Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Effects of s.c. doses of morphine and verapamil, alone and in combination, on arterial blood gases and pH, mean blood pressure and heart rate were assessed in partially restrained, awake Fischer-344 rats. As expected, morphine (4-16 mg/kg) produced a dose-dependent respiratory depression, as indicated by hypoxia, hypercapnia and acidosis. Verapamil, a calcium channel antagonist, alone (10 mg/kg) did not affect these parameters; however, it significantly attenuated and delayed the aforementioned effects of morphine. Morphine caused a slight increase in mean blood pressure, which was not dose dependent, whereas verapamil reduced blood pressure dramatically even in the presence of morphine. All groups showed some tachycardia, but rats treated with morphine alone showed the most pronounced increase in heart rate, which was antagonized by verapamil. The authors conclude that the interaction of verapamil with morphine's respiratory depressant effects differs from the previously reported potentiation of morphine's antinociceptive and hypothermic actions.
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PMID:Interactions between verapamil and morphine on physiological parameters in rats. 372 97

The authors report two cases of Bipolar Affective Disorder which were responsive to Lithium therapy in the past, but could no longer be treated with Lithium due to hyperparathyroidism in the first case and noncompliance in the second. In both cases, successful control of hypomania was achieved with Verapamil, but treatment of depression required the addition of Trazodone. The rationale for employing a calcium channel blocking agent, such as Verapamil, in bipolar illness is reviewed.
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PMID:Verapamil in bipolar illness. 373 Oct 14

The calcium channel blocker, verapamil (0.1-1.0 mg/kg, i.v.) was administered to anesthetized rats to determine its effects on ventilation and on ventilatory responses to hypoxia and CO2. Verapamil produced a dose-dependent increase in tidal volume (VT) and a decrease in respiration rate (f). The bradypnea due to verapamil was characterized by an increase in expiratory duration (TE) and no change of inspiratory duration (TI). Verapamil produced similar changes in VT and f in vagotomized rats. The increase in respiration rate and minute volume due to hypoxia were inhibited by verapamil (0.5 and 1.0 mg/kg) but the increase in tidal volume due to hypoxia was depressed only with the 1.0 mg/kg dose. On the other hand, the increase in VT due to breathing CO2 was not changed by verapamil (0.1-1.0 mg/kg), but depression of the respiratory frequency response to CO2 occurred with 1.0 mg/kg of verapamil. These results indicate that verapamil produced slow, deep breathing and these responses were not mediated by vagal mechanisms. Ventilatory responses to hypoxia were depressed by verapamil. However, since the calcium blocker demonstrated no effect on the VT-CO2 relationship, verapamil did not change ventilatory chemosensitivity to CO2. The data also suggest that mechanisms governing the control of respiratory frequency are more sensitive to verapamil than tidal volume responses.
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PMID:Effect of verapamil on ventilation and chemical control of breathing in anesthetized rats. 393 39

The effects of intravenous dantrolene sodium, alone and in combination with verapamil, upon atrioventricular conduction, cardiovascular function, and neuromuscular function were studied in chloralose-urethane anesthetized dogs. Hemodynamic variables (systemic arterial, central venous, and pulmonary arterial pressures and cardiac output) and His-bundle electrograms were monitored, and measurements were made during atrial pacing at 175 beats/min, as well as at the spontaneous heart rate. In one part of the study animals received dantrolene sodium incrementally at 30-min intervals to cumulative doses of 1, 2.5, 5, and 10 mg/kg. Subsequently, verapamil was administered incrementally at 30-min intervals to cumulative doses of 0.1, 0.2, 0.4, and 0.6 mg/kg. In the second part of the study, dogs received identical dosage sequences, but verapamil preceded dantrolene administration. Dantrolene caused no significant depression of atrioventricular conduction or cardiac performance but did increase systemic vascular resistance at doses above 2.5 mg/kg. Verapamil alone (greater than or equal to 0.2 mg/kg) or with dantrolene (greater than or equal to 0.1 mg/kg) increased the atrial-His-bundle conduction interval. In the presence of verapamil, dantrolene (greater than or equal to 2.5 mg/kg) decreased cardiac index and increased pulmonary artery occlusion pressure. Although 0.6 mg/kg verapamil depressed cardiac index and increased pulmonary artery occlusion pressure, this effect was observed at 0.4 mg/kg after prior treatment with dantrolene. Verapamil did not augment the dose-dependent twitch depression observed with dantrolene. Dantrolene alone had no apparent effect on atrioventricular conduction and caused little enhancement of the effects of verapamil. However, each drug appeared to enhance the myocardial depressant effects of the other.
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PMID:Effects of dantrolene and verapamil on atrioventricular conduction and cardiovascular performance in dogs. 395 91

