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PubMed1989

Regional effects of 6-hydroxydopamine (6-OHDA) on free radical scavengers in rat brain.

Superoxide dismutase (SOD), catalase, glutathione (GSH), and glutathione peroxidase (GSH-Px) were measured in the caudate-putamen (CPu), the hippocampus (HIP), and the brainstem (BS) of the brains of control animals and of rats treated with one intracerebroventricular infusion of 6-hydroxydopamine (6-OHDA). Injection of 6-OHDA resulted in significant decreases in the activity of SOD in the CPu, the BS, and in the HIP. There were decreases in catalase in the CPu and in the BS, but not in the HIP. GSH was reduced in the CPu and the BS but not changed in the HIP. There were small decreases in the activity of GSH-Px only in the BS. These changes may be secondary to the production of free radicals after the infusion of 6-OHDA in rat brain.

Animals↗
PubMed1986

Cerebrospinal fluid pressure of anaesthetized rats during intracerebroventricular infusion.

Increases in cerebrospinal fluid pressure (CSFP) were measured in the lateral ventricle in barbiturate anaesthetized male Sprague Dawley rats during intracerebroventricular (IVT) infusions into the contralateral ventricle. IVT infusions of isotonic artificial CSF (art-CSF) solutions at 10 and 38 microliters/hr increased mean CSFP from control preinfusion level of 3.6 cm H2O to 4.6 cm H20 (n.s.) and 5.2 cm H2O (p less than 0.01) respectively with CSFP appearing to attain equilibrium after 30-60 min of infusion. IVT infusion of hyperosmolar art CSF solutions (saccharide and salt solutions of approximate 1000 mOsm/kg) at 38 microliters/hr resulted in a larger increase of CSFP which equilibrated at 8.5 cm H2O (p less than 0.001) after 90 min of infusion. It is suggested that on the basis of CSFP measurements in these and other experiments cited that IVT infusions be run at infusion rates of less than 40 microliters/hr to ensure minimal physiological change.

Animals↗
PubMed1988

Ingestion, body weight and activity of rats receiving repeated intracerebroventricular infusions of rat satietin.

Satietin is a putative satiety agent that is found in a variety of species including man and the rat. In the first experiment male Sprague-Dawley rats were fitted with chronic third ventricle cannulas and placed in activity wheels. After recovery, animals were intracerebroventricularly (ICV) infused with either sterile rat satietin (r-SAT) (100 micrograms/rat) dissolved in 10 microliters saline (n = 6) or sterile saline (n = 8). Infusions were repeated the next two days. Infusions of r-SAT had no effect on the rats' water intake or activity but did suppress (p less than 0.05) their food consumption when compared to the controls, but only after the first and second infusions. Thus tolerance to r-SAT quickly developed using this schedule of administration. Notably, body weight of the r-SAT infused rats remained attenuated (p less than 0.01) for four days following the first infusion. In the second experiment the rats were ICV infused every fourth day with either r-SAT (100 micrograms/rat) (n = 10) or saline (n = 8) for a total of three infusions. Food, but not water, intake was significantly suppressed after the first and second infusions and lowered nonsignificantly after the third. Body weight was significantly reduced after the first r-SAT infusion and remained statistically reduced for seven days after the third infusion; at a time when the rats' food intake was normal. These data suggest that in addition to a r-SAT suppression of feeding, other r-SAT induced changes (possibly metabolic) may help reduce the rats' body weight. The above dose of r-SAT had no affect on the animals' rectal temperature. The data of the above two experiments reveal that r-SAT infused ICV into rats can suppress the animals' food intake and lead to a prolonged attenuation of body weight.

Animals↗
PubMed1982

Alcohol drinking in the rat: increases following intracerebroventricular treatment with tetrahydro-beta-carbolines.

