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*

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*

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

To elucidate the role of CNS GABA ergic system in the regulation of cardiovascular function, the effects of intracerebroventricular(icv) bicuculline(BIC), a selective GABAA antagonist, on blood pressure and heart rate were investigated in urethane anesthetized rabbits. 1) Icv BIC produced dose-dependent pressor and bradycardiac effect, while intravenous(iv) BIC had no effect on blood pressure and heart rate. 2) The pressor effect of BIC(10(g) was significantly attenuated by pretreatments with icv ketamine(5 mg) or icv diazepam(0.1 mg, 1 mg). Bilateral vagotomy and pretreatment with icv mecamylamine(0.2 mg), iv chlorisondamine(1 mg/kg), in phentolamine(1 mg/kg) did not affect the pressor action. 3) The bradycardiac effect of BIC(10(g) was abolished or reversed to slight tachycardia by bilateral vagotomy and pretreatment with icv ketamine(2.5 mg, 5 mg), icv diazepam(0.1 mg, 1 mg) and iv chlorisondamine(1 mg/kg). Neither icv mecamylamine(0.2 mg) nor iv phentolamine(1 mg/kg) affected the bradycardia. These results suggest that blockade of GABAA receptor produce pressor action which is associated with central excitatory amino acid system and produce reflex bradycardia induced by the pressor effect, and that sympathetic nervous system might not be involved in the pressor effect.
Bicuculline* ; Blood Pressure* ; Bradycardia ; Excitatory Amino Acids ; gamma-Aminobutyric Acid ; Heart Rate* ; Heart* ; Rabbits* ; Reflex ; Sympathetic Nervous System ; Tachycardia ; Urethane ; Vagotomy

The authors represented an analysis on 10 patients with traumatic epidural hematomas of the posterior fossa who had treated successfully from January 1984 to October 1985. The result were summarized as follows ; 1) Age incidence comprised ranging from 4 to 62 years and 6 were males and 4 were females. 2) Site of hematoma was related with fracture site closely and bleeding source confirmed during operation was transverse sinus in 4 cases, occipital sinus in 1 case, fracture site in 3 cases and unknown in 2 cases and it had close relationship between fracture site and large venous sinus. 3) Outcome was good in most cases except death in 1 and moderate disability in 1 case. Factors contributing to outcome were early detection and adequate treatment and also associated supratentorial injury.
Female ; Hematoma* ; Hemorrhage ; Humans ; Incidence ; Male ; Skull Fractures

It is well known that bloody cerebrospinal fluid(BCSF) obtained from patient with subarachnoid hemorrhage will contracts isolated brain arteries, but the effects of non-bloody CSF(non-BCSF), which does not contain blood components, has not been reported yet. In this study, CSFs were obtained from 12 patients hospitalized at the Department of Neurosurgery, Chonnam University Hospital from February to September 1994. Among the CSFs from these 12 patients, 3 cases were bloody and 9 cases were not. It was found that all BCSFs produced marked contractions in ring preparations of porcine isolated basilar and circle of Willis arteries. The non-BCSFs fell into two groups:one which contracted the preparations in a volume-dependent fashion(30-1000 microliter) and the other did not. The purpose of this study was to investigate the mechanism(s) of contractile response to the first group on-BCSF in the porcine isolated brain artery. Concentration-dependent contractions induced by KCl were not affected by the pretreatment with 500 microliter non-BCSF, while contraction induced by 5-hydroxytryptamine(5-HT) and phenylephrine(PE) were significantly potentiated by the same pretreatment of non-BCSF. Although volume-dependent contractions induced by the non-BCSF were not affected by the pretreatment with 10(-6) M phentolamine and 10(-4) M L-NAME, the contractions was significantly attenuated by the presence of 10(-6) M indomethacin and nimodipine. It was also found that the contraction induced by prostaglandin F2alpha(PGF2alpha) was relaxed by nitroprusside and atriopeptin(ANP) in a concentration-dependent manner and such relaxations were not affected by nitroprusside and ANP were not affected in the presence of 500 microliter non-BCSF. Above observations suggest that components, of non-BCSF from patients with brain lesion contains an unknown substance(s) that induces contraction of porcine isolated brain arteries and the above contractile effect involves the extracellular calcium influx and/or cyclooxygenaseprostaglandin system but not the NO-guanylate cyclase system.
Arteries* ; Atrial Natriuretic Factor ; Brain* ; Calcium ; Cerebrospinal Fluid* ; Circle of Willis ; Humans ; Indomethacin ; Jeollanam-do ; Neurosurgery ; NG-Nitroarginine Methyl Ester ; Nimodipine ; Nitroprusside ; Phentolamine ; Relaxation ; Subarachnoid Hemorrhage

