Background and Purpose-The association between elevated blood pressure (BP) and hematoma enlargement in acute intracerebral hemorrhage (ICH) has not been clarified. We investigated the association between maximum systolic BP (SBP) and hematoma enlargement, measuring SBP between a baseline and a second CT scan in patients with hypertensive ICH. Methods-We assessed 76 consecutive patients with hypertensive ICH retrospectively. We usually attempted to lower SBP below targets of 140, 150, or 160 mm Hg. Recordings of serial BP from admission until the second CT scan were assessed. A neuroradiologist, who was not informed of the aim of this study, reviewed CT films. Hematoma enlargement was defined as an increase in volume of Ն140% or 12.5 cm 3 . Results-Hematoma enlargement occurred in 16 patients. Maximum SBP was significantly associated with hematoma enlargement (Pϭ0.0074). A logistic regression model for predicting hematoma enlargement was constructed with the use of maximum SBP, hematoma volume, and Glasgow Coma Scale score at admission. After adjustment for these factors, maximum SBP was independently associated with hematoma enlargement (odds ratio per mm Hg, 1.04; 95% CI, 1.01 to 1.07). Target SBPs of Ն160 mm Hg were significantly associated with hematoma enlargement compared with those of Յ150 mm Hg (Pϭ0.025). Conclusions-Our findings suggest that elevated BP increases the risk of hematoma enlargement. Efforts to lower SBP below 150 mm Hg may prevent this risk.

We evaluated the effects of aging and hypertension on endothelium-dependent relaxation of rat common carotid arteries using 14-week-old (young) and 11-month-old (old) Wistar-Kyoto rats (WKY) and age-matched spontaneously hypertensive rats (SHR). Isometric tension of common carotid artery ring segments was measured. With a resting tension of 2.0 g determined from the baseline tension-contraction curves, precontraction was induced by 10" and hypertension 13 -16 on vascular reactivity in general have been extensively studied. In addition, there are several reports examining the influence of aging or hypertension on endothelium-dependent vasodilatations. 17 -21 In these studies, ACh-induced relaxation of rat mesenteric artery was unaffected by age, 17 whereas hypertension impaired endothelium-dependent relaxation in experimental animals. 18 -21 There are at present, however, noFrom the Department of Neurosurgery, University of Virginia School of Medicine, Charlottesville, Virginia.Address for correspondence: Neal F. Kassell, MD, Department of Neurosurgery, Box 212, Medical Center, University of Virginia, Charlottesville, VA 22908.Received June 30, 1987; accepted February 3, 1988. reports of the effects of aging or hypertension on the endothelium-dependent relaxations of cephalic arteries. This is surprising considering the major effects that aging and hypertension are thought to exert on the cerebral circulation.Recently Freiman et al 22 demonstrated that atherosclerosis impairs endothelium-dependent vascular relaxation to ACh and thrombin in monkeys. The common carotid artery, which is often affected by disorders such as atherosclerosis, has a great influence on cerebral circulation. Therefore, it seems pertinent to investigate the effects of aging and hypertension on the endothelium-dependent vascular relaxation in a cephalic artery such as the common carotid artery. Our experiments were designed to demonstrate these effects using young and old Wistar-Kyoto rats (WKY) and young and old spontaneously hypertensive rats (SHR).

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The combinatorial approach, guided by the break points, is so simple and systematic that it can be used again in the future when revision of the grading scale becomes necessary after development of new and effective treatment modalities that improve patients' overall outcome.

The effect of subarachnoid hemorrhage (SAH) on endotbelium-dependent vasodilation of isolated rabbit basilar artery was examined using an isometric tension recording method. Thirty-five rabbits that had 2 successive blood injections were divided into 3 groups: normal animals (control), 4 days, and 3 weeks after the first SAH. Acetylcholine (ACh) (10~6-10~4 M) and adenosine triphosphate (ATP) (10~6-10~4 M) were used to evoke dose-dependent vasodilation of isolated arterial rings previously contracted by 10~6 M serotonin. In the animals killed 4 days after the first SAH, both AChand ATP-induced relaxation were suppressed, and the degree of relaxation of this group was 38 ± 4.5% (mean ± SEM) and 22 ± 3.9% of the initial contractile tone in response to 10" 3 Despite extensive efforts to identify measures to dilate the narrowed arteries, no reliable measure exists for preventing vasospasm from developing or for reversing it. One of the major reasons for this inadequacy is a lack in understanding the pathogenesis of vasospasm. The cause of cerebral vasospasm following SAH is likely to be multifactorial.It has been recently suggested that impairment of the vasodilatory activity of cerebral arteries following SAH may play an important role in the pathogenesis of vasospasm. Arterial wall prostacyclin, a powerful vasodilator, decreases progressively following SAH. 8 It is well documented that endothelial damage occurs frequently after SAH. We have recently demonstrated that endothelium-dependent vasodilation induced by adenosine triphosphate (ATP) is impaired after SAH in a rabbit single hemorrhage model (T. Nakagomi, unpublished data). However, acetylcholine (ACh)-induced vasodilation was well preserved following SAH in that model. This may reflect a partial, less severe damage to the endothelium. The present experiments were conducted to investigate 1) the effect of SAH on endothelium-dependent vasodilation induced by ACh and ATP in a rabbit double hemorrhage model, which should result in more severe damage to the endothelium than a single injection model, and 2) to study the inhibitory effect of hemoglobin on endothelium-dependent vasodilation in basilar arteries exposed to SAH. Materials and Methods Animal PreparationsThirty-five male New Zealand white rabbits weighing 2.9-3.4 kg were anesthetized with an i.m. injection of ketamine (20 mg/kg), xylazine (5 mg/kg), and acepromazine (0.25 mg/kg) in a ratio of 8:1:1. The animals were intubated and received muscular paralysis with i.v. pancuronium bromide (0.08 mg/kg). Ventilation was maintained with a Harvard dual-phase control respirator. In each animal, the left ear artery was cannulated for monitoring blood pressure and withdrawing arterial blood.A 23-gauge butterfly needle was inserted into the cisterna magna percutaneously and connected to a pressure transducer via one outlet of a three-way stopcock. The other outlet was used for the injection of arterial blood. Intracranial pressure (ICP) was monitored immediately after the injection of arterial blood through the st...