Voluntary alcohol intake has been reported to increase in rats after the repeated intracerebroventricular (ICV) administration of 1,2,3,4-tetrahydro-beta-carboline (THBC) and some tetrahydroisoquinolines, although negative results have also been reported. THBC is a normal constituent in human plasma and platelets; 1-methyl-1,2,3,4-tetrahydro-beta-carboline (1-Me-THBC), however, occurs in the blood after a person drinks alcohol. We have evaluated the effects of two doses of THBC and 1-Me-THBC on voluntary alcohol consumption in rats. ICV infusions were given with Alzet minipumps for 14 days rather than giving repeated ICV injections. Stability of the drugs in the pump was verified using mass spectrometry. On each day the rats chose between water, alcohol (increasing concentrations from 3 to 30%) and an empty bottle. Alcohol intake increased by about 100% (p less than 0.05) during the last six days when 47 nmoles/hr of either THBC or 1-Me-THBC was infused. At the end of the experiment elevated blood concentrations of alcohol (0.02-0.78(0)/00) were found in rats belonging to the THBC or 1-Me-THBC groups and drinking 30% alcohol. The infusion of 0.47 nmoles/hr of either drug did not increase alcohol intake as compared to control.

Alcohol Drinking↗
PubMedDate not supplied

Acute and chronic intracerebroventricular morphine infusions affect long-term potentiation differently in the lateral perforant path.

Experiments were performed to investigate the effects of acute and chronic intracerebroventricular (icv) morphine infusions via osmotic minipumps on long-term potentiation (LTP) in the lateral perforant path (LPP)-granule cell synapse of the rat dentate gyrus. Although significant antinociceptive activity was observed when morphine was infused (25 nmol/microl/h) for 30 min or 1 h, the activity was not observed in rats receiving morphine chronically for 72 h, and the tail-flick latency of this group was comparable to that of rats receiving saline. LTP induction was significantly attenuated after acute morphine infusion (1 h) in LPP-granule cell synapses of the dentate gyrus. In contrast, LTP induction was augmented after chronic morphine infusion for 72 h. Bath-perfused morphine augmented the baseline population spike (PS) amplitude in rats treated with saline, whereas it attenuated the LTP induced by chronic morphine infusion. Returning the LTP to the level of saline infusion after in vitro morphine perfusion suggests that enhancement of the LTP is a withdrawal-like phenomenon. These results suggest a difference between the effects of acute and chronic intracerebroventricular morphine infusions on synaptic plasticity in the LPP-granule cell synapses of the dentate gyrus.

Analgesics, Opioid↗
PubMed1996

Binge ethanol-induced brain damage in rats: effect of inhibitors of nitric oxide synthase.

Testing the possible role of endogenous nitric oxide (NO) in the neurotoxicity of ethanol, we examined how two different NO synthase (NOS) inhibitors affected the extent cerebrocortical and olfactory neuronal damage in a modified "binge intoxication" rat model (Collins et al., Alcohol Clin. Exp. Res. 20:284-292, 1996). Male rats intragastrically fed ethanol (6.5 to 12 g/kg/day) in nutrient solution three times daily for 4 days also received NG-nitro-L-arginine methyl ester by chronic intracerebroventricular infusion or 7-nitro-indazole by daily intraperitoneal injection; control rats were given nutrient solution only and/or vehicles. Blood ethanol levels did not differ among the ethanol-treated groups. The amount of ethanol-dependent neuronal degeneration in the entorihinal cortex, dentate gyrus, and olfactory bulb glomeruli--visualized with the de Olmos cupric silver stain and quantitatively assessed in the binge-intoxicated rats--was either unchanged or significantly increased by the NOS inhibitors. Although the efficacies of the inhibitors cannot be directly compared because of various NOS forms were probably inhibited to differing extents, the results do not support the idea that endogenous NO is a neurotoxic mediator of ethanol's effects. Rather NO may have a modest neuroprotectant role in this model of early brain damage induced by ethanol. In addition, the NOS that is localized histochemically as NADPH diaphorase was present primarily in regions and/or cells not damaged by binge ethanol treatment. Assuming that NADPH diaphorase represents most of the NO forming enzyme(s) this suggests a transcellular mechanism for NO. A further observation was that hippocampal CA pyramidal neuron degeneration was extensive in rats infused centrally with NG-nitro-L-arginine methyl ester.

Alcoholic Intoxication↗
PubMed1988

Histaminergic mediation of the stress-induced release of prolactin in male rats.

