The mortality and morbidity of the intraventricular hemorrhage(IVH) has been decreased since the introduction of external ventricular drainage(EVD) and direct intraventricular infusion of urokinase as an effective therapeutic method. In 1989, we already reported a series of 54 cases of IVH treated with simple EVD or EVD with urokinase irrigation in a few cases. Authors analyzed again a series of 50 cases of IVH treated by EVD with direct intraventricular urokinase irrigation after the pervious report. The mortality rate was 55.5% in former occasion, however 18% in this study and the complications were considerably low. We experienced again that the EVD with urokinase irrigation is an effective method and convenient, simple technique in the management of IVH even though there is no ICP monitoring. So we prefer EVD with urokinase irrigation therapy in managing the IVH even if the patient is moribund state.
Drainage* ; Hemorrhage* ; Humans ; Infusions, Intraventricular ; Mortality ; Urokinase-Type Plasminogen Activator*

Phamacokinetic study of the antibiotic concentrations in the cerebrospinal fluid was done with high pressure liquid chromatography of CSF samples from twelve patients who had various amount of continuous extra-ventricular drainage during antibiotic administration. Five patients with large amount(over 150cc/day) of drainage had decreased CSF antibiotic concentrations dramatically below the effective concentration within 4 hours after intraventricular antibiotic administration, but six patients with small(less than 150cc/day) drainage maintained CSF antibiotic level above effective concentration even 24 hours after administration. In conclusion, repeated intraventricular administration of antibiotic is necessary to maintain the effective drug level in the patient with CSF drainage over 150cc/day.
Cerebrospinal Fluid* ; Chromatography, Liquid ; Drainage* ; Humans ; Infusions, Intraventricular*

Among all of the spontaneous TCH(intracerebral hemorrhage), the presence of IVH(intraventricular hemorrhage) is showing higher mortality and morbidity. Since the introduction of EVD(extraventricular drainage) and direct intraventricular infusion of Urokinase as a effective therapeutic methods of IVH, it's mortality and morbidity has been decreased. But, in cases of hemorrhage extended into all ventricular chambers showes poor prognosis even the EVD and infusion of Urokinase. Authors analyzed 40 cases of IVH treated with simple EVD or direct intraven-tricular infusion of Urokinase. The results were as follows: 1) The most common age groups of IVH patients were 5th and 6th decades and 22 patients were male, 18 patients were female. 2) All 15 cases of Urokinase treated group revealted over the 7 point of Graeb score. 3) On admission, Glasgow coma scale scores were under the 8 at the 11 cases(73%) of Urokinase treated group and 18 cases(72%) of simple EVD group. 4) Time of cleared ventricles showed fast at the Urokinase treated group than simple EVD group. 5) Incidence of complications were similar on both groups. 6) Prognosis revealed lower morbidity and mortality at the Urokinase treated group than simple EVD group. 7) In cases of high Graeb score and low Glasgow coma scale on admission showed poor prognosis in both groups.
Female ; Glasgow Coma Scale ; Hemorrhage* ; Humans ; Incidence ; Infusions, Intraventricular ; Male ; Mortality ; Prognosis ; Urokinase-Type Plasminogen Activator*

BACKGROUND: To evaluate the efficacy of modified ventriculolumbar perfusion (VLP) chemotherapy with methotrexate on leptomeningeal carcinomatosis in terms of symptomatic response and side effects. METHODS: Previous infusion rate of 20 mL/h was reduced to 15 mL/h for the purpose of decreasing constitutional side effects of VLP such as nausea/vomiting, insomnia and confusion. The primary outcome was the response rate of increased intracranial pressure (ICP), and the secondary outcome was the occurrence of side effects compared to previous 20 mL/h trial. This interim analysis to validate the reduced infusion rate is not to affect the original effect of VLP chemotherapy. RESULTS: All forty-seven patients were enrolled including 22 patients with increased ICP. Thirteen patients out of these (59%) got normalized ICP after VLP chemotherapy. Moderate to severe (grade 2–3) confusion was observed in 3 patients (6%) and it was significantly reduced compared to those (23%) in the VLP 20 mL/h (p=0.017). Grade 2–3 nausea/vomiting was also reduced from 64% to 45% but failed to reach statistical significance (p=0.08). Median overall survival (OS) was 5.3 months (95% confidence interval, 3.55–7.05) and patients OS, who received maintenance VLP was significantly prolonged compared to patients who underwent induction VLP only (5.8 vs. 3.4 months, p=0.025). CONCLUSION: VLP of reduced perfusion rate (15 mL/h) showed compatible control rate of increased ICP at this interim analysis. Decreased moderate to severe side effects and prolonged OS in patients received maintenance VLP encourage us to evaluate the effectiveness of this trial further.
Drug Therapy ; Humans ; Infusions, Intraventricular ; Intracranial Pressure ; Meningeal Carcinomatosis ; Methotrexate ; Perfusion ; Sleep Initiation and Maintenance Disorders

