Effects of nitric oxide donor on hepatic arterial buffer response in anesthetized pigs.
ABSTRACT The effects of systemic administration of exogenous nitric oxide (NO) donor on hepatic arterial buffer response (HABR) have not yet been studied in an anesthetized model. In this study, 28 anesthetized pigs received administration of sodium nitroprusside (SNP) or nitroglycerin (NTG) as exogenous NO donors. Pressure-flow (P-Q) relationships in the hepatic artery defined the pressure at zero flow (P(Qha = 0)) and flow-dependent resistance (R). The magnitude of HABR was evaluated by comparing the change in hepatic arterial blood flow (DeltaQha) divided by the change in portal venous blood flow (DeltaQpv), using the index of change in blood flow (DeltaQha/DeltaQpv). Mean arterial pressure decreased from baseline (95.6 +/- 3.8 mmHg) to SNP condition (68.3 +/- 1.9 mmHg) and decreased from baseline (92.7 +/- 4.4 mmHg) to NTG condition (66.2 +/- 1.7 mmHg). Mean index of change in blood flow (DeltaQha/DeltaQpv) was also significantly increased from baseline (0.19 +/- 0.12) to SNP condition (0.28 +/- 0.17; p = .009) and from baseline (0.18 +/- 0.17) to NTG (0.28 +/- 0.20; p < .05). In conclusion, systemic administration of SNP and NTG increases HABR with reduced hepatic arterial tone under decreased mean arterial pressure, presumably via exogenous NO enhancing another regulatory system and reducing the pressure gradient for sinusoidal washout.
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ABSTRACT: Changes in hepatic plasma flow (HPF) during sodium nitroprusside (SNP) induced hypotension were studied in 14 patients undergoing intracranial aneurysm surgery under neurolept anesthesia. Patients were monitored with the use of a radial artery catheter and a thermistor-tipped Swan-Ganz catheter. Hypotension was induced with incremental increases in the rate of SNP infusion until a stable mean arterial pressure (MAP) 35-55 mmHg had been achieved. In one group (Group A) of 10 patients, indocyanine green (ICG) clearance was determined simultaneously with hemodynamic variables, before and during SNP hypotension. In a second group (Group B) of four patients, a catheter was inserted into a hepatic vein to determine the ICG hepatic extraction (HE) coefficient. In Group A, MAP decreased from 73 +/- 10 (SD) to 41 +/- 9 mmHg, while cardiac index (CI) decreased in six patients and increased in four patients. However, the mean value of CI did not change significantly. The mean value of ICG clearance was not significantly affected by SNP hypotension. Nevertheless, a positive linear correlation existed between individual variation in CI and ICG clearance (r = 0.96). On the other hand, no correlation was noted between the change in MAP and ICG clearance. In Group B patients, the ICG HE coefficient remained unchanged during SNP hypotension, suggesting that ICG clearance varies only according to the variation in HPF. In conclusion, this study demonstrated that HPF did not decrease, despite a range of 20-60% decrease in blood pressure when CI is maintained during SNP hypotension.Anesthesiology 10/1985; 63(3):287-93. · 5.16 Impact Factor
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ABSTRACT: Central and splanchnic hemodynamic effects during controlled hypotension induced by the administration of the endogenous vasodilator adenosine were studied in ten artificially ventilated dogs under neurolept anesthesia. Adenosine was administered as a continuous infusion in the aorta (n = 3), in the inferior vena cava (n = 3), and after pretreatment with dipyridamole (which inhibits the cellular uptake of adenosine) (n = 4) in a dose sufficient to maintain a mean arterial blood pressure (MABP) level of approximately 50 mmHg. Observations were made before and after 20 min of controlled hypotension. Basal arterial plasma levels of adenosine were in the 10(-7) M range (means = 0.4 microM). The hemodynamic response was similar in all three settings. Adenosine caused a profound decrease in systemic vascular resistance (SVR) (52%, P less than 0.01) and preportal vascular resistance (PPR) (64%, P less than 0.01), while hepatic arterial vascular resistance ( HAR ) increased by 49% (P less than 0.05). Cardiac output increased (22%, P less than 0.05) through increase of stroke volume (77%, P less than 0.01), while heart rate decreased (28%, P less than 0.01). Whole-body oxygen uptake decreased (14%, P less than 0.01). Portal venous blood flow increased by 28% (P less than 0.05), whereas hepatic arterial blood flow decreased by 70% (P less than 0.01). In the preportal tissues, oxygen uptake decreased by 21% (P less than 0.01). In contrast, hepatic oxygen consumption increased (53%, P less than 0.05). Adenosine-induced hypotension was not associated with changes in plasma renin activity or the plasma concentration of norepinephrine. It is concluded that adenosine causes a rapidly induced and easily maintained hypotension and may be a potentially useful agent for controlled hypotension in patients.Anesthesiology 07/1984; 60(6):547-52. · 5.16 Impact Factor
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ABSTRACT: Controversial studies have been published concerning the role of nitric oxide (NO) release (beneficial or deleterious) during sepsis. Severe hypotension has been treated by NO inhibitors in humans, but animal studies described an increased mortality rate with this treatment. We hypothesized that an NO donor might be beneficial in maintaining liver flow during endotoxemia. To answer that question, mean arterial pressure (MAP), aortic, hepatic artery, and portal vein blood flow velocities (AoV, HAV, and PVV) (Doppler technique) were measured after endotoxin injection (Escherichia coli, Salmonella minnesota, and Salmonella enteritidis, 400 micrograms each, intravenously) in anesthetized and mechanically ventilated rabbits. Fifteen animals were treated with saline solution (10 mL/hr) or linsidomine perfusion (2 mg over 3 hours, 10 mL/hr). Saline-treated animals experienced a hypodynamic shock with a decrease in MAP, AoV, and PVV. In contrast, HAV increased without fully compensating the PVV decrease. In linsidomine-perfused rabbits, AoV and PVV remained at control level, and HAV increased without any further effect on MAP. Serum lactate levels increased in the saline-treated group and did not change in linsidomine-treated animals. These findings show that at the early phase of an endotoxin shock, and in the absence of intense fluid resuscitation, linsidomine perfusion is beneficial in maintaining systemic and hepatic perfusion while preventing lactic acidosis. These data suggest that, in the early phase of endotoxemia, NO is insufficiently released to allow adequate liver perfusion.Hepatology 12/1995; 22(5):1547-53. · 12.00 Impact Factor