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At least 19 recordsLinked to original sources
PubMed1992

Cardiovascular effects of Acanthaster planci venom in the rat: possible involvement of PAF in its hypotensive effect.

Cardiovascular effects of the crowns-of-thorns starfish (Acanthaster planci) venom were examined in rats. The crude venom extracted from the spines of A. planci caused systemic hypotension associated with an increase in heart rate and a decrease in renal cortical blood flow when given i.v. The hypotensive effect of the venom was not inhibited by pretreatment with atropine, indomethacin or aprotinin, but was significantly inhibited by SRI 63-441, a platelet activating factor (PAF) antagonist. The venom caused dose-dependent vasorelaxation of the isolated rat aortic ring preparation precontracted by noradrenaline, an effect which was significantly attenuated by pretreatment with SRI 63-441, methylene blue or parabromophenacyl bromide. Denudation of the endothelium also diminished the vasorelaxing effect of the venom. Both the vasorelaxing and the hypotensive effects showed tachyphylaxis. These results suggest the release of PAF or a PAF-like substance from the endothelium by the venom.

Animals↗
PubMedDate not supplied

Adverse cardiovascular effects of anti-arrhythmia drugs. Part I: Proarrhythmic effects.

Antiarrhythmic drugs are able to save patients from emergency dysrhythmic situations or to avoid symptomatic disorders when used in a prophylactic goal. However they can also induce adverse effects. Cardiovascular adverse effects, and especially proarrhythmic effects, are the most dreaded. Analysis of the underlying mechanisms of the onset and perpetuation of sustained arrhythmias could lead to a better understanding of causes of proarrhythmic effects and thus to a limitation of their occurrence. Antiarrhythmic drugs can modulate the three principal factors which are involved in the onset of arrhythmias: individual predisposing factors, trigger mechanisms and environmental factors. This multiparameter modulation will conduct either to suppress the arrhythmic disorders (antiarrhythmic effect) or to impair it (proarrhythmic effect). According to the numerous factors which take part in the onset and perpetuation of arrhythmia, incidence of proarrhythmic effect of antiarrhythmic drugs is very difficult to evaluate.

Anti-Arrhythmia Agents↗
PubMed1992

Ethanol/cocaine interaction: cocaine and cocaethylene plasma concentrations and their relationship to subjective and cardiovascular effects.

To investigate the pharmacologic effects of the interaction between ethanol and cocaine, eleven male, paid volunteers familiar with the use of both ethanol and cocaine were tested in a dose-response, placebo-controlled, single-blind, randomly-assigned, cross-over design. Ethanol (0.85 g/kg) or placebo was administered in divided doses over a thirty minute period. Fifteen minutes after the termination of ethanol ingestion, cocaine HCl (1.25 and 1.9 mg/kg) or placebo (lidocaine and mannitol) was given by nasal insufflation (snorting). Cocaine and cocaethylene plasma concentrations, blood ethanol levels, subjective ratings of drug effects, and cardiovascular parameters were measured. Statistical analysis of the results indicate that: 1) cocaine administration did not alter blood ethanol concentrations nor the ratings of ethanol intoxication; 2) ethanol caused a significant increase in cocaine plasma concentrations, ratings of cocaine "high", and heart rate; 3) acute tolerance to the subjective and heart rate effects of cocaine was observed; 4) when combined with cocaine, ethanol led to the slow formation of cocaethylene in amounts much lower than those of its parent compound; and 5) the appearance of cocaethylene in plasma did not alter cocaine's subjective and cardiovascular effects.

Alcoholic Intoxication↗
PubMedDate not supplied

Cardiovascular effects of benzquinamide.

The cardiovascular effects of benzquinamide were evaluated in anesthetized dogs. Intravenous benzquinamide, 0.5 to 5 mg/kg, caused tachycardia, elevated blood norepinephrine levels, frequent ventricular arrhythmias, and brief hypotension. Ganglionic blockade by hexamethonium prior to administration of benzquinamide prevented the tachycardia and alterations in norepinephrine levels but prolonged the period of hypotension. In isolated mesenteric arterial preparations benzquinamide interfered with contractile force generated by potassium chloride, norepinephrine, and prostaglandin F2 alpha. It is concluded that benzquinamide directly relaxes vascular smooth muscle thereby producing in vivo reduced peripheral vascular resistance and hypotension, which are compensated for by reflex sympathetic activation.

