
M. Bauer ◽  
G. F. Noldge-Schomburg ◽  
J. X. Zhang ◽  
J. L. Robotham ◽  
...  
Keyword(s):  
Blood Flow ◽  
Hemorrhagic Shock ◽  
Receptor Antagonist ◽  
Hepatic Blood Flow ◽  
Vehicle Group ◽  
Venous Flow ◽  
Systemic Hemodynamic ◽  
Eta Receptor ◽  
Eta Receptor Antagonist

We determined the role of nitric oxide (NO) and endothelins (ETs) in the regulation of hepatic blood flow during resuscitation from hemorrhagic shock (HS) in anesthetized rats. Volume resuscitation restored systemic hemodynamics and increased hepatic arterial and portal venous flow above baseline in the vehicle group. Presence of N omega-nitro-L-arginine methyl ester (L-NAME, 1 mg/kg) during resuscitation increased systemic vascular resistance (SVR) above baseline, prevented the restoration of hepatic arterial flow, and abolished portal hyperemia. Although the ETA+B-receptor antagonist bosentan (10 mg/kg) did not alter the systemic hemodynamic response, it abolished the hepatic arterial and portal hyperemia. The ETA-receptor antagonist BQ-610 (150 micrograms/kg) reduced SVR below baseline, allowed hepatic arterial hyperemia to occur, and further enhanced the portal venous hyperemia. This indicates that 1) NO reduces SVR and acts to preserve hepatic blood flow during resuscitation from HS; 2) ETA-receptor-mediated vasoconstriction counteracts the systemic and portal hemodynamic effects of NO; and 3) simultaneous ETB-receptor stimulation enhances blood flow to the liver and may serve to modulate the ETA-receptor-mediated vasoconstrictive effects of ETs.

Decreased endothelium-dependent relaxation in subarachnoid hemorrhage-induced vasospasm: role of ET-1

1995 ◽  
Vol 269 (3) ◽  
pp. H1009-H1015 ◽  
Author(s):  
M. Zuccarello ◽  
A. Romano ◽  
M. Passalacqua ◽  
R. M. Rapoport
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Receptor Antagonist ◽  
Basilar Artery ◽  
Arterial Blood ◽  
Eta Receptor ◽  
Eta Receptor Antagonist ◽  
Endothelium Dependent Relaxation

The purpose of this study was to test whether endothelium-dependent relaxation is decreased during acute vasospasm following subarachnoid hemorrhage (SAH) and the mechanism underlying the decrease. Basilar artery in situ was 35% constricted 3 days following injection of autologous arterial blood into the rabbit cisterna magna compared with vessels from control rabbits. In situ suffusion with the endothelium-dependent relaxant, acetylcholine (ACh; 10 microM), relaxed resting and serotonin (5-HT)-contracted control vessels but not vasospastic and 5-HT-contracted vasospastic vessels. In contrast, the relaxant potency and efficacy of ACh was similar in control and vasospastic vessels contracted with 5-HT in vitro. In situ suffusion with the ETA-receptor antagonist, BQ-123 (1 microM), reversed the vasospasm by 51% and restored the magnitude of ACh relaxation of vasospastic and 5-HT-contracted vasospastic vessels to that of controls. ACh in situ and in vitro relaxed endothelin-1 (ET-1)-contracted control vessels to a smaller magnitude than 5-HT-contracted control vessels. These results suggest, in contrast to previous studies, that endothelium-dependent relaxation is decreased during acute vasospasm following SAH. The decreased endothelium-dependent relaxation is secondary to the underlying ET-1-mediated spasm. The inhibition of endothelium-dependent relaxation observed in situ following SAH cannot be demonstrated in vitro, presumably due to loss of the ET-1-mediated vasospasm.

Differential regulation of renal regional blood flow by endothelin-1

1996 ◽  
Vol 271 (6) ◽  
pp. F1166-F1172 ◽  
Author(s):  
K. Gurbanov ◽  
I. Rubinstein ◽  
A. Hoffman ◽  
Z. Abassi ◽  
O. S. Better ◽  
...  
Keyword(s):  
Blood Flow ◽  
Receptor Antagonist ◽  
Bolus Injection ◽  
Regional Blood Flow ◽  
Doppler Flowmetry ◽  
Endothelin 1 ◽  
Male Wistar Rats ◽  
Eta Receptor ◽  
Etb Receptor ◽  
Eta Receptor Antagonist

The present study evaluated the effects and mechanisms of action of endothelin-1 (ET-1) on medullary and cortical blood flow (MBF and CBF, respectively). CBF and MBF were measured simultaneously by laser-Doppler flowmetry in anesthetized male Wistar rats. Bolus injection of ET-1 (1.0 nmol/kg iv) produced a sustained decrease in CBF (delta = -30%) and a transient increase in MBF (delta = +35%). The medullary vasodilation induced by ET-1 was observed with doses lower than that required to produce cortical vasoconstriction; was completely blocked by bosentan, a mixed ETA/B-receptor antagonist; and was mimicked by IRL-1620, a specific ETB-receptor agonist. In contrast, BQ-123, an ETA-receptor antagonist, failed to inhibit the ET-1-dependent medullary vasodilation but effectively blocked the cortical vasoconstriction induced by the peptide. Finally, inhibition of nitric oxide (NO) synthase completely abolished, whereas cylooxygenase inhibition attenuated, the effect of ET-1 on MBF. The data demonstrate that ET-1 exerts opposite effects on renal cortical and medullary circulation, i.e., ETA-receptor-mediated cortical vasoconstriction and ETB-mediated medullary vasodilation. Furthermore, the medullary vasodilation induced by ET-1 is dependent on the NO system and, to a lesser extent, on prostaglandin generation.

