Classification of CSDHs according to the internal architecture and intracranial extension may be useful for predicting the risk of postoperative recurrence.

In an anesthetized canine model in which ischemia was induced by incremental air embo-lism, 16 animals were exposed to 1 hr of ischemia and monitored for 10 min (n = 4), 60 min (n = 6), or 240 min (n = 6). Fourteen animals were observed for corresponding periods without being subjected to ischemia 70 min (n = 4), 120 min (n = 4), or 300 min (n = 6). Autologous granulocytes were labeled with '"in and reinfused just before ischemia. At the conclusion of each experiment, a M C-iodoantipyrine autoradiographic blood flow study was performed. Granulocyte accumulation measured by gamma scintig-raphy (cpm/gm) occurred in the injured hemisphere of ischemic animals at 60 min in anterior brain segments and at 240 min in anterior, middle, and posterior segments. By means of a double-label autoradiography technique, clustering of punctate granulocyte images was detected in regions of low flow or heterogeneous flow in half of the animals at both 60 min and 240 min post ischemia. Granulocyte clustering did not occur in the autoradiograms of nonischemic animals. The results implicate granulocyte participation hi the acute phase of ischemic brain injury and signal a convergence of hemostatk and inflammatory processes during the immediate postischemic period.

The incidence of postoperative fluid reaccumulation seems to be reduced by placing the tip of the drainage catheter in the frontal convexity and by removing subdural air during or after surgery.

No abstract

✓ Recent studies suggest the possible role of the red blood cell (RBC) in causing chronic cerebral vasospasm. However, the basic action of hemoglobin (Hb), the major component of the RBC, on cerebral arteries remains unknown. The present study was undertaken to analyze the contractile effects of human Hb (purified by ion-exchange chromatography) on canine arteries in vitro. The contractile activity of lysed RBC was shown to be derived from Hb. Hemoglobin in oxygenated form (oxyHb) caused a maximum contraction equal to about 70% of that induced by serotonin in the basilar artery. Ferrous Hb's (oxyHb and carboxyHb) produced much greater contraction than ferric Hb's (methemoglobin and cyanmethemoglobin), suggesting that superoxide radicals, an active species of oxygen, may be related to the contractile activity of Hb. Neither methysergide, phentolamine, mepyramine, nor aspirin inhibited the vasoconstrictive activity of oxyHb. This finding indicates that the activation of serotonergic, alpha-adrenergic, or histaminergic H1 receptors, or prostaglandin synthesis may not be involved in the mechanism of action of oxyHb. The constituents of Hb caused little or no contraction as compared with Hb as a whole. The basilar artery was more highly sensitive to Hb than arteries from other anatomical locations. Cyclic adenosine monophosphate caused a very slight decrease in the Hb-induced contraction. It is concluded that oxyHb can contract cerebral arteries in vitro. These results, coupled with recent reports on the participation of the RBC in producing chronic vasospasm, strongly suggest that oxyHb released from RBC's plays an important role in the pathogenesis of chronic cerebral vasospasm.