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PubMed1986

Interferon in experimental autoimmune encephalomyelitis: intraventricular administration.

Highly purified rat fibroblast-derived interferon (RfIFN), was administered intraventricularly to Lewis rats affected with experimental autoimmune encephalomyelitis (EAE). Its effects on both the active and passive forms of EAE were studied. A method was devised to deliver, via a syringe pump, RfIFN (sp. act. 10(8) U/mg) into the third ventricle of control and experimental animals. Rats with either the active form of EAE (produced by injection with myelin basic protein (MBP) in Freund's complete adjuvant) or with adoptively transferred EAE were treated with RfIFN either therapeutically and/or prophylactically. In no instance was a significant difference observed, on the course of EAE, between those animals receiving RfIFN and those receiving "mock" IFN. The pharmacokinetics of the infused RfIFN were also studied.

Animals↗
PubMed1988

Antagonism of quinidine's electrophysiologic effects by epinephrine in patients with ventricular tachycardia.

The purpose of this study was to determine whether pharmacologically induced elevations in the plasma epinephrine concentration within reported physiologic limits alter the response to quinidine during electropharmacologic testing. Twenty-one patients with coronary artery disease and a history of unimorphic ventricular tachycardia were found to have inducible sustained unimorphic ventricular tachycardia that was suppressed by treatment with oral quinidine gluconate. Epinephrine was then infused at a rate of either 25 or 50 ng/kg per min and testing was repeated. These infusion rates of epinephrine were previously demonstrated to result in elevations of the plasma epinephrine concentration in the range of concentrations that occur during a variety of stresses. Quinidine significantly lengthened the ventricular refractory periods and the QRS duration at a ventricular pacing cycle length of 350 ms, which was used as an index of intraventricular conduction. Epinephrine partially or completely reversed the effects of quinidine on ventricular refractory periods, but had no effect on QRS duration. During electropharmacologic testing of quinidine, no ventricular tachycardia was inducible in 12 patients, and only nonsustained ventricular tachycardia, 8 to 48 beats in duration, was inducible in 9 patients. Retesting during infusion of epinephrine demonstrated inducible sustained unimorphic ventricular tachycardia in 2 of the 12 patients in whom quinidine had completely suppressed the induction of ventricular tachycardia and in 8 of the 9 patients in whom only nonsustained ventricular tachycardia had been inducible during testing of quinidine. In conclusion, physiologic elevations in the plasma epinephrine concentration may reverse quinidine-induced prolongation of ventricular refractoriness but not intraventricular conduction.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1994

Deficits in the activation and phosphorylation of hippocampal tyrosine hydroxylase in the aged Fischer 344 rat following intraventricular administration of 6-hydroxydopamine.

Tyrosine hydroxylase activity was measured under optimal and suboptimal assay conditions in hippocampal extracts from young (2 month), mature (12 month), and old (24 month) Fischer 344 male rats 72 h after the infusion of 200 micrograms of the neurotoxin 6-hydroxydopamine or vehicle into the lateral ventricle. The lesion resulted in a 45-55% decrease of tyrosine hydroxylase activity measured under optimal conditions (pH 6.1, 3.0 mM 6-methyl-5,6,7,8-tetrahydropterin) and an approximately 35% decrease in the relative concentration of immunoreactive tyrosine hydroxylase. When measured under suboptimal conditions (pH 6.6, 0.7 mM 6-methyl-5,6,7,8-tetrahydropterin), tyrosine hydroxylase activity in 2- and 12-month-old lesioned animals was twice that measured in vehicle-treated animals. However, in the old lesioned animals, tyrosine hydroxylase activity measured under suboptimal conditions was not different from that measured in age-matched vehicle-treated animals. Isoforms of tyrosine hydroxylase were identified on immunoblots after two-dimensional gel electrophoresis using enhanced chemiluminescence. The relative proportion of lower pI isoforms of tyrosine hydroxylase in the 2-month-old lesioned animals was greater than that observed in vehicle-treated controls. In contrast, no difference was seen in the relative proportion of tyrosine hydroxylase isoforms in the 24-month-old lesioned versus control animals. These data indicate that the ability of locus ceruleus neurons to rapidly respond to and compensate for insult is attenuated in 24-month-old Fischer 344 rats due to a deficit in stimulus-evoked enzyme phosphorylation.

