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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intravenous amitraz caused significant hypotension and bradycardia in pentobarbitone anaesthetized guinea-pigs. Depression of blood pressure reached a plateau with a dose of 10 mg/kg but heart rate continued to fall in a dose-dependent manner, up to a fall of 90 beats per minute after a total of 160 mg/kg/min. Amitraz was then tested on spontaneously beating guinea-pig isolated atria. The maximum bath concentration approximated a blood concentration produced by 5 mg/kg amitraz in the guinea-pig (2.3 X 10(-4) M). Amitraz did not significantly shift the dose-response curve to isoprenaline or acetylcholine but antagonized histamine rate responses competitively in the presence of propranolol (2 X 10(-6) M). Propranolol unmasked a dose-dependent depressant effect of amitraz on atrial rate, an effect abolished with atropine (1 X 10(-5) M). Amitraz increased atrial force of contraction, an effect which was not seen when propranolol was present in the bath solution. Amitraz also depressed atrial rate directly, but this effect was minor in comparison to bradycardia seen in the guinea-pig. It is likely that the cardiovascular depression seen in the guinea-pig following amitraz i.v. is caused by an alteration in autonomic drive rather than a significant direct cardiac effect.
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PMID:The cardiac effects of amitraz in the guinea-pig in vivo and in vitro. 287 7

The interaction between beta-adrenoreceptor blockers and calcium antagonists may occasionally be dangerous. The effects of the new calcium antagonist PN 200-110 (isradipine) were compared with those of verapamil in 3 groups of conscious rabbits pretreated with either pindolol 0.3 mg/kg, propranolol 1 mg/kg intravenously or placebo. Each animal received PN 200-110 (0.01, 0.03 and 0.1 mg/kg) and 2 or more days later verapamil (0.1, 0.3 and 1 mg/kg). The calcium antagonists were given to lower mean blood pressure to the same extent as in the placebo group. This blood pressure effect remained unchanged after pretreatment with pindolol or propranolol. Both PIN 200-110 and verapamil increased heart rate to the same extent as in the placebo group. Both beta blockers blunted the effect of PN 200-110 on heart rate but converted the verapamil-induced tachycardia to bradycardia. Propranolol blunted the PN 200-110-induced increase in cardiac output and total peripheral conductance, whereas the high verapamil dose decreased cardiac output and caused peripheral vasoconstriction in propranolol-pretreated animals. Thus, both agents lowered blood pressure by peripheral vasodilatation in the placebo group, after beta blockade; however, the mechanism of the verapamil-induced blood pressure decrease changed from pure vasodilation to a decrease in cardiac output, i.e., cardiac depression. Verapamil but not PN 200-110 prolonged the PQ interval, especially in animals who had received beta blockade. Most differences in the interaction were attributable to differences between the 2 calcium antagonists; the differences between the beta blockers were small and in favor of pindolol.
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PMID:Interaction between two calcium antagonists and two beta blockers in conscious rabbits: hemodynamic consequences of differing cardiodepressant properties. 288 Apr 95

Studies evaluating the antianxiety and antipanic properties of beta-blockers do not support their routine use in treating either generalized anxiety disorder or panic disorder. The use of propranolol for anxiety disorders accompanied by physical symptoms, especially cardiovascular complaints, may be effective in some patients when combined with benzodiazepines or perhaps in some non-responders to conventional treatment. Better designed studies are needed to evaluate the exact role of beta-blocking agents in treating anxiety. The efficacy of propranolol in patients with panic disorder has not been widely researched, but preliminary results have not been encouraging. Propranolol may provide symptomatic relief in some patients with residual somatic complaints (i.e., palpitations and tachycardia), when combined with the patient's ongoing drug regimen. Because beta-blockers may induce depression, they should be used cautiously--if at all--in panic patients with concurrent depressive illness.
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PMID:Beta-blockers in anxiety disorders. 289 Jun 77

The effects of somatostatin on lateral hypothalamic self-stimulation were investigated in rats pretreated with haloperidol, bicuculline, phenoxybenzamine or propranolol. Somatostatin decreased the rate of self-stimulation. Halperidol, bicuculline and phenoxybenzamine potentiated the somatostatin-induced depression of self-stimulation behaviour. Propranolol had no effect. It is suggested that dopaminergic, GABAergic and noradrenergic systems are involved in the somatostatin-induced depression of self-stimulation.
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PMID:Effects of somatostatin on self-stimulation behaviour in rats pretreated with a receptor blocker. 289 12

