Pentoxifylline ameliorates postischemic delayed hypoperfusion of the cerebral cortex following cardiac arrest in cats: J Neurol Sci 1995; 132/2 (105–109)

Abstract

Two major events occurring in the cerebral hemodynamics after successful resuscitation from cardiac arrest are reactive hyperemia and postischemic hypoperfusion. We examined the effect of pentoxifylline on the feline cerebral hemodynamics following cardiac arrest. Fifteen cats were anesthetized and artificially ventilated. Using our photoelectric method, the local cerebral blood volume (CBV), mean transit time of blood (MTT), and cerebral blood flow (CBF) in the parietotemporal region were measured. Thoracotomy was performed, and cardiac arrest (ventricular fibrillation) was induced by direct application of a 2-V DC countershock. The heart was resuscitated with a DC countershock at 30 sec after cardiac arrest. In 9 cats, pentoxifylline (25 mg/kg) was infused into the femoral vein at 5 min before cardiac arrest (PTX group). The other 6 cats served as controls (control group). In both groups, the CBV, CBF and mean arterial blood pressure (MABP) overshot the control levels just after resuscitation, whereas the MTT was decreased. In the control group, postischemic hypoperfusion was detected at 30–180 min after resuscitation from cardiac arrest (CBF (ml/100 g/min): 51 ± 4 (control), 38 ± 4 (30 min, p < 0.05), and 23 ± 3 (180 min, p < 0.05)). However, the postischemic hypoperfusion was not observed in the PTX group. Pentoxifylline ameliorated postischemic delayed hypoperfusion in the cerebral cortex after a short period of cardiac arrest. Pentoxifylline may be useful in the emergency situations following cardiac arrest.