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Biomedical subjects

B Levitt

Publications and source records attributed to B Levitt.

At least 37 records · Page 2Linked to original sources
PubMed1984

High-pressure liquid chromatographic-fluorometric detection of adenosine and adenine nucleotides: application to endogenous content and electrically induced release of adenyl purines in guinea pig vas deferens.

To avoid some of the disadvantages associated with using radiolabeling to investigate adenyl purine content and release from excitable tissues, a reverse-phase high-pressure liquid chromatographic method utilizing fluorescence detection for the measurement of picomole amounts of endogenous ATP and its 6-amino purine analogs has been developed. This procedure has been used to determine the content of adenyl purines in the guinea pig vas deferens and that released from the tissue following stimulation of adrenergic nerves. The total tissue content was measured to be 1.6, 0.76, and 0.10 mumol/g of ATP, ADP, and AMP, respectively. However, adenosine could not be detected. Hypoxia caused a significant decrease in ATP content concomitant with an increase in adenosine content to 0.04 mumol/g. Following transmural electrical stimulation of the guniea pig vas deferens, the release of the following purine compounds was detected: ATP (0.106 nmol/g), ADP (0.242 nmol/g), AMP (0.035 nmol/g), and adenosine (0.454 nmol/g).

Acetaldehyde↗
PubMed1983

The dissociation of the exaggerated prolactin and thyrotropin responses in seminiferous tubule failure following the administration of a double-pulse of thyrotropin-releasing hormone.

PRL and TSH secretion has been evaluated in 11 patients with seminiferous tubule failure and 9 controls. When compared to the controls, the patients had increased basal FSH, TSH and PRL levels. However, LH, E2, T and thyroid hormone levels were similar to the controls. Both groups were given two pulses of TRH (200 micrograms) at 30 min intervals. Following the initial pulse of TRH, the patients demonstrated exaggerated TSH and PRL responses. The administration of a second pulse of TRH led to a further increment of TSH secretion in the patients. There was, however, no PRL response to the second TRH pulse in either patients or controls although mean PRL levels remained significantly greater in the patients.

Adult↗
PubMed1983

The cimetidine-lidocaine interaction.

Lidocaine is a widely used antiarrhythmic agent whose plasma clearance varies with changes in hepatic blood flow. Cimetidine, an H2-receptor antagonist, has been shown to decrease hepatic blood flow. To ascertain whether cimetidine affected serum lidocaine concentration, we studied 21 patients receiving lidocaine infusions and divided them into two groups. Fifteen patients received cimetidine, 300 mg every 6 hours, in addition to lidocaine; six patients received only lidocaine. In 14 of the 15 patients receiving both lidocaine and cimetidine, a rise in serum lidocaine levels was seen, whereas no change was noted in the control group. Six of the 15 patients were found to have levels in the toxic range and two had symptoms. An additional three patients on lidocaine received diphenhydramine, an H1-receptor antagonist. No elevation in serum lidocaine levels was noted after administration of diphenhydramine. We conclude that there exists an interaction between lidocaine and cimetidine and that the rise in serum lidocaine levels may be mediated by cimetidine's inhibition of the H2 receptor.

Cimetidine↗
PubMed1982

Factors influencing the release of purines and norepinephrine in the rabbit portal vein.