Aging↗
PubMed1992

Modification of late potentials by intracoronary ethanol infusion.

Antiarrhythmic drugs have no consistent effects on the signal-averaged electrocardiogram (ECG) while successful surgical ablation of ventricular tachycardia is known to abolish late potentials. Ten patients with prior myocardial infarction had successful ablation of recurrent sustained ventricular tachycardia by selective ethanol infusion into a small coronary vessel supplying the tachycardia origin. Signal-averaged ECGs were performed before and after initially successful ablation in patients without pacemaker dependence or intraventricular conduction delay to assess the effects on late potentials and to determine if the signal-averaged ECG could predict ventricular tachycardia recurrence. Only four of ten patients were eligible for study and all four had late potentials prior to ethanol ablation. Late potentials were abolished in one patient who has not had an arrhythmia recurrence in 25 months. One patient with sudden death and another patient with ventricular tachycardia recurrence had persistent late potentials post procedure that were modified by a reduction in terminal voltage and lengthening of terminal low amplitude signal. The fourth patient who receives chronic amiodarone had no arrhythmia recurrence in spite of persistent but modified late potentials. Thus, the abolition of late potentials after ethanol ablation may predict freedom from arrhythmia recurrence.

Cardiac Pacing, Artificial↗
PubMed1988

Adenosine stimulates glucose uptake in the isolated rat heart.

Adenosine (Ado) is a potent coronary vasodilator. Recent studies suggest that Ado may also have an important effect on myocardial carbohydrate metabolism. To determine whether Ado has a direct effect on myocardial glucose uptake, a recirculating, constant-flow, isolated rat-heart preparation was used. The hearts were perfused with Krebs-Henseleit buffer solution with an initial glucose concentration of 11 mmol/L. A control group was compared with hearts treated with Ado infusions (50 and 100 micrograms/min) or insulin (100, 200, and 300 microU/ml). In a separate series of experiments, nitroprusside was used to evaluate the effect of a nonspecific coronary vasodilator. The rate of glucose uptake was calculated as the amount of glucose removed from the perfusate normalized for heart weight and time. Developed pressure (DP) was assessed with an intraventricular balloon, and the coronary perfusion pressure (CPP) was monitored. At the end of 1 hour, the hearts were freeze-clamped and adenine nucleotide content was measured with HPLC. Ado treatment increased glucose uptake by 80% and 140%, respectively, at the two infusion rates (p less than 0.001). Myocardial adenosine triphosphate content was 18% and 26% higher in the Ado-treated hearts than in the controls (p less than 0.001). Ado also decreased the mean DP by 30% and 36% (p less than 0.001) and decreased CPP by 10% and 22%, respectively (p less than 0.001). Insulin increased glucose uptake in a similar dose response fashion but had no effect on myocardial nucleotide content, DP, or CPP. Nitroprusside decreased CPP but had no effect on glucose uptake, adenine nucleotide content, or DP. These results suggest that Ado may have a direct effect on glucose uptake independent of its properties as a coronary vasodilator.

Adenosine↗
PubMed1998

Cerebrospinal fluid concentrations of propofol during anaesthesia in humans.

The concentration of propofol in and surrounding the human brain during propofol anaesthesia is unknown. We measured simultaneously the concentration of propofol in cerebrospinal fluid (CSF) from an indwelling intraventricular catheter and the concentration in arterial blood in five neurosurgical patients before, during induction (at 2.5 and 5 min) and during a maintenance propofol infusion (at 15 and 30 min). After induction of anaesthesia with propofol 2 mg kg-1, anaesthesia was maintained with an infusion of 8 mg kg-1 h-1 for 15 min and then reduced to 6 mg kg-1 h-1. The plasma concentration of propofol increased rapidly during induction and reached a plateau concentration of mean 2.24 (SD 0.66) micrograms ml-1 after 5 min. The concentration of propofol in CSF showed a slower increase during induction and remained almost constant at 35.5 (19.6) ng ml-1 at 15-30 min after induction. The CSF concentration of propofol that we measured was 1.6% of the plasma concentration and consistent with the high protein binding of the drug in plasma.

Adult↗
PubMed2005

Pharmacologic resolution of functional outflow tract obstruction after mitral valve repair.

