Enoxaparin therapy initiated at the time of anesthesia induction increases postoperative intracranial hemorrhage.

Summary: Brain edema formation was investigated in the vasopressin-deficient Brattleboro rat using a middle cere bral artery occlusion model of early ischemic injury. Wa ter and sodium accumulation after 4 h of ischemia were attenuated 36 and 20%, respectively, in the Brattleboro strain as compared to the control Long-Evans strain. This effect was independent of differences in animal size and state of hydration. In addition, measurements of ce rebral blood flow indicated that Brattleboro and Long Evans rats had equal levels of ischemia following middle cerebral artery occlusion. Systemic treatment of Brattle boro rats with vasopressin normalized their serum elec trolyte concentrations and osmolarity but did not alter sodium or water accumulation in the ischemic brain. In contrast, intraventricular administration of vasopressin inThe ionic composition of the extracellular fluid compartment of the central nervous system is main tained remarkably constant (Bradbury, 1979). This suggests the presence of potent regulatory mecha nisms. It has been postulated that a central neuro endocrine system may monitor and regulate the electrolyte composition and volume of the brain, analogous to the hypothalamic control of systemic volume homeostasis (Raichle, 1981). Many of the hormones involved in systemic volume regulation, such as vasopressin, atrial natriuretic peptide, and angiotensin II, are synthesized and released within the central nervous system (Buijs et aI., 1978; Phil lips, 1987; Zamir et aI., 1986). These centrally re leased neuropeptides may act locally on adjacent target cells, or at more distant intracerebral sites 681Brattleboro rats increased edema formation to that seen in control rats. The reduced water and sodium accumu lation in Brattleboro rats subjected to middle cerebral ar tery occlusion may be related to alterations in blood brain barrier permeability since the blood-to-brain so dium flux was 36% less in the ischemic tissue of the Brattleboro as compared to the Long-Evans strain. These results support the hypothesis that central vaso pressin is a regulator of brain volume and electrolyte ho meostasis. Furthermore, our findings suggest a role for central vasopressin in the development of ischemic brain edema. Key Words: Brattleboro rat-Cerebral ischemia Vasopressin-Blood-brain barrier permeability Sodium-Middle cerebral artery occlusion.

The vasa vasorum have not been previously reported to contribute to the revascularization of occluded arteries. The four cases presented in this report suggest that the vasa vasorum can be a source of collateral circulation after carotid artery occlusion secondary to atherosclerotic disease.

There was a tendency toward left VA dominance in the hypertensive group compared with the control group, although a significant difference was shown by only one of the four reviewers. There were no differences in brainstem compression or rotation between the hypertensive and nonhypertensive groups. These results are contrary to those of recently published studies in which MR imaging and/or MR angiography revealed lateral brainstem vascular compression in hypertensive patients but not in nonhypertensive (control) patients. Reasons for this discrepancy are discussed. On the basis of their own experience and that of others, the authors believe that neurogenic hypertension does exist. However, thin-slice MR imaging may not be a reliable method for detecting neurovascularly induced essential hypertension and the prevalence of neurovascular compression as the source of hypertension may be overestimated when using current imaging techniques.