The Effects of Cross-Linked Hemoglobin on Regional Vascular Conductance in Dogs

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Abstract
Hemoglobin (Hgb) solutions cause systemic vasocon- striction, which might limit their use as intraoperative blood substitutes. This constriction is thought to be caused by interaction between Hgb and nitric oxide (NO). To determine whether (Y-(Y cross-linked hemoglo- bin (XL-Hgb) interferes with NO-mediated vasodila- tion caused by acetylcholine (ACh) and sodium nitro- prusside (NTP), we infused these compounds into the femoral, superior mesenteric, and circumflex coronary arteries of anesthetized dogs (n = 6) before and after partial exchange transfusion with XL-Hgb. Additional animals (n = 6) were studied after treatment with 5% albumin. XL-Hgb administration increased mean arte- rial pressure (MAP) from 81 ? 5 to 112 2 8 (P < 0.05). Albumin reduced MAP from 84 +- 4 mm Hg to 76 ? 4 mm Hg (P < 0.05). Vascular conductance after XL- Hgb decreased in the femoral artery, was not changed in the mesenteric bed, and increased modestly in the coronary artery (from 0.19 ? 0.03 to 0.26 t 0.02 mL * mm Hg-' * min-', P < 0.05). After albumin, conductance was unchanged in the femoral artery and increased in the mesenteric artery. Conductance also increased in the coronary bed (from 0.25 ? 0.02 to 0.49 ? 0.03 mL * mm Hg-' * mini I, P < 0.05). The vasodilator response to ACh in the femoral or mesenteric beds was either unaffected or augmented by either XL-Hgb or albumin. In the coronary bed, XL-Hgb blunted the dila- tor responses to ACh and NTP, while albumin aug- mented the coronary dilator responses to ACh. In five additional dogs, the NO synthase inhibitor p- monomethyl L-arginine caused MAP to increase from 85 -C 4 to 90 + 8 mm Hg and blunted the coronary dila- tor responses to ACh by approximately 25%. Subse- quent XL-Hgb administration caused a further increase in MAP to 112 t 19 mm Hg (P < 0.05) and also further blunted ACh-mediated vasodilator responses in the coronary circulation. XL-Hgb has complex effects on the circulatory system, including a reduction in the va- sodilator responses to ACh and NTP in canine coronary arteries in z&o. The potential impact of these events on patients with significant coexisting disease is unclear. (Anesth Analg 1997;85:265-73)