A 74-year-old woman with mitral regurgitation secondary to ruptured chordae tendineae, complicated by a cleft in the posterior mitral leaflet and a severely calcified mitral annulus, underwent mitral valve repair by implantation of polytetrafluoroethylene chords and closure of the cleft, without the use of an annuloplasty ring. Immediately after the repair severe left ventricular outflow tract obstruction developed secondary to the systolic anterior motion of the mitral valve. Echocardiography identified the cause as functional, in the presence of a hypertrophic left ventricle with no significant preoperative intraventricular dynamic gradient. The obstruction was severe enough to render impossible the weaning of the patient from cardiopulmonary bypass. This problem was reversed by the infusion of beta-blocking agents into the extracorporeal circuit.

Adrenergic beta-Antagonists↗
PubMed1996

Continuous warm versus intermittent cold cardioplegic infusion: a comparison of energy metabolism, sodium-potassium adenosine triphosphatase activity, and postischemic functional recovery in the blood-perfused rat heart.

We used metabolic, enzymatic, and functional end points to compare the protective properties of continuous warm and intermittent cold cardioplegic infusion in isolated, blood-perfused rat hearts. After excision, hearts (n = 12 per group) were preserved for 3 hours by one of the following cardioplegic procedures: (1) continuous infusion of warm (37 degrees C) blood cardioplegic solution prepared by mixing Fremes' solution with rat arterial blood in a ratio of 1:4, (2) continuous infusion of warm (37 degrees C) crystalloid cardioplegic solution prepared by mixing Fremes' solution with bicarbonate buffer solution in a ratio of 1:4, or (3) intermittent infusion of cold (20 degrees C) St. Thomas' Hospital cardioplegic solution number 2 infused for 3 minutes every 30 minutes during a 3-hour period of ischemia. In the continuous-infusion cardioplegic groups, the solution was infused through the aorta at a flow rate of 0.8 ml.min-1.gm-1 heart. At the end of the 3-hour preservation period, myocardial sodium-potassium adenosine triphosphatase activity (an index of ion-exchange activity) was assessed in six hearts in each group. The remaining hearts in each group were then aerobically perfused at 37 degrees C with arterial blood (from a support rat) for a further 50 minutes, during which time they were atrially paced at 320 beats/min. At the end of this period, left ventricular developed and end-diastolic pressures were assessed with an intraventricular balloon; the hearts were then freeze-clamped and taken for the measurement of tissue adenosine triphosphate and creatine phosphate content. Hearts (n = 6) aerobically perfused with blood for 50 minutes (no cardioplegic infusion) served as control preparations. At a balloon volume of 180 microliters, the mean final values for left ventricular developed pressure in the continuous warm blood, continuous warm crystalloid, and intermittent cold cardioplegic groups were 98 +/- 5 mm Hg (p < 0.05), 70 +/- 5 mm Hg, and 78 +/- 5 mm Hg, respectively. This was compared with 122 +/- 5 mm Hg in control hearts (p < 0.05 vs the rest). For left ventricular end-diastolic pressure, the corresponding values were 33 +/- 3 mm Hg, 32 +/- 6 mm Hg, and 14 +/- 4 mm Hg (p < 0.05), respectively. The control value was 16 +/- 3 mm Hg (p < 0.05 vs continuous warm blood and continuous warm crystalloid groups). Tissue content of adenosine triphosphate was similarly reduced to approximately 50% of control values in all groups, and creatine phosphate content fully recovered in all groups. Sodium-potassium adenosine triphosphatase activity was poorly preserved in continuous warm crystalloid-treated hearts (0.012 +/- 0.003 vs 0.030 +/- 0.008 mumol inorganic phosphate-mg-1.min-1.

Adenosine Triphosphate↗
PubMed1988

Effect of taurine on growth hormone and prolactin secretion in rats: possible interaction with opioid peptidergic system.

The effect of taurine on growth hormone (GH) and prolactin (PRL) secretion was investigated in the urethane-alpha-chloralose anesthetized rats, considering the interaction with endogenous opioid peptidergic system. Intraventricular injection of taurine (0.25 and 1.0 mumol) stimulated GH and PRL secretion in a dose-dependent manner. However, 4.0 mumol taurine failed to show these effect. The intravenous infusion of naloxone (4 mg/kg b.w.) completely inhibited both the GH and PRL secretion induced by taurine (1.0 mumol). The combined treatment of taurine (1.0 mumol) and FK33-824 (Met-enkephalin derivative, 100 micrograms/kg b.w., i.v.) significantly increased GH and PRL responses induced by taurine or FK33-824 alone. These results indicate that taurine is an effective stimulator of GH and PRL secretion in rats, and that the mechanism of this action involves the opioid peptidergic system in the hypothalamus.