Histamine (HA) is likely to participate in the neuroendocrine regulation of prolactin (PRL) secretion. We, therefore, studied the possible involvement of HA in the stress-induced release of PRL in conscious male rats. HA (30 micrograms) infused intracerebroventricularly 15 min before decapitation elevated PRL plasma levels from 5 +/- 1 to 54 +/- 6 ng/ml (p less than 0.01). Intracerebroventricular infusion of the H2 receptor antagonists cimetidine (CIM: 100 micrograms) or ranitidine (RAN: 125 micrograms) abolished the PRL response to HA (p less than 0.01), while intracerebroventricular infusion of the H1 receptor antagonist mepyramine (MEP; 100 micrograms) inhibited the response only 40% (p less than 0.05). Intra-arterial infusion of CIM (2,000 micrograms) or RAN (2,500 micrograms) inhibited the HA-stimulated PRL secretion 52% (p less than 0.01) or 63% (p less than 0.01), respectively. The H1 receptor antagonists MEP (1,000 micrograms) and SKF-93944 (1,500 micrograms) had no effect following intra-arterial administration. Restraint stress increased the PRL level to 84 +/- 6 ng/ml (p less than 0.01 vs. control). This effect was prevented by intracerebroventricular infusion of CIM or RAN (p less than 0.01) and inhibited 75% by MEP (p less than 0.01). Intra-arterial infusion of CIM, MEP, and SKF-93944 inhibited the stress response about 50% (p less than 0.01), while RAN decreased the response only 25% (p less than 0.05). Ether stress elevated the plasma PRL concentration to 46 +/- 5 ng/ml (p less than 0.01 vs. control). When infused intracerebroventricularly CIM or RAN prevented the response (p less than 0.01), while MEP had no effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

[Mortality and survival rate in pulmonary atresia with intact intraventricular septum. Determining factors].

Sixty nine children with pulmonary atresia and intact ventricular septum diagnosed by catheterization from 1971 to 1988 are reviewed. These patients are the 2.9% of the 2,322 children diagnosed of congenital heart disease by catheterization and angiography in this 17 year period. The overall mortality was 72.4%. Twenty children died at a mean age of 37 days before cardiac surgery was performed, mostly before 1982, before the use of prostaglandin infusion. Forty seven children received surgical treatment, with a surgical mortality rate of 74% at the period 1971-1982 and 54% at the period 1983-1988. The right ventricular hypoplasia was the anatomic factor of dismal outlook. The actuarial survival in the patients without hypoplastic right ventricle and surgical treatment was 52% in the period 1971-1988 and near 80% in the first 3 years of life in the period 1983-1988. The use of preoperative prostaglandin infusion and improved operative techniques has changed the natural history of this malformation.

Angiocardiography↗
PubMed1986

Efficacy of baclofen and phenobarbital against the kainic acid limbic seizure-brain damage syndrome.

Baclofen and phenobarbital were tested for anticonvulsant efficacy against limbic seizures produced by i.c.v. infusion of kainic acid (KA) in unanesthetized rats. All rats treated with KA alone developed a prolonged status epilepticus associated with extensive neuronal degeneration. When administered immediately after the KA infusion, baclofen (5 mg/kg i.p.) protected five of six animals against the development of status epilepticus and did not alter the behavioral expression of the residual discrete electrographic seizures. Phenobarbital (40 mg/kg i.p.) given 15 min before KA also prevented the development of status epilepticus in five of six rats, but blocked the behavioral expression of the residual electrographic seizures. In two of five additional rats, baclofen prevented or reversed status epilepticus when administered 50 to 60 min after the end of the KA infusion. The ability of these drugs to prevent KA-induced neuronal degeneration correlated with their anticonvulsant action.

Animals↗
PubMed1991

Effects of DPI 201-106, a novel cardiotonic agent, on hemodynamics, cardiac electrophysiology and arrhythmias induced by programmed ventricular stimulation in dogs with subacute myocardial infarction: a comparative study with dobutamine.

