Intratracheally-instilled antileukoprotease and alpha 1-proteinase inhibitor: effect on human neutrophil elastase-induced experimental emphysema and pulmonary localization.

The protective capacities of intratracheally-instilled antileukoprotease and alpha 1-proteinase inhibitor towards human neutrophil elastase (HNE)-induced pulmonary injuries were compared in hamsters. The antiproteases were instilled in equimolar amounts up to 20 h before HNE instillation. At all intervals, both inhibitors were able to inhibit HNE-induced emphysema efficiently.

Prevention of cumene hydroperoxide induced oxidative stress in cultured neonatal rat myocytes by scavengers and enzyme inhibitors.

Oxidative stress induced by cumene hydroperoxide was studied in cultured neonatal rat myocytes. A progressive increase of irreversible cell injury as determined by leakage of the cytoplastic enzyme alpha-hydroxybutyrate dehydrogenase (alpha-HBDH) from the cells was noted at concentrations ranging from 25-100 microM cumene hydroperoxide (incubation time 90 min). Cumene hydroperoxide-induced damage was reduced or prevented by several compounds: the application of Trolox C, a water-soluble vitamin E analogue, and of phospholipase A2 inhibitors chlorpromazine and (to a lesser extent) quinacrine prevented alpha-HBDH release.

Isoproterenol-induced cytotoxicity in neonatal rat heart cell cultures is mediated by free radical formation.

The cardiotoxic effect of the beta-adrenergic agonist isoproterenol was studied in cultured neonatal rat myocytes. A progressive increase in irreversible cell injury as determined by leakage of the cytoplasmic enzyme alpha-hydroxybutyrate dehydrogenase (alpha-HBDH) from the cells was noted at concentrations above 2.5 x 10(-4) M isoproterenol (exposure time 6 h).

Delayed recovery of homogeneous perfusion distribution in isolated rat heart after vasodilatation induced by alpha 1 adrenoceptor blockade during postischaemic reperfusion.

The purpose of this study was to investigate whether vasodilatation induced by doxazosin, an alpha 1 adrenoceptor blocker, during postischaemic reperfusion was able to accelerate reflow in unperfused myocardium. Isolated isovolumetrically beating rat hearts were exposed to global ischaemia by perfusion at 15 mm Hg for 2 h, resulting in an end ischaemic coronary flow rate of 2.3 (SD 1.

Diltiazem (0.5 mg/l) decreases coronary vascular resistance during reperfusion, but not during low flow ischemia, in the isolated perfused rat heart.

Isolated rat hearts underwent low flow perfusion with a perfusion pressure of 15 mmHg for two hours followed by reperfusion at a perfusion pressure of 80 mmHg for two hours. In these severely damaged hearts we tested whether diltiazem (0.5 mg/l) administered during ischemia or during reperfusion had vasodilatory effects.