Effect of nitric oxide synthase inhibition on the pial arteriolar crosslinked hemoglobin transfusion

We investigated whether exchange transfusion of crosslinked hemoglobin, sufficient to reduce hematocrit to 17%, causes pial arteriolar constriction by scavenging nitric oxide (NO). Diameter of small (<50 μm), medium (50-100 μm) and large (> 100 μm) arterioles were measured through closed cranial windows of pentobarbital-anesthetized cats. Transfusion of crosslinked hemoglobin decreased diameter by 11±2.6, 9±1.3 and 8±2.5% (±SE; n=8) in small, medium and large arterioles, respectively. In contrast, transfusion of an albumin-containing solution to equivalent hematocrit increased the corresponding diameters by 12±3.8, 7±2.9, and 15±3.8% (n=6). In another group (n=9), L-nitroarginine (L-NA; 3 × 10^-4M) was applied locally before hemoglobin transfusion to inhibit local NO synthesis. Subsequent hemoglobin transfusion transiently decreased diameter during the transfusion (14±1, 13±1.5, 9±0.7%) when arterial pressure transiently increased. When L-NA was locally administered and hypertension was controlled by removal of additional blood during the crosslinked hemoglobin transfusion, diameter remained unchanged. However, vasodilation did not occur as in the albumin transfused group. We conclude that a component of the constrictor response is an autoregulatory response to hypertension rather than scavenging NO in brain. The greater cerebral vasodilation with albumin transfusion than with hemoglobin transfusion at equivalent hematocrit is presumably related to greater oxygenation with the hemoglobin O₂ carrier.