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We studied the effects of long-term fish oil (FO) dietary supplementation on brain edema, polymorphonuclear neutrophil (PMN) infiltration, and infarct size in a rat stroke model. Rats were given regular rat chow with or without FO supplement (20 of total calories) for 7 weeks. Body weight did not differ between the two groups. In the FO group, an increase in eicosapentaenoic acid and a decrease in arachidonic acid content in hepatic phospholipids were significant in the phosphatidylcholine, phosphatidylethanolamine, and phosphatidylserine but not in the phosphoinositol fraction. Platelet activity reflected by serum thromboxane B2levels was reduced in the FO group. Postischemic brain edema and PMN infiltration were not different between the two groups. The infarct volume was significantly greater in the FO group (controls: 96 ±7 mm3, n 49; FO group: 124 ± 6 mm3, n 53; p0.0036). The greater ischemic brain injury in the FO-supplemented animals is probably related to the intraischemic hyperglycemia, which was worse in the FO group than in the control group (controls: 265 ± 19 mg/dl, n 14; FO group: 340 ± 18 mg/dl, n 16; p0.0079).

In 14 members of four families with a hereditary syndrome of exertional myalgia, five of eight muscle biopsies from symptomatic individuals showed histochemical and biochemical absence of myoadenylate deaminase (MADA). In the others, MADA biochemical activity was normal in two and reduced but not absent (intermediate level) in one. Asymptomatic relatives had normal histochemical MADA activity, but three had intermediate biochemical levels.

Although hyperglycemia has been shown to consistently exacerbate ischemic brain injury following global or diffuse cerebral ischemia, the effect of hyperglycemia in unilateral focal cerebral ischemia remains controversial. Recent advances in thrombolytic therapy have enhanced the clinical significance of postischemic reperfusion. We studied the effect of plasma glucose on ischemic brain injury in a newly developed focal cerebral ischemia-reperfusion model. Rats allowed free access to food until ischemic insult developed intra-and postischemic hyperglycemia and cortical infarction. Rats fasted for 24 hours had blunted hyperglycemic responses. Infarct volumes were correspondingly smaller. The protective effect of fasting was partially abolished by glucose loading during ischemia to induce intra-ischemic hyperglycemia. Glucose loading immediately or 3 hours after focal cerebral ischemia did not significantly alter the protective effect of fasting. Insulin treatment in fed rats before ischemia also reduced hyperglycemic responses and infarct volume. Timing of insulin treatment was also critical in the reduction of ischemic injury. These findings indicate that plasma glucose during the period of ischemia is an important determinant of brain injury in focal cerebral ischemia-reperfusion and there is a therapeutic window for normalization of plasma glucose to be efficacious.

We measured levels of thromboxane B2and 6-keto-PGF10in rabbit spinal cord and cat CSF after impact injury to spinal cord. Rabbit tiissue thromboxane B2levels increased more than 6-keto-PGF10. In cat, CSF thromboxane B, was higher the first hour postinjury; CSF 6-keto-PGF10also increased, but less so. These results imply activation of arachidonic acid metabolism. The relatively greater increase of thromboxane B, suggests that thromboxane-prostacyclin imbalance may contribute to post-traumatic ischemia.

Hypertensive intracerebral hemorrhage (HICH) is generally considered to be a monophasic event. Enlargement of the initial hematoma after several hours or days has rarely been documented. We describe the clinical and CT findings in 8 patients (5 men, 3 women, aged 39 to 68 years) with continued bleeding or rebleeding during the acute phase of HICH. The thalamus was the most frequent site of hemorrhage (6/8). The neurologic status deteriorated in all: 6 within 24 hours, and 2 after 5 and 7 days. Persistent hypertension was common (6/8) prior to extension of the hemorrhage. The 2nd CT revealed an obvious increase in hematoma size in all cases. Four patients died and 4 survived with severe neurologic disability. These serial studies indicate that active bleeding or rebleeding can occur in HICH and suggests that the risk is particularly high with thalamic hemorrhage. We conclude that meticulous control of hypertension after HICH may be justified in selected patients.

Three degrees of focal ischemic infarction in the rat were created in the cerebral cortex supplied by the right middle cerebral artery, by ligation of the right middle cerebral artery and the right common carotid artery and temporary clip compression of the left common carotid artery, in succession. The postischemic accumulation of calcium in cerebral cortex of the right middle cerebral artery territory, determined by atomic absorption spectrometry, correlated with the infarct volume. The results are consistent with the hypothesis that calcium has role as a mediator in the pathogenesis of cerebral infarction.