[An experimental study on shock after temporary hepatic inflow occlusion and platelet activating factor (PAF)].
The potential effect of CV6209, a platelet activating factor (PAF) antagonist, on shock after temporary hepatic inflow occlusion was investigated. Five groups of rats were given following chemicals i.v. (Group A: both 3 mg/kg of CV6209 and 100 U/kg of heparin, Group B: 3 mg/kg of CV6209, Group C: 100 U/kg of heparin, Group D: 4 ml/kg of normal saline, Group E: 4 ml/kg of normal saline under splanchnic decompression with port-jugular bypass) and were subjected to 45 minutes of hepatic inflow occlusion. The survival rates 24 hours after the occlusion were 80%, 60% 45%, 30% and 80% in groups A, B, C, D and E, respectively. All rats except for those in group E developed hypotension during the occlusion period. The blood pressure was reversed to pre-occlusion level after declamping in groups A and B, although hypotension continued in groups C and D. Blood chemistry also revealed diminished elevation of serum mitochondrial GOT after the occlusion in PAF antagonist group. These results suggest that portal congestion is the most responsible for shock and death after temporary hepatic inflow occlusion and PAF is a mediator of the injury.
Fukuoka
T
T
First Department of Surgery, Nara Medical University, Kashihara, Japan.
D000818:Animals; D001219:Aspartate Aminotransferases / Q000097:blood; D001794:Blood Pressure / Q000187:drug effects; D003250:Constriction; D008099:Liver / Q000098:blood supply*; D008297:Male; D008928:Mitochondria / Q000201:enzymology; D010972:Platelet Activating Factor / Q000037:antagonists & inhibitors / Q000502:physiology*; D011170:Portasystemic Shunt, Surgical; D011726:Pyridinium Compounds / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D012769:Shock / Q000378:metabolism* / Q000503:physiopathology / Q000517:prevention & control
D010972:Platelet Activating Factor; D011726:Pyridinium Compounds; C053321:CV 6209; D001219:Aspartate Aminotransferases