Near-infrared spectroscopy (NIRS) may be a useful method for monitoring the regional oxygen saturation (rSO(2)) of the lower extremity during endovascular aortic repair. Eighteen patients with thoracic descending and/or abdominal aortic aneurysm were enrolled in this study. NIRS probes were placed bilaterally on the calves. Muscular rSO(2) (mrSO(2)) was monitored every 30 s throughout the operation. In the leg in which the femoral artery was clamped, mrSO(2) values were selected at 3 or 4 points-just before clamping (control value), 30 min after clamping, 10 min after the first declamping, and 10 min after the second declamping following repair of the femoral artery, if necessary. In all patients, mrSO(2) decreased significantly during clamping, from 64 ± 11 % (mean ± SD) of the control value to 32 ± 15 %. After declamping, mrSO(2) recovered to 69 ± 14 % of the control value in 16 patients. In the 2 other patients, however, mrSO(2) did not recover after the first declamping, because of femoral artery dissection. After additional repair, mrSO(2) recovered quickly to the control value. These data suggested NIRS may objectively and quantitatively reflect oxygenation of the lower extremities, and may indicate an ischemic event that needs additional repair during endovascular aortic repair.
The role of poly (adenosine diphosphate-ribose) synthetase (PARS) in the contractile and relaxant responses of pulmonary arteries injured by ischemia and reperfusion (IR) of splanchnic artery has not been evaluated. We examined these responses by using 3-aminobenzamide, a pharmacological inhibitor of PARS. IR models in rats were induced by clamping the superior mesenteric artery for 60 min, followed by release of the clamp for 60 min. In the 2 treated groups, 5 or 10 mg/kg of 3-aminobenzamide was administered as an IV bolus at 10 min before reperfusion, followed by infusion rates of 5 and 10 mg.kg(-1).h(-1), respectively, during the period of reperfusion (IR + PARS inhibitor 5 and 10 groups). In the vehicle-treated group, 3-aminobenzamide was not given, but IV saline was administered (IR group). In the control group, surgery was performed, but the superior mesenteric artery was not occluded (sham group). The pulmonary arteries were isolated, and effects of drugs were evaluated in vitro. The IR group showed no attenuation of the contractile responses of the pulmonary artery to phenylephrine. The relaxant responses to endothelium-dependent vasodilators, acetylcholine, and A23187 in the IR group were significantly inhibited when compared with the sham group. The reduction in the relaxant response to endothelium-dependent vasodilators was improved in the IR + PARS inhibitor 5 and 10 groups when compared with the IR group. We concluded that IR attenuated the relaxant responses of the pulmonary artery to endothelium-dependent vasodilators and that PARS inhibitors ameliorate the reduction in the relaxant response.
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