The combined depressant effects of verapamil and halothane on myocardial contractility were studied using isolated papillary muscle from the rabbit. Verapamil alone (0.5 microM) significantly decreased peak developed tension (PDT) by 15 +/- 2%, time to peak tension (TPT) by 10 +/- 1%, and maximum rate of increase of tension (+dT/dt) by 5 +/- 1%, but not maximum rate of decrease of tension (-dT/dt). Halothane alone (0.8%) significantly decreased PDT by 56 +/- 2%, TPT by 11 +/- 2%, +dT/dt by 53 +/- 2%, and -dT/dt by 56 +/- 2%. During the exposure period, the combination of verapamil and halothane together produced a simple additive effect (no significant interaction effect by two-way analysis of variance), with PDT decreased by 68 +/- 2%, TPT by 20 +/- 3%, +dT/dt by 62 +/- 2%, and -dT/dt by 65 +/- 2%. The reversibility of halothane-induced depression was also studied. Peak developed tension showed complete reversibility 30 min after discontinuing halothane. In the presence of verapamil, however, the reversibility of halothane-induced depression was not complete, and significant residual depression of PDT (19 +/- 3%) was observed. We conclude that the acute depressant effect of verapamil plus halothane in isolated papillary muscle is additive, but reversibility of halothane-induced depression may be impaired or prolonged in the presence of verapamil.
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PMID:Interaction of halothane and verapamil in isolated papillary muscle. 396 31

The antihypertensive effect of finoptin (verapamil) and corinfar (nifedipin) and their impact on the hemodynamics and the repolarization complex of the ECG were studied in 52 patients with essential hypertension and 48 patients with secondary arterial hypertension. The calcium antagonists were found to effectively decrease the blood pressure by reducing the peripheral resistance. Verapamil may be recommended for the monotherapy of mild and moderate forms of arterial hypertension, whereas corinfar should be used in cases of marked hypertension and at the third stage of therapy. Patients with electrocardiographic signs of myocardial ischemia show the normalization of the ST segment and a decreased depression of T wave under the impact of corinfar.
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PMID:[Treatment of arterial hypertension with calcium antagonists]. 398 59

We have investigated the hypothesis that the calcium antagonist verapamil might be useful for prevention or treatment of malignant hyperthermia (MH) in MH-susceptible (MHS) swine. MH episodes were triggered in four groups of four swine with halothane alone or combined with succinylcholine (SCh) and, with and without verapamil. MH episodes were reversed by therapy with dantrolene and NaHCO3 in all groups. Verapamil did not alter MH episodes triggered by halothane alone or combined with SCh. The dantrolene-NaHCO3 requirements for reversal of MH were greater for the groups receiving halothane-SCh, but did not differ in groups pretreated with and without verapamil. In vitro verapamil (25 microM) did not reduce responses of intact muscle fibers to halothane and, in fact, exaggerated some halothane-induced responses. High concentrations of verapamil (0.5 mM) caused contractures in MHS but not in normal muscles. Neither our in vivo nor in vitro results support the use of verapamil in the treatment of MH. Further, doses of dantrolene used to reverse these MH episodes, although admittedly small (1-2 mg/kg), did not produce myocardial depression when used in combination with verapamil.
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PMID:Verapamil is not a therapeutic adjunct to dantrolene in porcine malignant hyperthermia. 400 78