The present study was performed in order to evaluate whether norepinephrine (NE) can modulate the synthesis and release of 1 and 2 series of prostaglandins (PGs) by the isthmic region of preovulatory sow oviducts and also to clarify whether the action of the neurotransmitter is mediated through alpha, through beta or through both types of tissue adrenoreceptors. NE, at a concentration of 1 microgram/ml, depressed significantly (P less than 0.05) the basal output of PGE1 and enhanced (P less than 0.01) the release of PGE2 but, did not modify, the output of "PGF2 alpha-like material". Propranolol (10(-7)M) failed to alter the basal output of "PGE1, PGE2 or PGF2 alpha-like material". In the presence of this beta-adrenoreceptor blocker, the depression induced by NE on PGE1 output, was abolished; its stimulatory influence on the release of PGE2, was eliminated and no effect was detected regarding PGF2 alpha. On the other hand, phentolamine (10(-6)M) did not alter the basal output of "PGE1, PGE2 or PGF2 alpha-like material" and also failed to modify the depression induced by NE on PGE1 release. However, this alpha adrenoceptor blocker completely inhibited the stimulatory action of NE on the output of PGE2 into the incubating medium. The foregoing results document opposite actions of NE on PGE1 and PGE2 outputs from the isthmic region of proestrous sow oviducts and suggest the involvement of beta-adrenoreceptors in both disparate influences. The activation of alpha adrenoreceptors also appears associated with the enhancing effect of the agonist on the release of PGE2. The possible physiological significance of these findings is discussed in terms of the function of the isthmic region as an "adrenergic sphincter" able to influence ovum transport around the moment of ovulation.
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PMID:On the synthesis of prostaglandins E1, E2 and E2 alpha by sow oviducts. Differential modulation of 1 and 2 series of prostaglandins by norepinephrine. 298 54

Because both long-term adrenoceptor agonist administration and antidepressant treatment in animals down-regulate CNS beta-adrenoceptors and attenuate brain adenylate cyclase activity, beta-adrenoceptor agonists may also possess antidepressant properties. We compared the effects of the centrally acting beta-adrenoceptor agonist clenbuterol (5, 10 and 35 mg/kg per day), and the combination of propranolol (5 mg/kg per day) and clenbuterol (10 mg/kg per day), with desipramine (15 mg/kg per day) on forced swim test performance and on cortical beta-adrenoceptors in rats following 7 days of drug administration. Desipramine (15 mg/kg per day), and clenbuterol (10 and 35 mg/kg per day, but not 5 mg/kg per day) both significantly reduced immobility in the forced swim test. Frontal cortex beta-adrenoceptors were significantly down-regulated after desipramine and all 3 doses of clenbuterol. The co-administration of propranolol (5 mg/kg per day) blocked both the reduction in immobility and down-regulation of cortical beta-receptors induced by clenbuterol (10 mg/kg per day). Propranolol (5 mg/kg per day) alone up-regulated frontal cortex beta-adrenoceptors, but had no significant effect on swimming performance. These data suggest that the physiological consequences of beta-adrenoceptor down-regulation are important in the mechanism of action of antidepressants. The results also suggest that clenbuterol may be useful in the treatment of depression.
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PMID:A comparison of the neurochemical and behavioral effects of clenbuterol and desipramine. 303 50

The effects of nifedipine (60 to 90 mg/day) and propranolol (240 mg/day) on symptoms, angina threshold and cardiac function were compared in a placebo-controlled, double-blind, crossover study. Five-week treatment periods with nifedipine and propranolol were compared with 2 weeks of placebo treatment in 21 men with chronic stable angina pectoris, 13 of whom had symptoms both at rest and on exertion. Compared with placebo, New York Heart Association functional class improved in patients equally with nifedipine (p = 0.001) and propranolol (p = 0.006). Frequency of chest pain decreased with nifedipine (p = 0.001) and propranolol (p = 0.01), and nitroglycerin consumption similarly decreased with both treatments. Nifedipine significantly delayed the onset of chest pain (p = 0.01) and 1 mm of ST-segment depression (p = 0.002) during bicycle exercise; smaller increases with propranolol were not statistically significant. A preferential clinical response to nifedipine (9 patients) or propranolol (6 patients) was unrelated to the presence or absence of pain at rest or to any baseline hemodynamic finding. Nifedipine and propranolol were equally effective in relieving exertional ischemia as shown by improvements in ejection fraction at identical workloads, from 0.48 +/- 0.11 to 0.58 +/- 0.12 (p less than 0.001) and 0.56 +/- 0.14 (p less than 0.001), respectively. Exercise wall motion, assessed by a semiquantitative wall motion score, also improved with both drugs. Propranolol treatment decreased exercise cardiac output by 14% (p = 0.01) through its effect on heart rate. In contrast, nifedipine treatment had no effect on cardiac output.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of nifedipine alone with propranolol alone for stable angina pectoris including hemodynamics at rest and during exercise. 308 64