DPI 201-106 (DPI), a novel and potent cardiotonic agent, exhibits its effects by prolonging the open state of Na+ channels, resulting in an increase in action potential duration, and thus, is supposed to share the class III antiarrhythmic activity. The effects of DPI on the hemodynamics, intraventricular conduction and refractoriness of heart, and the incidence of arrhythmias induced by programmed electrical ventricular stimulation (PES) were compared with (+/-)-dobutamine. Dogs which survived for 5 to 7 days after the induction of myocardial infarction were used as the model. The presence of subacute myocardial infarction caused by occluding the left anterior descending coronary artery elicited a mild left ventricular dysfunction represented by a significant decrease in peak LV dp/dt by about 20%. Both i.v. bolus injection of DPI (1, 3 and 5 mg/kg) and i.v. continuous infusion of dobutamine (3, 5 and 10 micrograms/kg/min), which were administered in a cumulative manner, dose-dependently improved the hemodynamic parameters. At the higher doses of both DPI (3 and 5 mg/kg) and dobutamine (5 and 10 micrograms/kg/min) the control values were reached or even exceeded. DPI dose-dependently increased the effective refractory period (ERP) of both non-infarcted and infarcted ventricular myocardia to a similar degree, but the conduction time showed a frequency-dependent increase in the infarcted myocardium to a greater degree than in the non-infarcted myocardium after DPI. In contrast, dobutamine decreased the ERP in both non-infarcted and infarcted myocardia, and slightly increased the difference of refractoriness between the non-infarcted and infarcted zones with no effect on the intraventricular conduction. In the PES study, DPI (3 and 5 mg/kg) produced a significant decrease in the incidence of ventricular tachycardia, whereas dobutamine (5 and 10 micrograms/kg/min) tended to worsen the arrhythmias. These findings suggest that cardiotonic agents with a class III antiarrhythmic property such as DPI may be potentially useful for the management of heart failure accompanied by ischemic heart disease.

Animals↗
PubMed1981

Yohimbine diastereoisomers: cardiovascular effects after central and peripheral application in the rat.

The cardiovascular effects of four yohimbine diastereoisomers, yohimbine, rauwolscine, corynanthine, and 3-epi-alpha-yohimbine, were compared in urethane-anaesthetized and conscious, normotensive Sprague-Dawley rats. Intravenous cumulative infusions (10--500 microgram) of the drugs to anaesthetized rats decreased blood pressure and blunted the pressor response to intravenous adrenaline injections. Corynanthine was the most potent isomer in this regard, followed by yohimbine, rauwolscine, and 3-epi-alpha-yohimbine. Depressor responses following intravenous bolus doses (40 microgram) showed a similar ranking. Intraventricular injections of yohimbine to anaesthetized rats decreased blood pressure dose-dependently, as did injections of corynanthine and rauwolscine. Responses indicated the ranking to be yohimbine greater or equal to rauwolscine greater than corynanthine for this effect at the 40 microgram dose. Heart rate was also decreased by these isomers, but not in a dose-dependent fashion. In conscious rats, the intraventricular injection of these isomers (20 microgram) increased blood pressure and heart rate. No differences were noted in terms of blood pressure responses; but, in causing tachycardia, the ranking was rauwolscine greater than yohimbine greater than corynanthine. These data suggest that after intraventricular application in anaesthetized rats, the effects of these alpha-adrenoceptor blockers are related to their individual affinity for the alpha 2 adrenoceptor.

Animals↗
PubMed1990

Measuring left ventricular dimensions by conductance catheter in the rabbit.

