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- W2007890201 abstract "We previously reported that nitric oxide (NO) in the brain cortex increases during hemorrhagic shock (HS) and then recovers to a baseline level by a retransfusion. Accordingly, we suggested that NO may play a role in blood redistribution during HS. To ascertain whether or not NO contributes to blood redistribution, we have investigated the changes in the liver's NO production during HS. Mongrel dogs were used in the study. After each dog was anesthetized with pentobarbital, an NO-selective electrode was placed in its liver, and a probe to measure hepatic blood flow (HF) was placed on the liver's surface. HS was induced until a mean arterial blood pressure of <40 mmHg was reached. In Group I (n=5), HS was maintained for 30 min. In Group II (n=7), shed blood was reinfused at 10 min after HS. In Group III (n=7), 10 min after NG-nitro-L-arginine methyl ester 30 mg/kg intravenously (i.v.), the same procedures were performed as in Group II. In Groups II and III, although 10 min of HS produced an increase in NO-related electrical current [Group II, 2,197+/-786 pA; Group III, 983+/-77 pA (mean+/-standard error)], reinfusion of shed blood restored the NO-related electrical current to its baseline value. HF in Groups I and II decreased continuously during HS, and it recovered to baseline after the restoration from HS in Group II. In Group III, NG-nitro-L-arginine methyl ester 30 mg/kg i.v. decreased HF 12.7+/-.7 to 10.2+/-.6 mL/min/100 g (mean+/-standard error, p < .05). In conclusion, although NO produced in the liver might play an important pathophysiologic role in HS, it may not affect the blood redistribution during HS, such as in mean arterial blood pressure <40 mmHg." @default.
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- W2007890201 date "1998-05-01" @default.
- W2007890201 modified "2023-09-25" @default.
- W2007890201 title "NITRIC OXIDE IN THE LIVER MAY NOT BE INVOLVED IN BLOOD REDISTRIBUTION DURING HEMORRHAGIC SHOCK IN THE DOG" @default.
- W2007890201 doi "https://doi.org/10.1097/00024382-199805000-00012" @default.
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