Plasma-based hemoglobin may provide a more effective sink for NO than red cell-based hemoglobin. We tested the hypothesis that cell-free hemoglobin transfusion impairs dilation to acetylcholine (Ach) in pial arterioles with tight endothelial junctions. Exchange transfusion of approximately 5-7 g of crosslink! hemoglobin in 8 pentobarbital-anesthetized cats resulted in a decrease in hematocrit (30±1 to 18±1%; ±SE), an increase in arterial pressure (112±4 to 138±6 mmHg), and a decrease in diameter in small (2550 urn; 11±3%), medium (50-100 jim; 9±1%) and large (>100 iaa); 8±3%) arterioles. Topical Ach (SxlO'M) increased diameter by 31±4, 21±3 and 22±6%, respectively. The corresponding increases in 7 time controls cats at 33% hematocrit (38±10, 21±4, 19±4%), and in 6 albumin transfused cats at 18% hematocrit (20±4, 17±4, 13±5%) were similar to those in hemoglobin transfused cats. Likewise, size-dependent dilation to the NO donor SIN-1 (10-6M) in the hemoglobin group (23 ±4,16±3,9±2%) was similar to that in the control group (19±3, 12±2, 9±3%) and in the albumin group(23±4,18±4,7±1%). TopicalL-nitroarginine(3×104M) attenuated Ach but not SIN-1 dilation in all groups. We conclude that crosslinked hemoglobin transfusion does not impair dilation to Ach or SIN-1. Close contact of cell-free hemoglobin with the luminal endothelial glycocalyx does not appear to substantially impair abluminal diffusion of NO or a nitrosothiol to the smooth muscle.
|Original language||English (US)|
|State||Published - Dec 1 1996|
ASJC Scopus subject areas
- Molecular Biology