Nitric oxide generation in a rat model of acute portal hypertension

Citation
Lm. Howe et al., Nitric oxide generation in a rat model of acute portal hypertension, AM J VET RE, 61(10), 2000, pp. 1173-1177
Citations number
45
Categorie Soggetti
Veterinary Medicine/Animal Health
Journal title
AMERICAN JOURNAL OF VETERINARY RESEARCH
ISSN journal
00029645 → ACNP
Volume
61
Issue
10
Year of publication
2000
Pages
1173 - 1177
Database
ISI
SICI code
0002-9645(200010)61:10<1173:NOGIAR>2.0.ZU;2-X
Abstract
Objective-To document blood nitric oxide concentrations in the portal vein and systemic circulation in a rat model of acute portal hypertension and co mpare values with a control group and a sham surgical group. Animals-50 rats; 10 controls (group 1), 10 sham surgical (group 2), and 10 rats with surgically induced acute portal hypertension (group 3). Procedure-Following induction of anesthesia, catheters were placed surgical ly in the carotid artery, jugular, and portal veins of group 2 and 3 rats a nd in the carotid artery and jugular vein of group 1 rats. Baseline heart a nd respiratory rates, rectal temperature, and vascular pressure measurement s were obtained, and blood was drawn from all catheters for baseline nitric oxide (NO) concentrations. Acute portal hypertension was induced in the gr oup 3 rats by tying a partially occluding suture around the portal vein and a 22-gauge catheter. The catheter was then removed, resulting in a repeata ble degree of portal vein impingement. After catheter placement, all variab les were remeasured at 15-minute intervals for 3 hours. Results-Blood nitric oxide concentrations were greater in all vessels teste d in group 3 than in group 2 rats. Conclusions and Clinical Relevance-Acute portal hypertension in this experi mental model results in increased concentrations of NO in the systemic and portal circulation. On the basis of information in the rat, it is possible that increased NO concentrations may develop in dogs following surgical tre atment of congenital portosystemic shunts if acute life-threatening portal hypertension develops. Increased NO concentrations may contribute to the sh ock syndrome that develops in these dogs.