Anesthesia↗
PubMed1975

Effect of cerebral intraventricular insulin on pancreatic insulin secretion in the dog.

The effect of cerebral intraventricular insulin on pancreatic insulin secretion was investigated. An extracorporeal pancreatic blood circuit was established after laparotomy to monitor blood flow and insulin concentration directly from the superior pancreaticoduodenal vein. Phentolamine was infused throughout (0.2 mg./min. intravenously) to block alpha-adrenergic effects of any catecholamine secretion induced by surgical stress. Glucose (1.5 mg./kg./min. intravenously) was infused to maintain a constant baseline stimulation of insulin secretion. Six dogs received insulin and six control dogs received saline through a spinal needle stereotaxically placed into the left lateral cerebral ventricle. After central injection of insulin (0.2 U./kg.) there was a significant increase of pancreatic output as early as five minutes. It is concluded that the pancreatic beta-cells are under the influence of insulin-sensitive cells of the CNS.

Animals↗
PubMed2004

Review of hemoglobin-induced myocardial lesions.

Over 100 preclinical studies in several small and large animal species were performed to evaluate the safety and efficacy of diaspirin cross-linked hemoglobin (DCLHb; Baxter Healthcare Corp.) as an oxygen therapeutic. During the preclinical evaluation of DCLHb, myocardial lesions were observed following the administration of DCLHb to certain species. These lesions were characterized as minimal to moderate, focal-to-multifocal myocardial degeneration and/or necrosis that were scored using a severity scale of minimal to marked in relative severity. The lesions were typically observed 24-48 h after single topload infusions of DCLHb into rhesus monkeys or pigs at doses as low as 200 or 700 mg/kg, respectively. Dogs, sheep, and rats did not develop these lesions after single-dose administrations of DCLHb. The left ventricular myocardium, typically near the base of or including the papillary muscles, was the most severely affected region, followed by the intraventricular septum and the right ventricle. The left and right atria were usually not affected. In a study in rhesus monkeys, morphometric analysis revealed that these lesions comprised less than 3% of the total myocardium. Although increases in serum enzyme activities (AST, CK, LDH) were observed after infusion of DCLHb, myocardial-related isoenzymes did not increase. ECG analysis and echocardiography were not altered by these lesions, and there was no observable adverse effect on myocardial function. Polymerization of DCLHb reduced, but did not eliminate, the incidence and severity of the lesions. However, infusion of hemoglobin solutions with reduced reaction rates with nitric oxide (NO) resulted in a significant decrease in lesion incidence and severity, while administration of L-NAME, an NO synthase inhibitor, resulted in the appearance of lesions that were indistinguishable from those induced by hemoglobin, suggesting that reduction in normal NO levels is an important mechanistic factor. Overall, the presence of myocardial lesions represents a histopathologic finding that must be considered during the preclinical testing and development of new HBOCs.

Animals↗
PubMedDate not supplied

Management of progressive pain in a patient with intramedullary chordoma of the spine.

OBJECTIVES: The case here presented adequately reflects the difficulties involved in the treatment of pain in patients where the neuropathic component of pain predominates, and shows the different therapeutic steps that may be taken-from surgery and radiotherapy, to the administration of different drugs via the spinal route, to, finally, the presently little-used option of a direct intraventricular access. CONCLUSIONS: Spinal tumors are infrequent, but pose great difficulties for the management and control of the pain they cause. The utility of the spinal route as an early approach for the provision of adequate analgesia seems clear. However, it also appears to lose efficacy with time, and dose incrementing and/or the addition of drugs that enhance the analgesic action of morphine are not always effective. In such selected cases, the intraventricular route may constitute a useful alternative, allowing improved symptoms control with lower morphine doses, and the use of the system previously implanted for intrathecal spinal infusion.

Analgesics↗
PubMed1986

Protective actions of carbocromene against amitriptyline-induced cardiotoxicity in anesthetized rats.