To investigate neuronal injury developed in an experimental model of temporal lobe epilepsy, the expression of c-FOS, c-JUN and HSP72 on the amygdala, hippocampus and temporal neocortex was studied. Epileptic seizure was induced in rats by microinjection of kainic acid(1microgrm/microl) dissolved in phosphate buffer(0.1 M, pH 7.4) into the left amygdala. Selective and delayed neuronal injuries appeared in the CA3 region of the hippocampus after 14 days and were characterized by swelling of cytoplasm and neurites, nuclear pyknosis and loss of neurons. Early induction of c-FOS and c-JUN was noted on the injection-side amygdala at 1-12h, and delayed expression developed at 7 days after the injection. HSP72 expression appeared continuously 3 hrs after the injection. Delayed induction of c-FOS, c-JUN and continuous expression of HSP72 were observed in the hippocampus and entorhinal cortex. In the hippocampus, c-FOS expression was relatively strong in the neurons of CA3 and dentate gyrus at 7~14 days after the injection. Similar findings were also noted in the neurons of the entorhinal cortex. Induction of HSP72 occurred slightly later than on that of c-FOS and c-JUN in the amygdala, with the prominent induction being noted in the neurons of amygdala, CA2, CA3, CA4 and dentate gyrus at 3 to 21 days after the injection. These results suggested that the delayed expressions of c-FOS and c-JUN in the hippocampus correlated well with impending clinical epileptic seizure.
Amygdala ; Animals ; Cytoplasm ; Dentate Gyrus ; Entorhinal Cortex ; Epilepsy ; Epilepsy, Temporal Lobe* ; Hippocampus ; Hydrogen-Ion Concentration ; Kainic Acid ; Microinjections ; Models, Theoretical ; Neocortex ; Neurites ; Neurons ; Rats* ; Temporal Lobe*

Influences of intracerebroventricular(icv) ouabain on cardiovascular system and on pressor response to raised intracranial pressure(ICP) were investigated in urethane-anesthetized rabbits. Intravenous(iv) 40 microgram/kg ouabain did not affect blood pressure of rabbit. Icv ouabain(5, 10, 20 microgram/kg) and digoxin(6.25, 12.5 microgram/kg) produced dose-dependent pressor responses and marked decrease of heart rate. After bilateral vagotomy, the bradycardiac effect of ouabain disappeared, while the pressor effect was significantly potentiated. The ouabain-induced pressor effect was not affected by iv and icy phentolamine or propranolol, and significantly inhibited by icy infusion of lidocaine(0.1 mg/kg/min) and diazepam(0.025 mg/kg/min). The pressor response to raised ICP was not affected by iv 40 microgram/kg ouabain but disappeared by icy 10 microgram/kg ouabain and 6.25 microgram/kg digoxin. These data suggests that ouabain causes pressor effect through direct interaction with a site(s) in central nervous system and bradycardiac effect by direct activation of vagal center, and ouabain blocks central sympathetic stimulation by increase of ICP in rabbits.
Blood Pressure ; Cardiovascular System* ; Central Nervous System ; Digitalis* ; Digoxin ; Heart Rate ; Intracranial Pressure ; Ouabain ; Phentolamine ; Propranolol ; Rabbits* ; Vagotomy