Angiotensin I ; pharmacology ; Animals ; Blood Pressure ; drug effects ; physiology ; Infusions, Intraventricular ; Male ; Peptide Fragments ; pharmacology ; Pulmonary Artery ; physiology ; Rats ; Rats, Sprague-Dawley

BACKGROUND: The sodium concentration in the central nervous system may play an important role in cardiovascular function and body fluid regulation. The purpose of this investigation was to examine the effects of intracerebroventricular (ICV) infusion of hypertonic NaCl solutions on the cardiovascular responses in normotensive and 2-kidney, 1 clip (2K1C) renal hypertensive rats. METHODS: 2K1C hypertension was made by clipping the left renal artery and were used 4 weeks later. Age-matched control rats received a sham treatment. Under thiopental (50 mg/kg, IP) anesthesia, both isotonic and hypertonic NaCl solutions (0.15 M, 0.6 M and 1.2 M) were ICV applied, while blood pressure and heart rate (HR) responses were continuously monitored. RESULTS: Central administration of hypertonic NaCl solution caused an elevation in mean arterial pressure (MAP) and HR in both normotensive and 2K1C hypertensive rats. The response magnitude in the blood pressure was positively correlated to the NaCl concentration in normotensive rats, while the pressor responses to hypertonic NaCl were comparable regardless of the concentration of NaCl in hypertensive rats. Despite of the HR responses were similar in between two groups, the magnitude of the MAP increases were more elevated in hypertensive than in normotensive control rats. Isotonic NaCl solution, when centrally applied, caused an elevation in blood pressure only in hypertensive rats. CONCLUSION: These results indicate that the central sensitivity to sodium chloride is altered in 2K1C renal hypertensive rats.
Anesthesia ; Animals ; Arterial Pressure ; Blood Pressure ; Body Fluids ; Central Nervous System ; Heart Rate ; Hypertension ; Hypertension, Renal ; Infusions, Intraventricular* ; Placebos ; Rats* ; Renal Artery ; Sodium ; Sodium Chloride ; Thiopental

