ABNORMAL IN-VIVO RESPONSE TO SODIUM-NITROPRUSSIDE AFTER PORCINE SINGLE-LUNG TRANSPLANTATION

Citation
S. Kukkonen et al., ABNORMAL IN-VIVO RESPONSE TO SODIUM-NITROPRUSSIDE AFTER PORCINE SINGLE-LUNG TRANSPLANTATION, Transplantation, 61(10), 1996, pp. 1435-1439
Citations number
28
Categorie Soggetti
Immunology,Surgery,Transplantation
Journal title
ISSN journal
00411337
Volume
61
Issue
10
Year of publication
1996
Pages
1435 - 1439
Database
ISI
SICI code
0041-1337(1996)61:10<1435:AIRTSA>2.0.ZU;2-Z
Abstract
The chronic increase of pulmonary vascular resistance after lung trans plantation is only partly due to an active increase in baseline vasomo tor tone, but the nature of the acute pulmonary hypertension after isc hemia and reperfusion is not known. We studied the effects of sodium n itroprusside on pulmonary hemodynamics during reperfusion in porcine l eft lung allotransplants. In twelve pigs (weight: 18 to 24 kg) pulmona ry arteries of the native and the transplanted lung were cannulated fo r right-heart bypass. The total blood flow was 2 L/min. Flow distribut ion between the lungs was measured at equal mean pulmonary artery pres sure, and pulmonary vascular resistance at equal and constant flow-i.e ., 1 L/min to each lung. After baseline measurements sodium nitropruss ide (1, 3, and 9 mu g/kg/min) was administered to sig animals (SNP gro up). The control group (n=6) received an equal amount of the vehicle. After 30 min of discontinuation of the drug infusion, the schedule was repeated. In the transplanted lung, pulmonary vascular resistance dec reased in all animals during the first hour of reperfusion. During the second drug infusion pulmonary vascular resistance was significantly lower in the SNP group compared with the control group only at the hig hest infusion rate of the drug (9 mu g/kg/min), which also induced a 4 4% decrease in systemic vascular resistance. Arterial oxygen tension r emained comparable in the two groups throughout the study. Our data su ggest that other factors besides active vasoconstriction may contribut e to the acute increase of pulmonary vascular resistance after lung tr ansplantation.