This study was undertaken to observe the effects of centrally administred antihistamines on the blood pressure. Diphenhydramine(DPH), a H1-receptor antagonist, and ranitidine(RAN), a H2-receptor antagonist were administered intracerebroventricularly(icv) on urethane-anesthetized rabbits. 1) Both DPH and RAN administered intraccebroventricularly increased blood pressure, however the intravenous(iv) adminstration of them did not affect blood pressure. The pressor response to icv DPH was dose-dependent, but that to icv RAN was not. 2) The pressor response to icv DPH(1mg) was either markedly attenuated or reversed to depressor response by the pretreatment with icv phentolamine(250,500ug), and iv chlorisondamine(0.1, 1mg/Kg) and iv phenoxybenzamine(1mg/Kg). In cord-sectioned rabbtis, icv RAN) 1mg) did not produce pressor response. 3) The pressor responsr to icv RAN(1mg) was not affected by the pretreatment with icv phentolamine(500ug), iv chlorisondamin(1mg/Kg) and iv phenoxybenzamine(1mg/Kg), and iv phenoxybenzamine(1mg/Kg). RAN also producted pressor response in cordsectioned rabbits. These results suggest that the pressor response to icv DPH is elecited by increasing peripheral sympathetic tone via the stimulation of central alpha-adrenoreceptors and the pressor response to icv RAN is produced by releasing some humoral facotr which can increase blood pressure.
Blood Pressure ; Diphenhydramine* ; Histamine Antagonists ; Rabbits* ; Ranitidine*

Intracerebral hemorrhage secondary to vitamin K deficiency is presented in three newborn infants: 4 days, 28 days and 21 days of age respectively. After the administration of vitamin K(5-10 mg) either intravenously or intramusculary, prolonged prothrombin time(PT) and partial thromboplastin time(PTT) were corrected promptly. Vitamin K dependent coagulation factor deficiency due to vitamin K deficiency is accounted for the pathogenesis of hemorrhage. The possible causes of vitamin K deficiency, diagnostic methods and treatment of this disease entity are reviewed. Neurosurgeons as well as pediatricians should remain alert for the development of intracerebral hemorrhage caused by vitamin K deficiency in neonatal period.
Blood Coagulation Factors ; Cerebral Hemorrhage* ; Hemorrhage ; Humans ; Infant, Newborn* ; Partial Thromboplastin Time ; Prothrombin ; Prothrombin Time ; Thromboplastin ; Vitamin K Deficiency* ; Vitamin K* ; Vitamins*

The effect of nicardipine was investigated on hypertension due to raised intracranial pressure, pressor response of alpha-adrenoceptor agonists in the dissected thoracic aorta. Intracerebroventricular(icv) and intravenous(iv) nicardipine produced dose-dependent depressor response and bradycardiac effect, especially marked response was observed following iv injection. The pressor response to raised intracranial pressures was potentiated following iv injection of 50 microgram/kg nicardipine but was markedly inhibited following iv 100 microgram/kg injection, and was not affected following icv 50 microgram/kg administration but was markedly inhibited following icv administration of 100-200 microgram/kg nicardipine. The nicardipine inhibited contractile effect of KCI 35 mM in a dose-dependent fashion but did not affect that of Ne and ME. These data suggest that nicardipine caused hypotensive effect by blocking calcium influx in the peripheral vessels and that direct effect of nicardipine on central nervous system involves the hypotensive action. Conclusively, the inhibitory effect of nicardipine on the pressor response to the intracranial pressure elevation may be induced by these two mechanisms.
Aorta, Thoracic ; Calcium ; Central Nervous System ; Hypertension ; Intracranial Pressure* ; Nicardipine*

Effect of infusion and bolus injection of lidocaine on the pressure response to the increased intracranial pressure(ICP) was investigated in urethane-anesthetized rabbits. 1) Arterial blood pressure(BP) and ICP were significantly raised by infusing saline(0.05ml/min) into an epidural balloon. 2) Infusing of lidocaine(0.5mg/kg/min) into an ear vein minutely inhibited the elevation of BP and ICP when infusing saline into an epidural balloon. However, infusion of lidocaine(1.5mg/kg/min) markedly inhibited the elevation of BP and ICP. 3) Repeating the infusion of saline into the epidural balloon with intervals, the duration reached to the level of 80-10 mmHg ICP was gradually shortened. Each depressor response to the first, second and third injection of lidocaine(3 mg/kg) was similar. The first injection transiently reduced the elevated ICP, but the second and third injection reduced that significantly and the reducing effect was gradually prolonged according to repeating the lidocaine injection. These results show that lidocaine could delay the elevation of ICP and reduce the previously increased ICP by infusing saline into an epidural balloon.
Ear ; Intracranial Hypertension* ; Lidocaine* ; Rabbits* ; Veins