A miniaturized (3.5 F), six-electrode conductance catheter was tested in 18 anaesthetized adult rabbits (weight 3.8-4.6 kg, ethylurethane 2.5 g kg-1). In eight animals, the reference stroke volume (ref-SV) was obtained by an electromagnetic flow probe, while reference end-diastolic volume (ref-LVEDV) was computed by dividing ref-SV by undamped thermal dilution ejection fraction (ref-EF) estimates. Comparisons with conductance indexes (z-SV, z-LVEDV and z-EF) were made at baseline, subsequent levels of graded haemorrhage and reinfusion state. In 10 animals intraventricular segmental conductance was compared with echocardiographic left ventricular cross-section (5 MHz short-focus probe), in the basal state and during acute left ventricular volume changes generated by inferior vena cava balloon occlusion. In each experiment, parallel conductance due to the tissues surrounding the left ventricle (Gp) was determined by infusing a 5M NaCl solution bolus into the right ventricle. Linear regression analysis showed fairly good correlations between z-SV, z-LVEDV and z-EF and reference indexes (r = 0.84, r = 0.83, and r = 0.72, respectively; P less than 0.001 in all cases). A linear regression analysis from 17 interventions (inferior vena cava balloon occlusion) showed a good correlation between left ventricular echocardiographic cross-sectional area and conductance, and higher correlation coefficients, r ranging from 0.870 to 0.986 were obtained from continuously sampled conductance and echographic measurements. Parallel conductance Gp was correlated (r = 0.807, P less than 0.01) with the intercept of the regression line of echographic vs conductance data. The determination of Gp thus improved the accuracy of the left ventricular dimension estimate. These results add further evidence for the possibility of continuous monitoring of left ventricular dimension by means of a conductance catheter, and demonstrate the feasibility of such studies on small experimental animals.

Animals↗
PubMed1976

[A case of the lateral ventricular tumor (subependymal glomerate astrocytoma) with preceding Parkinsonian symptoms due to normal pressure hydrocephalus (author's transl)].

Authors report a patient with a subependymal glomerate astrocytoma in the right lateral ventricle. He maifested parkinsonian symptoms and dementia related to the preceding normal pressure hydrocephalus which was proved by an infusion test, and then advanced an akinetic mutism. Soon after a shunting operation was carried out he showed a full recovery from the symptoms, which may suggest that an incomplete block of the ventricular system is one cause of the normal pressure hydrocephalus. From pathology it was revealed that the tumor is an intraventricular astrocytoma with a fibrous stalk and was totally removed with an ease. The findings seem to accord with "Subependymal glomerate astrocytoma" (Boykin.) Further corroboration would be necessary to establish this entity.

Aged↗
PubMed1975

Pharmacological actions of the antihypertensive agent N-amidino-2-(2,6-dichlorophenyl)acetamide hydrochloride (BS 100-141).

Pharmacological properties characterizing N-amidino-2-(2,6-dichlorophenyl)acetamide hydrochloride (BS 100-141) as a centrally acting antihypertensive agent are described. Its action resembles that of clonidine in many respects but with important differences which are discussed. In DOCA-NaCl--hypertensive conscious rats, BS 100-141 lowers systemic blood pressure with oral doses of 0.3-5 mg/kg. Evidence for a central site of action is provided by the following findings. Infusion of BS 100-141 into the vertebral artery of anaesthetized dogs reduces blood pressure, the same dose being ineffective by i.v. route. Injection into the lateral cerebral ventricle of anaesthetized cats causes a marked reduction in blood pressure and heart rate, the same dose being ineffective when given i.v. The effects of intraventricular injection are inhibited by phentolamine administered by the same route. Intravenous administration of BS 100-141 induces dose-dependent reductions in the splanchnic (sympathetic) nerve activity in the cat. BS 100-141 reduces noradrenaline turnover in the brain stem of the rat as a result of central alpha-adrenoceptor stimulation. Doses which are effective in the hypertensive rat do not reduce dopamine turnover in the corpus striatum. The peripheral, direct alpha-sympathomimetic action of BS 100-141 was demonstrated by the transient increases in blood pressure observed in rats. These increases were unaffected by pretreatment with reserpine, but were antagonized by phentolamine. BS 100-141 was shown to induce contractions of isolated veins and arteries which were competitively inhibited by phentolamine. It stimulates presynaptic cardiac sympathetic alpha-adrenoceptors, thus inhibiting transmitter release to the heart. The sedative effects of BS 100-141 observed in dogs were slight compared to those of clonidine.

Animals↗
PubMed1978

Optimizing myocardial supply/demand balance with alpha-adrenergic drugs during cardiopulmonary resuscitation.