Propranolol hydrochloride is a beta-adrenergic blocking drug used in a variety of clinical conditions. Overdoses can result in severe hypotensive states usually associated with bradycardia or asystole or with profound myocardial depression. We report on an 18-year-old man who ingested a massive dose of propranolol HCl in a suicide attempt. The patient was brought to the hospital in an unresponsive state within 30 minutes of ingestion. He was initially stabilized but subsequently died nine hours after the drug was ingested. Invasive monitoring during this period revealed the shock to be secondary to marked depression of his systemic vascular resistance. Cardiac rhythm and left ventricular output were maintained throughout the attempted resuscitation. This hemodynamic picture suggests that decreased systemic vascular resistance may be another mechanism of shock in significant propranolol HCl overdoses.
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PMID:A fatal case of propranolol poisoning. 322 44

The effects of a novel piperazine derivative (INO 2628) on sinus node pacemaker activity and atrial contractile force were investigated in isolated, blood-perfused dog atrium. Injections of INO 2628 (0.03-100 mumol) into the sinus node artery of the isolated atrium induced a dose-dependent decrease in sinus rate and an increase in contractile force. The positive inotropic effects at more than 10 mumol were accompanied by a transient negative inotropism. Propranolol did not affect the positive inotropic response to INO 2628, but it significantly suppressed positive chronotropic and inotropic responses to norepinephrine. Atropine at a dose which completely blocked negative chronotropic and inotropic responses to carbachol, produced a slight but significant depression of INO 2628-induced negative chronotropic responses; inotropic responses were unaffected. These results suggest that INO 2628 induces noncholinergic negative chronotropic and nonadrenergic positive inotropic responses in isolated dog atria.
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PMID:Negative chronotropic and positive inotropic effects of a unique cardioactive agent, N,N'-dicyclopropyl methyl piperazine (bis) hydrochloride (INO 2628), in isolated, blood-perfused dog atria. 324 39

1. Ambulatory electrocardiography was used to compare the effects of propranolol and pindolol on symptoms, heart rate, arrhythmias and ST segments. Seventeen males (mean age 54 years) with a diagnosis of chronic stable angina pectoris (New York Heart Association Class II-III) were studied. Patients were treated on a double-blind cross-over basis with propranolol 80 mg three times daily or pindolol 5 mg three times daily for 14 days each. During the last 48 h of each treatment period ambulatory electrocardiography was performed. 2. Propranolol resulted in a significantly lower mean hourly, mean 24 h and minimum heart rate. Likewise propranolol caused a lower mean daytime and nocturnal heart rate. There was no significant difference in the frequency of angina between the treatments. The number of episodes of ST segment depression was not significantly different between the two drugs, although there was a trend in favour of propranolol. 3. Both the mean 24 h ST level and the maximum ST segment depression were lower during treatment with pindolol. Propranolol was associated with a total of 117 nocturnal pauses or episodes of asystole ranging in length from 1.5 to 2.8 s. During treatment with pindolol only one such period occurred. The number of premature ventricular contractions occurring during treatment with pindolol (1316 beats) was less than on propranolol (2010) and the mean hourly frequency of premature ventricular contractions was significantly lower during pindolol administration. 4. Pindolol is not significantly different from propranolol in the control of symptomatic and asymptomatic myocardial ischaemia and is associated with fewer premature ventricular contractions. However, there is no advantage in using pindolol in chronic stable angina.
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PMID:The influence of beta-adrenoceptor blockers with and without intrinsic sympathomimetic activity on heart rate, arrhythmias and ST-T segments, using ambulatory electrocardiography. 335 81


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