In our experience, adenosine-induced transient asystole was safe and helpful for satisfactory clipping of a complicated aneurysm. An estimated dose injection of adenosine was more convenient than the test-incremental method and did not result in serious cardiologic problems.

Abstract-Free hemoglobin (Hb) and red blood cells augment hypoxic pulmonary vasoconstriction (HPV) by scavenging nitric oxide (NO). S-nitrosation of Hb (SNO-Hb) may confer vasodilatory properties by allowing release of NO during deoxygenation and/or by interaction with small-molecular weight thiols. Likewise, cross-linking of free Hb may limit its vasoconstrictive effect by preventing abluminal movement of the molecule. We compared the effects of free SNO-Hb and Hb intramolecularly cross-linked at the ␤-cysteine 93 residue [Bis(maleidophenyl)-polyethylene glycol2000HbA (Bis-Mal-PEGHb)] to those of free oxyHb on pulmonary artery pressure (PAP), HPV, and exhaled NO (eNO) in isolated, perfused rat lungs. Ventilation of lungs with anoxic gas for 5 minutes reduced perfusate PO 2 to 11Ϯ1.0 Torr. Addition of SNO-Hb or Bis-Mal-PEGHb (100 mol/L) to buffer perfusate increased normoxic PAP and augmented HPV in similar magnitude as free oxyHb, but had no effect on eNO. Addition of the allosteric modulator inositol hexaphosphate to increase Hb P50 and the thiol glutathione (GSH) to allow removal of NO from Hb via transnitrosation to the perfusate did not reduce augmentation of HPV by SNO-Hb or increase eNO. GSH resulted in an Ϸ50% reduction in perfusate [S-nitrosothiol] T he rapid oxidation of nitric oxide (NO) by oxyhemoglobin (oxyHb) to form methemoglobin (metHb) and nitrate acts to limit the magnitude and duration of the vasorelaxant effects of NO. 1 In the pulmonary circulation, this is manifest as increased pulmonary vascular resistance (PVR) and augmentation of hypoxic pulmonary vasoconstriction (HPV) by red blood cells (RBCs) and free Hb. [2][3][4][5][6][7][8] An additional reaction of NO with Hb is S-nitrosation at the ␤-cysteine 93 (␤-cys93) residue to form S-nitrosoHb (SNO-Hb). 9 This reaction is also reversible, particularly in the presence of low-molecular weight thiols such as glutathione (GSH), 9,10 and/or under the allosteric influence of deoxygenation. 9,11,12 This dynamic, oxygen-linked property of SNO-Hb has led to the theory that Hb may act as a carrier of NO from the lung to the peripheral circulation, where it is released on deoxygenation of Hb. That free and intraerythrocytic SNO-Hb results in systemic and cerebral vasodilation supports this hypothesis. 9,11 Recently, we showed that free SNO-Hb is a potent a vasoconstrictor in the pulmonary circulation. 6 In addition, we were unable to demonstrate an allosteric effect of deoxygenation on NO release from SNO-Hb, although this observation was limited by the low P 50 of free SNO-Hb and the inability to reduce perfusate PO 2 below Ϸ38 Torr despite ventilation with anoxic gas in this model.In the present work, we again studied the effects of SNO-Hb on PVR and HPV. However, we expanded on our previous work by using a different animal model (isolated, perfused rat lungs), which allowed a reduction in the perfusate PO 2 to Ϸ10 Torr during anoxic ventilation, a level that should promote deoxygenation of SNO-Hb. In addition, we studied both lower and higher conce...

These data indicate isoflurane general anesthesia protects against noise-induced hearing loss and tissue damage in mice.