A K+-channel blocker, 4-aminopyridine(4-AP) increases neurotransmitter release from motor nerve terminals and has been shown to restore neuromuscular transmission in the myasthenic syndrome. It has been reported that the intravenous injection of 4-AP in the myasthenic patients caused many central adverse effects including anxiety and restlessness, but did not affect the blood pressure. The aim of this study was to observe the effect of intracerebroventricularly administered 4-AP on the blood pressure and to elucidate the mechanism of the action in urethane-anesthetized rabbits. Intracerebroventricular(icv) 4-AP produced pressor effects in a dose-dependent fashion, but intravenous(iv) 4-AP of the same dose did not altered the blood pressure. Tetraethylammonium, a K+-channel blocker which differs from 4-AP structurally, had little effect on the blood pressure, but 3,4-diaminopyridine, another derivative of the aminopyridine, produced pressor effect similar to 4-AP. The pressor effect of icv 4-AP was not affected by the treatment with iv phenoxybenzamine and chlorisondamine, and in bilateral adrenalectomized rabbits. These results suggest that the 4-AP pressor effect is not related to the periphral sympathetic nerve nor adrenal gland. The pretreatment with icv phentolamine and prazosin did not altered the 4-AP pressor. However, the icv 4-AP pressor effect was significantly attenuated by the treatment with icv yohimbine, and significantly potentiated by the treatment with icv clonidine. The treatment with icv diltiazem markedly inhibited the icv 4-AP pressor effect. It is concluded that 4-AP-sensitive K+-channels in rabbit brain might play a role in the regulation of blood pressure and that the 4-AP pressor effect is closely related to the central alpha2-adrenoceptors and L-type calcium channels.
4-Aminopyridine* ; Adrenal Glands ; Anxiety ; Arterial Pressure* ; Blood Pressure ; Brain ; Calcium Channels, L-Type ; Chlorisondamine ; Clonidine ; Diltiazem ; Humans ; Injections, Intravenous ; Neurotransmitter Agents ; Phenoxybenzamine ; Phentolamine ; Prazosin ; Psychomotor Agitation ; Rabbits ; Tetraethylammonium ; Yohimbine

This study was designed to observe anoxia-induced responses and to clarify their possible mechanisms in porcine basilar and circle of Willis arteries. Anoxia produced a transient vasoconstriction, which then recovered to the basal tension of a 3-5 min. later, and the reoxygenation that follows produced the biphasic(relaxation-contraction) response in the intact endothelial rings under resting tension. The anoxia-induced contraction was potentiated by pretreatment with KC1 and PGF2alpha. Reoxygenation produced only sustained relaxation. Removal of the endothelium and pretreatment with nimodipine or indomethacine markedly attenuated the anoxia-induced contractions. Anoxia transiently and significantly increased cyclic GMP contents in the endothelium-intact preparations, but did not affect them in the endothelium-removed ones. The above results suggest that anoxia-induced contraction is endothelium-dependent and is resultant to the release of a Prostaglandin-like substance(s) .
Anoxia* ; Arteries ; Cerebral Arteries* ; Circle of Willis ; Cyclic GMP ; Dinoprost ; Endothelium ; Indomethacin ; Nimodipine ; Relaxation ; Vasoconstriction

A silver staining technique was used in the study of nucleolar organizer regions(AgNORs) from the paraffin sections of 26 meningiomas. The specimens were divided into four groups as follows:benign(n=16), atypical(n=5), anaplastic or malignant(n=5) and recurrent without atypical histological findings(n=2) groups, and the mean number of AgNORs in each group was 1.47+/-0.27, 1.93+/-0.4, 2.00+/-0.27 and 1.49+/-0.53 respectively. We noted that the mean number of AgNORs reflected the cellular kinetics of a tumor and was related to histological grade. There was no significant difference between non-recurrent & recurrent benign meningiomas and it was thought that the main cause of recurrence in benign meningiomas was not perhaps cell proliferation but incomplete surgical removal.
Cell Proliferation ; Kinetics ; Meningioma* ; Nucleolus Organizer Region* ; Paraffin ; Prognosis* ; Recurrence ; Silver Staining

Hearing loss in the contralateral functioning ear is a rare and distressing complication after vetibular schwannoma removal. Various possible mechanisms have been proposed, however, the etiology of hearing loss is not clear. Fortunately, this is an extremely rare occurrence, sporadic case reports have appeared in the literatures. We report two cases of acute contralateral hearing loss after vestibular schwannoma removal and discuss the possible mechanisms of the phenomenon. Although permanent deafness may result, in our cases, the hearing loss was temporary, returning to near preoperative level within one month. The etiology of hearing loss in one case is thought to be cerebrospinal fluid leakage. However, in the other case, the cause of hearing loss is not clear. A better understanding of these events may lead to preventive measures to avoid contralateral hearing loss after vestibular schwannoma removal.
Cerebrospinal Fluid ; Deafness ; Ear* ; Hearing Loss* ; Hearing* ; Neurilemmoma ; Neuroma, Acoustic*

No abstract available.
Vulva* ; Vulvar Neoplasms*

No abstract available.
Vulva* ; Vulvar Neoplasms*