This study was designed to analyze the effects of carbocromene on circulatory and electrophysiologic failure in rats anesthetized with urethane. Amitriptyline was infused at 0.4 mg/kg/min (n = 12) until death of the animals at 30 +/- 6.7 min due to vascular collapse. Following initial heart rate increase and QRS prolongation, this was characterized by progressive hypotension, bradycardia, intraventricular conduction delay, S-T segment elevation and A-V block. In the initial 31 rats, carbocromene was administered i.v. with 4 mg/kg followed in two groups by 40 (n = 13) and 80 micrograms/kg/min (n = 18) i.v., respectively. The drug was effective in protecting the animals against the acute cardiovascular failure induced by amitriptyline. The preservation was associated with a diminution of the hypotension, negative chronotropic actions, S-T segment elevation and the incidence of A-V block produced by amitriptyline. Survival time of the rats increased to 46 +/- 5.3 min (p less than 0.05 vs. amitriptyline controls) and 63 +/- 6.5 min (p less than 0.01) with infusion of 40 and 80 micrograms/kg/min carbocromene, respectively. These results suggest that carbocromene is an effective treatment of amitriptyline-induced cardiotoxicity by massive overdose with beneficial effects largely due to hemodynamic and metabolic oxygen-sparing impact on the heart. Membrane stabilizing antiarrhythmic carbocromene effects may be contributory factors in its protective value in the treatment of acute amitriptyline poisoning.

Amitriptyline↗
PubMedDate not supplied

The effect of intraventricular 6-hydroxydopamine on the content of oxytocin and vasopressin in the hypothalamus and pituitary gland of water-deprived rats.

The effect of intraventricular 6-hydroxydopamine on the content of oxytocin and vasopressin in the hypothalamus and pituitary gland of water deprived rats. Acta Physiol. Pol., 1977, 28 (6): 497-504. Rats received one infusion of 200 microgram 6-hydroxydopamine with 25 microgram of ascorbic acid into the lateral cerebral ventricle. After 57 days some rats were deprived of water for 4, 8 or 12 days. Then, the animals were sacrificed by decapitation. Oxytocin was determined in extracts from the posterior pituitary lobe and hypothalamus by the method of Van Dongen and Hays, while the vasopressin content was determined by the method of Dekanski. It was found that 6-hydroxydopamine injection into the cerebral ventricles causes a rise in oxytocin content in the hypothalamus and prevents its fall during--4--12 days of dehydration.

Animals↗
PubMedDate not supplied

Cardioprotective effects of carbocromen in awake and anesthetized dogs with amitriptyline poisoning.

We studied the effects of the antianginal drug carbocromen (4 mg/kg bolus plus 80 micrograms/kg/min i.v.) on amitriptyline (400 micrograms/kg/min i.v.) toxicity. In anesthetized dogs, amitriptyline increased heart rate, left ventricular (LV) end-diastolic pressure, and the PR and QT intervals, the QRS complex, and the S-T segments of the peripheral electrocardiogram. Blood pressure, LV pressure, and LV dP/dtmax fell considerably. Survival time was 37 +/- 4 min in amitriptyline-treated dogs and 64 +/- 3 min (p less than 0.05) in those receiving amitriptyline plus carbocromen. The amount of amitriptyline consumed until death increased from 14.8 to 25.6 mg/kg (p less than 0.05) with carbocromen. In conscious dogs, the hemodynamic impact of intraatrial amitriptyline was similar to that in anesthetized animals, and changes in stroke volume resembled those of dP/dt. Cardiac output was not altered, and peripheral resistance decreased moderately. Carbocromen prevented most of the typical amitriptyline effects on the heart and circulation. Sustained ventricular arrhythmia occurred at 29 +/- 4 min with amitriptyline infusion but was delayed to 58 +/- 3 min (p less than 0.05) when carbocromen was added. These experiments demonstrate (a) amitriptyline intoxication produced ventricular tachyarrhythmia and cardiac failure if high agent concentrations were achieved; (b) these rhythm disorders were associated with slowing of intraventricular conduction, which could be enhanced by carbocromen; and (c) carbocromen might be an effective therapy for amitriptyline-caused arrhythmia with cardiovascular collapse.

Amitriptyline↗