Effect of NO on Brain Circulation fellowiy Reccvery from Organs Faitu

1996 Fiscal Year Final Research Report Summary

• Project/Area Number: 07457348
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Anesthesiology/Resuscitation studies
• Research Institution: University of TsukuBA
• Principal Investigator: SATO Shigehito University of TsukuBA,Institute of Clinical Medicine, Associate professor, 臨床医学系, 助教授 (30143176)
• Co-Investigator(Kenkyū-buntansha): MIYABE Masayuki University of TsukuBA,Institute of Clinica, Lecturer, 臨床医学系, 講師 (60145589) ; SAITO Shigeyuki University of TsukuBA,Institute of Clinical Medicine Lecturer, 臨床医学系, 講師 (20186935) ; NICHIKAWA Toshiaki Akita University School of Medicine, Professor, 医学部, 教授 (50156048)
• Project Period (FY): 1995 – 1996
• Keywords: NO(nitric oxide) / hemorrhagu shock / hepatic blood flow / es-NOS / L-NAME

Research Abstract

We previously reported that 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.In order 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 (MAP) of<40 mmHg was reached. In Gr. I(n=5), HS was maintained for 30 min. In Gr. II(n=7), shed blood was reinfused at 10 min after HS.In Gr. III(n=7), 10 min after N^G-nitro-L-arginine methylester (L-NAME) 30 mg/kg i.v., the same procedures were performed as in Gr. II.
In Gr. II and III, although 10 min of HS produced an increase in NO-REC (Gr. II ; 2,197 (]SY.+-。[) 786 pA, Gr. III ; 983 (]SY.+-。[) 77 pA, mean (]SY.+-。[) SEM), reinfusion of shed blood restored the NO-REC to its baseline value. HF in Gr. I and II decreased continuously during HS, and it recovered to baseline following the restoration from HS in Gr. II.In Gr. III, L-NAME 30 mg/kg i.v. decreased HF 12.7 (]SY.+-。[) 0.7 to 10.2 (]SY.+-。[) 0.6 ml/min/100g (mean (]SY.+-。[) SEM, p<0.05).
In conclusion, although NO produced in the liver might play an important pathophysiologic role HS, it may not affect the blood redistribution during HS, such as in MAP<40 mmHg.