This experiment was performed to define the paricipation of a discrete hypothalamic neural structure in the genesis of pulmonary edema and the effect of alpha adrenergic blockade. Fifty adult cats weighing 2.5 to 4.0 Kg, were used in this study. The components of the pathophysiological systemic changes, lung weight, and histopathological changes of lung and hypothalamus were studied in groups of animals when intracranial pressure(ICP) was raised to 200 mmH2O of 300 mmH2O for 2 hours by intraventricular infusion with normal saline. The animals were divided into 5 groups : The normal control group was comprised in 10 normal cats. Control and phentolamine treated animal groups which had an elevated ICP of up 200 mmH2O consisted of 10 cats each. Control and phentolamine treated animal groups which had an elevated ICP of up to 300 mmH2O consisted of 10 cats each. The results obtained were as follows : 1) In the animal groups of elevated ICP to 200 mmH2O or 300 mmH2O, there were hemodynamic systemic changes which were neurogenically mediated and caused an immediate elevation in blood pressure of 30 mmHg to 60 mmHg. The hemodynamic data of the animals that had an elevated ICP of up to 300 mmH2O were significantly more deviated from normal control values than the 200 mmH2O ICP groups. The hemodynamic responses of the phentolamine treated animal with elevated ICP of up to 200 and 300 mmH2O were less deviated from normal control values. 2) The lung weights of the animals with an elevated ICP of up to 200 and 300 mmH2O were significantly heavier than the normal control value(p<0.05) and the lung weights of the animals with an elevated ICP of 300 mmH2O were significantly heavier than those with an ICP of 200 mmH2O(p<0.01). The lung weights of the phentolamine treated animal groups were significantly lighter than the control group but showed little increase in the lung weight when compared to the normal value. 3) By controlling the elevated ICP above 200 mmH2O in the experimental animals we have confirmed gross and microscopic appearances of hemorrhagic pulmonary edema. Histopathological changes of the phentolamine treated animals were significantly less sever than in the control groups. 4) By elevating ICP above 200 mmH2O in the experimental animals, we have confirmed discrete bilateral hemorrhagic spots of the anterior hypothalamus, preoptic region induced by increased intracranial pressure. Histopathological changes of the phentolamine treated animals with the elevated ICP were significantly less severe than of the control groups. 5) This experimental model may define the specific particification of the hypothalamus in the pathophysiological pathogenesis of neurogenic pulmonary edema. These results suggest that the lungs are directly affected by the intense sympathetic discharge evoked by release phenomenon from the sympathoinhibitory influence of the hypothalamus, and pulmonary edema was effectively eliminated by alpha adrenergic blockade.
Adult ; Animals ; Blood Pressure ; Cats* ; Edema* ; Hemodynamics ; Humans ; Hypothalamus ; Hypothalamus, Anterior ; Infusions, Intraventricular ; Intracranial Pressure ; Lung* ; Models, Theoretical ; Phentolamine* ; Pulmonary Edema ; Reference Values ; Weights and Measures

Changes of blood pressure, heart rate, ECG, respiration rate and pupil size by intracerebroventricular(ICV) infusion of hypertonic NaCl with 0.04 ml/min for 5 min(total 0.2ml) were observed in urethane-anesthetized rabbits. ICV infusion of 0.75M NaCl produced slight pressor effect (11mmHg) and did not affect other parameters. ICV infusion of 1.5M NaCl began to increase blood pressure from 2~3 min after the infusion and produced maximal increase(24mmHg) at 5~10 min. Then the pressor effect was recovered to the original level at 30~60 min. Change of heart rate by the infusion was not clear, but ST-segment of ECG was markedly depressed. Respiration rate increased about 1.5 times than the control in accordance with the pressor effect and the state was continued even after the recover of the pressor effect. Both pupils dilated markedly and light-reflex was lost. Changes of parameters by ICV infusion of 3.0M NaCl were similar to those by 1.5M NaCl and some rabbits caused severe arrhythmias and died. The purpose of present study is to investigate the mechansim(s) of the pressor effect induced by the ICV infusion of 1.5M NaCl. The pressor effect of 1.5M NaCl was attenuated by the continuous infusion of vasopressin antagonist(20microm/kg/min) but not affected by intravenous treatment with 2mg/kg phentolamine, 2mg/kg propranolol and 1mg/kg chlorisondamine. The pressor effect was not altered with ICV 0.12mg/kg phenoxybenzamine, 0.4mg diltiazem, 0.1mg/kg mecamylamine and 0.2mg/kg atropine. After ICV infusion of 25microg/kg/min of diazepam, however, the pressor effect was completely abolished and restored 3~4 hours after stopping diazepam infusion. The pressor effect was rather potentiated than inhibited in bilateral adrenalectomized or nephrectomized rabbits. Infusion of 2microg/kg/min of saralasin for 10 min in the bliateral adrenalectomized rabbit did not affect the pressor effect at all. These results suggest that hypertensive effect induced by ICV infusion of hypertonic NaCl is mediated by the increase of vasopressin secretion.
Arrhythmias, Cardiac ; Atropine ; Blood Pressure ; Chlorisondamine ; Diazepam ; Diltiazem ; Electrocardiography ; Heart Rate ; Infusions, Intraventricular* ; Mecamylamine ; Phenoxybenzamine ; Phentolamine ; Propranolol ; Pupil ; Rabbits* ; Respiratory Rate ; Saralasin ; Vasopressins