Previous studies have shown that transmural electrical stimulation (TES) of the rabbit portal vein in vitro, results in the overflow of 3H-purines from tissues prelabelled with 3H-adenosine. The purpose of the present study was to assess the possible sites which contribute to the TES-induced overflow of purines in this adrenergically innervated tissue. The contribution to postjunctional elements to purine overflow was assessed with the alpha 1-adrenoceptor antagonist, prazosin. Prazosin (3 x 10(-7) M) did not affect the release of 3H-norepinephrine but markedly reduced the TES-induced contraction. The release of 3H-purines was reduced by 20% by prazosin, indicating that approximately 80% of the release is independent of the alpha 1-mediated postjunctional response and, therefore, probably originates from neuronal sites in the tissue. Two lines of evidence indicate that a considerable portion of the alpha 1-adrenoceptor-independent release of 3H-purines (i.e., in the presence of prazosin) arises from adrenergic nerves. First, the fractional release of 3H-purines was enhanced and reduced, respectively, by the alpha 2-adrenoceptor antagonist, yohimbine, and the alpha 2-adrenoceptor agonist, clonidine, in concentrations (10(-6) M) which did likewise to the fractional release of 3H-norepinephrine. Second, destruction of the adrenergic nerves by in vitro treatment with 6-hydroxydopamine reduced the fractional release of 3H-purines by 55%. The release of purines which remains after 6-hydroxydopamine treatment may occur from non-adrenergic nerves.

Adrenergic Fibers↗
PubMed1978

The influence of heart rate on ouabain cardiotoxicity in cats with spinal cord transection.

The dose, serum level and ventricular content of ouabain needed to produce cardiotoxicity were examined in control cats, cats with transected spinal cords and cats with transected spinal cords whose heart rates were restored to control values by artificial pacing. The lethal dose of ouabain was higher in cats with transected spinal cords and not paced than it was in the control group. However, the lethal dose of ouabain in spinal-sectioned cats with ventricular pacing was no different from that in controls. However, in both groups of spinal-sectioned cats, death was associated with higher ventricular and serum levels of ouabain than in controls. The ventricular ouabain content of paced animals with transected spinal cords was higher than that of controls and lower than that of unpaced spinal cats. Thus, restoration of heart rate to control levels in spinal animals appeared to accelerate myocardial ouabain uptake. The lower myocardial ouabain content in the spinal-sectioned animals which were paced suggests that pacing sensitizes the heart to cardiotoxicity. Spinal section itself appears to decrease the sensitivity to ouabain partly through a decrease in cardiac rate and partly through a loss of neurogenic influence.

Animals↗
PubMed1978

The effect of diphenidol on ouabain cardiotoxicity in the cat.

The capacity of diphenidol to influence ouabain-induced cardiotoxicity was studied in anaesthetized cats with and without spinal cord transection. 2 Diphenidol pretreatment increased the lethal dose of ouabain in both intact cats and cats in which the spinal cords had been transected. Diphenidol pretreatment increased the myocardial content of ouabain associated with death in the intact animals, but failed to influence the lethal ventricular concentration in cats with transected spinal cords. 3 The failure of diphenidol to influence tissue thresholds for toxicity in the spinal cat and the equivalence of tissue ouabain requirements for death in spinal cats and diphenidol-treated intact animals, suggest a neural mechanism for the protective effect in intact animals. 4 Ouabain administration prolonged atrio-ventricular conduction time in all animals and diphenidol attenuated this effect. Thus, the influence of both drugs on antrioventricular conduction may not be entirely mediated by central neurones.

Animals↗
PubMed1978

Blockade of tissue uptake of the antineoplastic agent, doxorubicin.

Myocardial uptake of doxorubicin (Adriamycin) and its inhibition by digoxin and propranolol were studied in paced, isolated perfused cat hearts using tritiated doxorubicin. Contractility was studied using a Walton-Brody strain gauge arch and its first derivative. Coronary blood flow was measured by collecting the effluent from the heart. The myocardial content of doxorubicin was 0.069 +/- 0.101 nmol/mg after 30 minutes. Combined administration of doxorubicin and digoxin reduced the myocardial content of doxorubicin to 0.025 +/- 0.010 nmol/mg (P less than .02). The combination increased contractility compared with doxorubicin alone and increased coronary blood flow compared with digoxin alone. The reduction in the myocardial content of digoxin by doxorubicin was not significant. Propranolol also reduced the myocardial uptake of doxorubicin (P less than .05) without changing coronary blood flow and without further reducing contractility. Thus, both propranolol and digoxin merit evaluation in preventing doxorubicin cardiotoxicity.