In 14 dogs the determinants of myocardial blood supply and metabolic demands were assessed during cardiopulmonary resuscitation (CPR) and under steady-state conditions in fibrillating hearts on cardiopulmonary bypass. During open chest cardiac massage (nine dogs), coronary diastolic blood pressure and blood flow were low. Vasopressor infusion (methoxamine or epinephrine) raised diastolic pressure from 33 +/- 3 to 55 +/- 3 mm. Hg and increased coronary blood flow (CBF) 124 percent (from 38 +/- 3 to 85 +/- 11 c.c. per 100 Gm. per minute. Comparison of these drugs in fibrillating hearts on cardiopulmonary bypass showed that epinephrine increased the "vigor of fibrillation" (intraventricular balloon pressure rose 24 percent and oxygen uptake increased 42%) but impeded subendocardial flow 53% (endocardial/epicardial flow ratio fell from 0.79 to 0.48). In contrast, methoxamine did not significantly change intraventricular balloon pressure, oxygen uptake, coronary flow, or its distribution. We conclude that augmentation of diastolic pressure with alpha adrenergic drugs during CPR improves coronary perfusion and that inotropic drugs may worsen myocardial ischemia during CPR by raising oxygen demands while simultaneously impeding subendocardial blood supply.

Animals↗
PubMed1991

Antiarrhythmic and proarrhythmic properties of diazepam demonstrated by electrophysiological study in humans.

We evaluated the electrophysiological parameters before and after the intravenous infusion of diazepam (0.2 mg/kg) in 20 cardiac patients to investigate the drug's antiarrhythmic effect. Diazepam did not significantly change the arterial pressure. After the intravenous infusion of diazepam, the sinus cycle length significantly shortened from 847 +/- 132 to 747 +/- 155 ms (p less than 0.01). No significant change in the maximal sinus node recovery time was noted. The AH interval at the atrial pacing length of 600 ms shortened significantly from 140 +/- 40 to 127 +/- 39 ms (p less than 0.05). However, there was no significant change after the administration of diazepam in the longest atrial pacing rate associated with Wenckebach conduction in the atrioventricular (AV) node, effective and functional refractory periods of the AV node, HV interval, and QRS width during ventricular pacing at the cycle length of 600 ms. The atrial and ventricular effective refractory periods remained unchanged after the administration of diazepam. Six of the eight patients who showed dual AV nodal refractory period curves in the control study did not demonstrate them after diazepam administration by increasing the atrial or AV node effective refractory period. Thus, diazepam showed significant electrophysiological effects of the heart including shortening of the sinus cycle length, improvement in AV node conduction, and no significant effect on the His-Purkinje or intraventricular conduction and refractoriness of the atrium, AV node and ventricle. On the other hand, diazepam may influence the inducibility of supraventricular reentrant tachycardia incorporating the AV node.

Adult↗
PubMed1991

Reversal of learning impairment in ventral globus pallidus-lesioned rats by combination of continuous intracerebroventricular choline infusion and oral cholinergic drug administration.

The effects of separate or combined oral administration of THA (9-amino-1,2,3,4-tetrahydroacridine hydrochloride) and NIK-247 (9-amino-2,3,5,6,7,8-hexahydro-1H-cyclopenta[b] quinoline monohydrate hydrochloride) and intracerebroventricular choline infusion using an osmotic minipump were investigated by observing locomotor activity, shock sensitivity, passive avoidance response and cerebral choline and acetylcholine contents in the bilateral ventral globus pallidus-lesioned rat. Evaluation of locomotor activity and shock sensitivity revealed no sensorimotor disturbances caused by combined administration. Intracerebroventricular choline infusion (100 mumol/day) and oral THA or NIK-247 administration (0.5 mg/kg) had no effect on the acquisition of the passive avoidance response, while the combination of oral THA or NIK-247 administration (0.5 mg/kg) and intracerebroventricular choline infusion (100 mumol/day) elicited good acquisition of passive avoidance learning and produced a significant increase of choline and acetylcholine in the cerebral cortex of the bilateral ventral globus pallidus-lesioned rat. These findings suggest that continuous intracerebroventricular choline infusion may intensify the ameliorating effect of THA or NIK-247 on learning disturbance.

Acetylcholine↗