This study tested the hypothesis that enhancement of blood cardioplegia with the nitric oxide donor agent SPM-5185 inhibits postischemic left ventricular and coronary endothelial dysfunction. Eighteen anesthetized dogs supported by total vented bypass were subjected to 30 minutes of normothermic ischemia followed by 4 degrees C multidose blood cardioplegia. Hearts received either standard blood cardioplegia (vehicle group; n = 6), blood cardioplegia with 1 mumol/L SPM-5185 (low-dose group; n = 6), or 10 mumol/L SPM-5185 (high-dose group; n = 6). After 60 minutes of cardioplegic arrest, the heart was reperfused for a total of 60 minutes, first in the beating empty state for 30 minutes and then after discontinuation of bypass for 30 minutes. Baseline and postischemic left ventricular function was assessed by the slope of the end-systolic pressure-volume (impedance catheter) relation. Postischemic end-systolic pressure-volume relation was depressed by 53.7% of preischemic values in the vehicle group (from 8.2 +/- 1.0 to 3.8 +/- 0.3 mm Hg/ml) and by 33.7% (from 9.2 +/- 1.1 to 6.1 +/- 0.5 mm Hg/ml) in the low-dose group. In contrast, there was complete postischemic functional recovery in the high-dose group (from 7.6 +/- 1.1 to 7.2 +/- 1.2 mm Hg/ml). In coronary arteries isolated from these hearts, endothelium-dependent maximal relaxation to acetylcholine was impaired by 27% in the vehicle group and by 18% in the low-dose group, whereas the high-dose group showed complete endothelium-dependent relaxation. Myeloperoxidase activity, an index of neutrophil accumulation in postischemic myocardium, was elevated in the vehicle and low-dose groups (3.36 +/- 0.58 and 2.56 +/- 0.68 U/100 mg tissue) but was significantly reduced in the high-dose group to 1.27 +/- 0.45 U/100 mg tissue. We conclude that inclusion of 10 mumol/L nitric oxide donor SPM-5185 in blood cardioplegia improves postischemic ventricular performance and endothelial function in ischemically injured hearts, possibly via inhibition of neutrophil-mediated damage.
Acadesine reduces infarct size by an adenosine mediated mechanism, but this cardioprotective action is not associated with significantly augmented interstitial fluid adenosine levels.
To define the value of renal duplex sonography (RDS) to detect the presence of critical renal artery (RA) stenosis or occlusion after surgical repair or percutaneous transluminal balloon angioplasty (PTRA), we retrospectively reviewed our recent 71-month experience. Methods: From January 1987 through November 1992, 272 patients underwent 279 operative RA repairs and 35 patients underwent PTRA. Three hundred twenty-five RDS examinations were performed in 176 patients after operative intervention or PTRA during the study period. Forty-one of these patients had conventional angiography providing 61 RA for RDS comparison, and these data form the basis of this analysis. Twenty-four women and 17 men (mean age 57 years) underwent 44 operative RA repairs or 17 PTRA for correction of atherosclerotic disease (51 arteries) or fibromuscular dysplasia (10 arteries). Before their renovascular procedure each patient had significant hypertension (mean 193/106 mm Hg). RDS after surgery or PTRA was technically complete for all 61 RA. Results: Compared with angiography RDS correctly identified 47 of 48 repairs with less than 60% RA stenosis, 7 of 11 repairs with 60% to 99% stenosis, and 2 renal artery occlusions, providing a 69% sensitivity rate, 98% specificity rate, 90% positive predictive value, and a 92% negative predictive value. These results were adversely affected by branch RA disease, which accounted for three of four false-negative RDS study results. For 50 kidneys undergoing correction of main RA disease, RDS demonstrated an 89% sensitivity rate, 98% specificity rate, and 96% overall accuracy. RDS results were equivalent for both surgical and PTRA treatment. Conclusions: From this experience we conclude that RDS is useful for anatomic evaluation after surgical RA repair or PTRA. A negative RDS result excludes stenosis or occlusion of a main RA reconstruction but does not exclude significant branch level disease. (J VASC StTRG 1993;18:381-90.) Confirmation of the anatomic success of renal revascularization is assumed on the basis of a favorable blood pressure response in many centers. The fallacy of this assumption, however, has been documented repeatedly by previous reports. 1-3 Those recorded experiences have clearly documented that a favorable blood pressure response can occur after
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