Y. Kinoshita

Long-term renal preservation after brain death maintained with vasopressin and epinephrine

In order to examine renal function after brain death, twenty-eight patients were randomly separated into two groups. The systemic blood pressure of ten patients was maintained with epinephrine alone (group 1). Eight of the ten patients experienced cardiac arrest within 48 h (range 6–87 h) despite the rather large dosage of epinephrine. Urine output was uncontrollable and renal function deteriorated progressively in this group. Eighteen patients were maintained with arginine vasopressin and epinephrine (group 2). Circulation was maintained with a smaller dosage of epinephrine than that given group 1 for at least 4 days (mean±SD 16.5±12.2 days). Urine output was controlled within the normal range and serum levels of blood urea nitrogen (BUN) and creatinine were normal for 14 days. Daily creatinine clearance was more than 80 ml/min. The combined administration of arginine vasopressin and epinephrine preserved the kidneys after brain death for more than a week. This method will be of great value in renal transplantation from brain-dead organ donors.

Morphological and functional alterations of the hypothalamic-pituitary system in brain death with long term bodily living

SummaryHypothalamic hormones as well as anterior pituitary hormones were detected in the peripheral plasma after the diagnosis of brain death. It is possible that residual hypothalamic tissue was functioning after satisfying the usual criteria of total brain death. To examine this possibility, endocrinological and morphological alterations of the hypothalamic-pituitary system was evaluated in 28 brain dead patients. Intrinsic ADH was depleted in the plasma shortly after the diagnosis of brain death. Anterior pituitary hormones were initially detected in all patients, but gradually disappeared. The direct TRH (thyrotropin releasing hormone) stimulation to the anterior lobe was responded to well. Morphological studies showed a partial necrosis of the anterior lobe and the preservation of the posterior lobe for as long as a week. These data prove that the pituitary is partially preserved after brain death.LH-RH (luteinizing hormone releasing hormone) was detected in the peripheral plasma of all patients and GRF (growth hormone releasing factor) was detected in half of the patients for as long as 15 days, but autopsy revealed the fact that the brain tissue including the hypothalamus became extensively necrotic after the sixth day of brain death. In order to solve this controversy it is proposed that these hormones originate from extracranial tissues such as pancreas. The detection of hypothalamic hormones after the diagnosis of brain death therefore is not contradictory to the concept of total brain death.

Transcatheter embolization in the treatment of massive bleeding due to maxillofacial injury

Thirty-one cases of massive bleeding due to blunt maxillofacial injuries were treated by several procedures. Blind techniques, such as nasal and/or oral packing or ligation of external carotid artery, failed to achieve hemostasis in 13 of the 18 cases (72.2%) in which they were employed before 1984. Since then, carotid angiography has documented the location of the bleeding in 12 of the 13 cases (92.3%) in which it was employed. Each of the four cases in which extravasation was visualized from the external carotid artery was successfully treated by transcatheter embolization. We conclude that selective, angiographically guided embolization can reliably achieve hemostasis in a high proportion of patients with maxillofacial injury who are in danger of exsanguination from the branches of the external carotid artery.

Computed tomographic imaging of the brain in after hypoglycemia coma

SummaryA case of severe hypoglycemic coma was studied by sequential Computed Tomographic Imaging (CT) of the brain. The CT 1) was normal in the early stage, 2) subsequently showed a low density area, which was enhanced by the contrast medium, in the cerebral cortex and the boundary zone between the major cerebral arteries, and 3) revealed marked enhancement in the entire cortical region and hypodensity in the periventricular region in the late stage. These CT findings, representing the course of neural cell damage by severe hypoglycemia, are discussed from the pathophysiological viewpoint.

Limb ischemia and reperfusion: relationship of functional recovery to nerve and muscle blood flow.

UNLABELLED The relative importance of nerve versus muscle injury in limb ischemia-reperfusion is poorly understood. We used 14C-butanol tissue distribution to measure regional blood flow simultaneously in the proximal and distal sciatic, the posterior tibial nerve trunk (NBF), and biceps femoris muscle (MBF) of rats during 3 hours of occlusion of the ipsilateral iliac and femoral arteries and subsequently for up to 9 days of reperfusion. Limb motor function was also serially assessed. The contralateral limbs served as controls. Experimental groups were untreated control (n = 16); methylprednisolone, 30 mg/kg (n = 13); the lazaroid U74389F, 3 mg/kg (n = 13); and lazaroid vehicle (n = 13), i.v. 15 minutes before occlusion and 15 minutes after reperfusion. RESULTS One hour after occlusion, NBF was -77% of the control value (p < 0.02) but MBF was unchanged (control NBF 15.2 +/- 3.3, control MBF 6.3 +/- 0.9, units mL.min-1 x 100 g-1). At both 2 and 21 hours of reperfusion, NBF was double that of control in all groups (p < 0.01); but MBF, which had been modestly elevated to 10.5 +/- 0.5 at 2 hours (p < 0.01), was already normal at 21 hours in all groups. During days 5 to 9 of reperfusion, NBF was still numerically elevated (NS); MBF remained at control. Functionally, test. limb scores were always grossly abnormal during occlusion (range: 7.1-8.5, normal = < 2). After 1 hour of reperfusion, all test limb scores were improved versus occlusion (p < 0.001, Wilcoxon rank-sum). Subsequently, there was gradual improvement in all groups, scores at 6 days ranging from 1.9 to 2.5. CONCLUSION NBF is rapidly and severely reduced during ischemia. During reperfusion, the hyperemic flow response in nerve is more prolonged than in muscle. Limb dysfunction during ischemia and reperfusion may be largely the result of axonal or neuromuscular junction injury or both. Neither of the two treatments had effects on blood flow or limb function.