scholarly journals Changes in Hepatic Hemodynamics due to Primary Liver Tumours

HPB Surgery ◽  
1996 ◽  
Vol 9 (4) ◽  
pp. 245-248 ◽  
Author(s):  
F. Jakab ◽  
Z. Ráth ◽  
F. Schmal ◽  
P. Nagy ◽  
J. Faller
Keyword(s):  
Hepatocellular Carcinoma ◽  
Blood Flow ◽  
Hepatic Artery ◽  
Hepatic Blood Flow ◽  
Primary Hepatocellular Carcinoma ◽  
Portal Venous Flow ◽  
Venous Flow ◽  
Control Value ◽  
Early Results ◽  
Total Hepatic Blood Flow

Data regarding the afferent circulation of the liver in patients with primary hepatocellular carcinoma are controversial, we have carried out measurement of hepatic arterial and portal venous flow intraoperatively by transit time ultrasonic volume flowmetry. In patients with primary hepatocellular carcinoma the hepatic artery flow increased to 0.55±0.211 compared with the control value of 0.37±0.102 1/min. (p<0.01). The portal venous flow decreased from 0.61±0.212 l/min, to 0.47±l/min. p<0.01). Due to the opposite changes in the afferent circulation the total hepatic blood flow did not change significantly, compared with controls.The ratio of hepatic arterial flow to portal vein flow increased to 1.239±0.246 in patients with hepatocellular carcinoma, which is double of the control value (0.66±0.259 l/min). After resection this ratio did not change.The resection did not alter hepatic artery or portal venous flow significantly, although the total hepatic blood flow decreased significantly (p<0.01).On the basis of our early results it is possible that the ratio of the two circulations may be to deel measured with doppler ultrasound and provide diagnostic information.

BQ123, an ETA Receptor Antagonist, Attenuates Endothelin-1-Induced Vasoconstriction in Rat Pulmonary Circulation

1993 ◽  
Vol 22 (1) ◽  
pp. 39-43 ◽  
Author(s):  
S. T. Bonvallet ◽  
M. Oka ◽  
M. Yano ◽  
M. R. Zamora ◽  
I. F. McMurtry ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Pulmonary Circulation ◽  
Endothelin 1 ◽  
Eta Receptor ◽  
Eta Receptor Antagonist

scholarly journals Salvianolic Acid A, as a Novel ETA Receptor Antagonist, Shows Inhibitory Effects on Tumor in Vitro

2016 ◽  
Vol 17 (8) ◽  
pp. 1244 ◽  
Author(s):  
Qiao Zhang ◽  
Shifeng Wang ◽  
Yangyang Yu ◽  
Shengnan Sun ◽  
Yuxin Zhang ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Inhibitory Effects ◽  
Salvianolic Acid ◽  
Salvianolic Acid A ◽  
Eta Receptor ◽  
Eta Receptor Antagonist

Superiority of YM598 over atrasentan as a selective endothelin ETA receptor antagonist

2004 ◽  
Vol 498 (1-3) ◽  
pp. 171-177 ◽  
Author(s):  
Hironori Yuyama ◽  
Yukiko Noguchi ◽  
Akira Fujimori ◽  
Masashi Ukai ◽  
Noriko Fujiyasu ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Eta Receptor ◽  
Eta Receptor Antagonist

scholarly journals Angiotensin 1-7 Administration Increases Renal Blood Flow in the Absence of Bradykinin B2 Receptor in Ovariectomized Estradiol Treated Rats: The Role of Mas Receptor

2019 ◽  
Author(s):  
Shadan Saberi ◽  
Aghdas Dehghani ◽  
Mehdi Nematbakhsh
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Ovariectomized Rats ◽  
Vehicle Group ◽  
Estradiol Valerate ◽  
Bradykinin B2 Receptor ◽  
Hoe 140 ◽  
Group 2 ◽  
Renal Vascular

Abstract- Renin angiotensin (RAS), kallikrein kinin (KKS), and sex hormonal systems demonstrate a complex contribution in kidney circulation. This study was designed to investigate the role of angiotensin 1-7 (Ang 1-7) receptor (MasR) and of bradykinin B2 receptor (B2R) in renal blood flow (RBF) response to Ang 1-7 infusion in ovariectomized estradiol treated rats. The ovariectomized rats received intramuscular vehicle (group 1, OV) or estradiol valerate (500 µg/Kg/week) (group 2, OVE) for two weeks. Then each group was divided into two subgroups subjected to receive B2R antagonist (HOE-140, subgroup A), or MasR antagonist (A779) plus HOE-140 (subgroup B). RBF and renal vascular resistance (RVR) responses to graded Ang 1-7 infusion were determined. In condition of B2R alone blocking, RBF response to Ang 1-7 in OVE group was significantly greater than that of OV group (P=0.05), however this response difference was failed by co-blockades of MasR and B2R. Estradiol could promote RBF response to graded Ang 1-7 infusion in the absence of B2R alone, however when both receptors (MasR and B2R) were blocked the role of estradiol was limited.

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