Augmentation of postischemic brain damage by severe intermittent hypertension.

The neurological recovery and histological changes were studied in monkeys after intermittent postischemic arterial hypertension after 16 min of global brain ischemia. Ischemia was produced with a high pressure (1500 mm Hg) neck tourniquet and systemic arterial hypotension. Intensive care and life support, including monitoring of physiological variables, were provided for 7 days. Postischemia all monkeys were immobilized; ventilation was controlled and mean arterial pressure was maintained between 85--115 mm Hg for the first 48 hours. Immediately postischemia in four monkeys, intermittent arterial hypertension (i.e., 150--190 mm Hg) was induced by norepinephrine infusion for 3--5 min. Hypertensive episodes were repeated at 15, 30, 60, and 120 min postischemia, once every hour for the first 24 hours and once every 2 hours between 24 and 48 hours. Thereafter, the monkeys were allowed to breathe spontaneously. Four control monkeys were similarly treated except that arterial hypertension was not induced. Neurological recovery was evaluated by EEG, intracranial pressure, neurological deficit scoring, and histological examination of the brain after killing on day 7 postischemia. The neurological deficit score (100 % = brain death; 50% = vegetative state; 0% = normal) in control monkeys on day 7 was 17.8 +/- 1.8 (SEM) % compared to 46.3 +/- 6.5% (p less than 0.05) in the hypertension group. EEG recovery was delayed and the postischemic increase in intracranial pressure was prolonged in the hypertension group. Histological damage scores in the brain correlated with neurological deficit scores. Severe intermittent hypertension has a deleterious effect on neurological recovery after global brain ischemia.

[Experimental study of barbiturate application following anoxic encephalopathy]. / Etude expérimentale de l'utilisation des barbiturates après l'encéphalopathie anoxique.

The protective effect of thiopental on neurological lesions provoked by cerebral anoxie was studied in the monkey. Cerebral ischemia was induced by a cervical tourniquet applied for a period of 16 minutes. A control series of 10 animals received only the normal resuscitation. A series of 27 monkeys received either 90 mg/kg of thiopental at 5, 10, 15, 30 or 60 minutes following ischemia, or 120 mg/kg at the 30th or 60th minute. One third of the dose was administered within 5 minutes and the rest during the following 55 minutes. The results shows that the prevention, by thiopental, of the clinical and histological lesion secondary to cerebral anoxia is effective when this drug is administered before the 15th minute. With 90 mg/kg administered at the 30th or 60th minute the improvement was slight: with 120 mg/kg it was greater if the injection was given at the 60th rather than at the 30th minute. These results, along with the mechanisms which may explain the action of thiopental, are discussed.

Evaluation of insecticide smears for the control of screw-worm fly, Chrysomya bezziana, in Papua New Guinea.

Three new insecticide smear preparations for the control of Chrysomya bezziana larvae infesting wounds of cattle have been tested under field and laboratory conditions and compared with an established preparation EQ 335 which is based on 3% lindane. Two preparations based on 3% coumaphos proved comparable to EQ 335 in the field trials and exhibited more prolonged residual effectiveness in laboratory tests. A smear preparation based on 2.5% methoxychlor was only effective in controlling 1 and 2 day-old larvae in wounds and was generally inferior to other smears tested in the laboratory.