Verapamil and propranolol, alone and in combination, were given intravenously to anesthetized dogs to analyze the interaction between drug-induced cardiovascular effects and the resulting changes in pharmacokinetics. Dosing regimens were used that produced steady state plasma levels of both drugs, and the observed effects were clearly related to the plasma concentrations of the agents. When given alone, at stable "therapeutic" levels in plasma, verapamil or propranolol decreased spontaneous heart rate, increased atrioventricular conduction time, and had opposite effects on cardiac output. At the same doses, the combined infusion of the 2 drugs rapidly resulted in profound depression in cardiac function; in addition, plasma concentrations of both agents increased into ranges associated with cardiovascular toxicity. When verapamil doses were reduced, combined infusion with propranolol decreased atrioventricular conduction and cardiac output, but drug plasma concentrations (and associated effects) remained stable. When reduced doses of propranolol were added to infusion of verapamil, similar effects on cardiovascular function occurred, but plasma drug levels increased progressively throughout the remainder of the study period. In all combinations studied, beta blockade with propranolol decreased liver plasma flow and, therefore, the systemic clearance of verapamil. The in vitro effects of propranolol on verapamil metabolism were small, although significant, and not clinically relevant. These acute studies suggest that the hemodynamic effects resulting from verapamil and propranolol in combination may significantly diminish clearance of 1 or both drugs, thereby resulting in accumulation during continued administration, increased drug effects with increasing plasma concentrations, and potentially lethal drug toxicity.
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PMID:Cardiovascular and pharmacokinetic consequences of combined administration of verapamil and propranolol in dogs. 401 21

In transversely sectioned rat hippocampal slices, the effects of low (20 Hz, 600 pulses) and high (400 Hz, 200 pulses) frequency tetani of Schaffer collaterals were examined on the CA1 population spike as well as on the binding of 3H-glutamate. The population spike was suppressed while 3H-glutamate binding greatly enhanced following a low frequency tetanus. Verapamil (1 micron), which does not block long-lasting potentiation (LLP), counteracted the depression of the population spike as well as the associated increase in 3H-glutamate binding. The high frequency tetanus induced LLP of the population spike but caused no change in the amino acid binding. These results indicate that the increase in the number of glutamate receptors is not a requirement for LLP.
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PMID:Long-lasting potentiation in hippocampus is not due to an increase in glutamate receptors. 614 35

Calcium channel blockers relax the arterial smooth vasculature and lower blood pressure when it is elevated because of excessive vasoconstriction. They may be regarded as ventricular unloading agents. Nifedipine (11 cases, Group 1) and verapamil (12 cases, Group 2) were tested in hypertensive patients with cardiac enlargement (LV diastolic diameter greater than or equal to 60 mm), ECG signs of LV strain, lung congestion and dyspnea at rest, in an acute (nifedipine 20 mg; verapamil 160 mg) and 1-month (nifedipine 20 mg q.i.d.; verapamil 160 mg t.i.d.) therapeutic evaluation. In the acute study nifedipine reduced systemic vascular resistance (SVR), mean arterial pressure (MAP), mean pulmonary wedge pressure (PWP) and LV diastolic diameter (DD) and improved cardiac index (CI) and Vcf. In Group 2 verapamil reduced SVR and MAP, improved CI and was not effective on PWP, LV DD and Vcf. Verapamil was discontinued in 2 patients who developed severe dyspnea at rest after 3-4 days of continued oral treatment. At the end of the trial Vcf, PWP and LV DD were unchanged in the remaining subjects in Group 2 despite persistent pressure reduction. In Group 1 all of the patients had relief of dyspnea and lung congestion, reduction of heart size, persistent decrease of MAP and PWP, and improvement in Vcf. The only side effect was ankle edema in 4 cases. A less potent vasodilating action of verapamil and a predominant depression in cardiac contractility may account for the different results with the two drugs, in spite of a shared antihypertensive effect. These findings prove that functional changes in the failing hypertensive heart may differ after nifedipine compared to verapamil as a result of interaction and relative preponderance of influences on afterload and contractility.
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PMID:Clinical use of calcium channel blockers as ventricular unloading agents. 622 Aug 95


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