Animals↗
PubMed1977

Effects of actodigin on the heart.

Actodigin is a new semisynthetic cardiac glycoside reported to have a rapid onset and brief duration of action in dogs. Five patients with congestive heart failure in normal sinus rhythm were given incremental doses of actodigin. Overall, there was no significant change in heart rate, aortic or pulmonary artery pressure, systemic vascular resistance, cardiac index, and stroke volume. This lack of response to actodigin is consistent with previous reports of acute administration of other cardiac glycosides. Four patients with atrial fibrillation and a rapid ventricular rate were given similar doses of actodigin. The ventricular rate was readily controlled. After drug administration was stopped, the ventricular rate quickly returned toward predrug levels. Thus, the rapid onset and brief duration of action of actodigin may be useful in the initial management of atrial fibrillation.

Adult↗
PubMed1977

A comparison of actodigin and ouabain in cats.

The effects of actodigin and ouabain at infusion rates which produce death in equivalent times were compared in anesthetized cats. Actodigin-induced ventricular tachycardia occurred sooner than that induced by ouabain. However, in animals in which the infusion of drug was stopped one minute after the onset of ventricular tachycardia, the arrhythmia terminated sooner in cats given actodigin than in those given ouabain. Actodigin produced a slower heart rate and greater prolongation of the PR interval than did ouabain suggesting a greater increase in vagal tone in the actodigin treated cats. Left ventricular pressure was not changed by either drug while peak dp/dt was increased after 30 min of the ouabain infusion but not significantly more than changes produced by actodigin. Thus, the use of actodigin may be limited by the early appearance of ventricular arrhythmias.

Animals↗
PubMed1977

The influence of prostaglandins E1 and E2 on ouabain cardiotoxicity in the cat.

The capacity of prostaglandins E1 (PGE1) and E2 (PGE2) to influence the lethal dose and lethal myocardial content of ouabain was studied in intact cats and cats whose spinal cords had been transected. The administration of PGE1 and PGE2 to intact cats was associated with an increase in lethal dose and ventricular content of ouabain. Spinal cord transection alone was also associated with an increase in lethal dose and ventricular content of ouabain. The administration of either PGE1 and PGE2 to animals whose spinal cords had been transected changed neither the lethal dose nor the lethal ventricular content of ouabain compared with cats whose spinal cords were transected but who received only ouabain. The present data suggest that PGE1 and PGE2 are effective agents for prophylaxis of ouabain-induced arrhythmias in the cat. The failure to observe an additional antiarrhythmic effect in animals whose spinal cords had been transected implies that the nervous system plays an important role in the antiarrhythmic action of the prostaglandins.

Animals↗
PubMed1976

Neural basis for the genesis and control of digitalis arrhythmias.

The pharmacokinetics of ouabain associated with toxicity were studied in the cat and the guinea pig both in vivo and in vitro using ouabain-H3. After spinal cord transection a higher dose of ouabain was required to reach the lethal endpoint. This intervention also increased the myocardial and serum levels associated with toxicity were studied in the cat and the guinea pig both in vivo and in vitro using ouabain-H3. After spinal cord transection a higher dose of ouabain was required to reach the lethal endpoint. This intervention also increased the myocardial and serum levels associated with death. These findings were corroborated in experiments using digitoxin H3. In vitro, substantially higher ouabain tissue contents were associated with a lethal event. In addition, in cats and guinea pigs, the lethal myocardial ouabain content did not change when the infusion rate of ouabain was varied in vivo or the perfusate ouabain concentration was changed in vitro. In vivo, propranolol increases the myocardial ouabain content associated with death to in vitro levels. In vitro, the drugs prolongs the time to death by retarding the myocardial uptake of ouabain. These data suggest that the toxic effects of ouabain in the whole animal are largely neural and in the isolated heart, substantially myocardial.

Animals↗