BACKGROUND: Production of neuronal progenitors is usually stimulated in the forebrain subventricular zone of mice after the intracerebroventricular infusion of prolactin. As a preliminary study, we infused prolactin to the male rat brain to test the hypothesis that prolactin promotes new cell proliferation in the brain and functional recovery after focal ischemia. METHODS: Male rats were subjected to intraluminal middle cerebral artery occlusion. Prolactin was administered to the surface of the brain for 5 or 14 days starting 24 or 48 hours after stroke onset at doses of 6.4 microgram per day. We administered the same volume of saline to the other ischemic rats used as a control group. Some rats were killed 6 or 17 days after stroke for analysis of infarct volume and newly generated cells within the subventricular zone and the striatum. The other rats were tested for neurological recovery 24 days after stroke. RESULTS: There was no significant difference of infarct volume among the experiment groups. Treatment with prolactin did not increase the numbers of bromodeoxyuridine-immunoreactive cells in the subventricular zone and the striatum. Treatment with prolactin did not enhance neurological recovery in all tests performed. CONCLUSIONS: In this preliminary study, prolactin did not enhance new cell generation in the male rat brain nor reduce the neurological deficits after ischemic stroke.
Adult* ; Animals ; Brain Ischemia* ; Brain* ; Cell Proliferation ; Humans ; Infarction, Middle Cerebral Artery ; Infusions, Intraventricular ; Ischemia ; Male* ; Mice ; Neurons ; Prolactin ; Prosencephalon ; Rats* ; Stem Cells ; Stroke

AIMTo further explore the role of adenosine A1 receptor in the neuroprotective effect of cerebral ischemic preconditioning, the present study was undertaken to observe the effect of inhibiting expression of adenosine Al receptor with adenosine A1 receptor antisense oligodeoxynucleotide (ARA1 As-ODN) on the neuroprotective effect of cerebral ischemic preconditioning against delayed neuronal death (DND) normally induced by lethal brain ischemia.

METHODThe rat 4-vessel occlusion global cerebral ischemic model was used. Forty-eight male Wistar rats with permanent occlusion of the bilateral vertebral arteries were divided into 8 groups: Sham, CIP, brain ischemic insult, CIP + brain ischemic insult, Distilled water + CIP + brain ischemic insult, ARA1 As-ODN, ARA1 As-ODN +CIP, ARA1 As-ODN+ CIP + brain ischemic insult(two doses of 10 nmol/5 microl and 20 nmol/5 microl were used) groups. ARA1 As-ODN was dissolved in distilled water and injected into the right lateral cerebral ventricle. To illustrate the profile of DND, histological grade (HG) and neuronal density (ND) in the CA1 region of the hippocampus were examined 7 d after the sham operation or the last time of ischemia under thionin staining.

RESULTSThe HG and ND in CIP group were similar to those in sham group. Brain ischemic insult induced obvious DND as represented with the increase in HG and decrease in ND significantly (P < 0.05 vs. sham and CIP groups). In CIP + ischemic insult group,no obvious DND was observed,which indicated that CIP protected pyramidal neurons against the ischemic insult.While the administration of ARA1 As-ODN in ARA1 As-ODN + CIP + brain ischemic insult group caused obvious increase in HG and decrease in ND compared with CIP + brain ischemic insult group (P < 0.05) in a dose dependent manner,which indicated that the neuroprotective effect of CIP against DND of hippocampal pyramidal neurons normally induced by ischemic insult was inhibited by the administration of ARA1 As-ODN.

CONCLUSIONThe results further demonstrate the association of up-regulation of adenosine A1 receptors with the induction of CIP-mediated BIT.

Animals ; Brain Ischemia ; physiopathology ; prevention & control ; Hippocampus ; physiopathology ; Infusions, Intraventricular ; Ischemic Preconditioning ; Male ; Oligodeoxyribonucleotides, Antisense ; administration & dosage ; pharmacology ; Random Allocation ; Rats ; Rats, Wistar ; Receptor, Adenosine A1 ; metabolism ; physiology ; Up-Regulation ; drug effects