Animals↗
PubMed1991

A comparison of the cardiovascular effects of phenylpropanolamine and phenylephrine containing proprietary cold remedies.

1. The cardiovascular effects of the proprietary cold remedies, Mu-cron and Boots Cold Relief tablets were compared with 'placebo' Boots Pain Relief tablets in a double-blind study involving 16 healthy volunteers. Measurements (impedance cardiography, forearm plethysmography) were made over 4 h after oral drug administration. 2. Two Mu-cron tablets (containing phenylpropanolamine [(1R,2S)- plus (1S,2R)-norephedrine] 50 mg) increased blood pressure (maximal effect 18 +/- 1/8 +/- 1 mm Hg (mean +/- s.e. mean), P less than 0.001), stroke volume (4.9 +/- 0.8 ml m-2, P less than 0.05), total peripheral resistance (243 +/- 27 dyn s cm-5 m2, P less than 0.001) and forearm vascular resistance (1.3 +/- 0.3 mm Hg ml-1 min, P less than 0.01) and reduced the ratio of pre-ejection period to ventricular ejection time (-0.031 +/- 0.003, P less than 0.05) and forearm blood flow (-2.6 +/- 0.5 ml min-1, P less than 0.05) but did not affect heart rate or cardiac index. 3. Two Boots Cold Relief tablets (containing phenylephrine 10 mg and caffeine 60 mg) caused a small and short-lived increase in total peripheral resistance but did not have consistent effects on other measurements. Two Boots Pain Relief tablets (containing caffeine 60 mg) did not have important cardiovascular effects. 4. The cardiovascular effects of phenylpropanolamine, including vasoconstriction and an increase in cardiac performance, are consistent with its alpha- and beta 1-adrenoceptor agonist action. While it may help the symptoms of rhinitis, its use in patients with heart disease or hypertension is hazardous.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1979

Noninvasive evaluation of cardiovascular effects of preoperative sedation in children.

The cardiovascular effects of two premedication regimes used in paediatric anaesthesia were studied. Eleven patients received rectal methohexitone (22 mg - kg) and 11 patients received intramuscular Innovar (0.03 ml - kg). The effect of these drugs on ventricular function was evaluated by measuring the shortening of the left ventricular minor dimension by echocardiography. No significant changes in this dimension, blood pressure, heart rate or respiratory rate were demonstrated with either drug. Both rectal methohexitone and intramuscular Innovar were shown to have minimal cardiovascular effects when used as preoperative sedation in paediatric patients. Echocardiography proved to be a valuable technique for the noninvasive evaluation of drug effects on myocardial contractility in children.

Child↗
PubMed1991

Cardiovascular effects of the new dihydropyridine derivative elgodipine.

The cardiovascular effects of elgodipine (IQB-875, CAS 119413-55-7), a new phenyldihydropyridine derivative, were studied and compared with those of other dihydropyridines. In isolated guinea-pig atria elgodipine, nifedipine and oxodipine decreased atrial rate and contractile force and in atrial and ventricular muscle fibres shortened the action potential duration (APD) at both 50% and 90% levels of repolarization, but had no effect on amplitude and Vmax of the upstroke or resting membrane potential. They also inhibited the amplitude of the slow contractions and decreased the amplitude and Vmax and shortened the APD of the slow action potentials elicited isoprenaline (isoproterenol) in K-depolarized fibres. In isolated perfused guinea-pig hearts elgodipine, oxodipine, nimodipine, nisoldipine, nitrendipine and nifedipine increased coronary flow and slowed conduction time through the A-V node, but they had no effect on intraatrial and intraventricular conduction times. In anaesthetized dogs the most marked effect of elgodipine was an arterial vasodilator action resulting in a decrease in systemic vascular resistance which explained the decrease in systemic blood pressure and improved left ventricular systolic performance (cardiac output and stroke volume) due to reduction of afterload. As a consequence elgodipine also decreased the pressure-rate product. It is concluded that elgodipine exerted cardiovascular effects qualitatively similar to those previously described with other Ca antagonists of the same class.

Action Potentials↗
PubMed1975

Modification by propranolol of cardiovascular effects of induced hypoglycaemia.

The cardiovascular effects of hypoglycaemia, with and without beta-blockade, were compared in fourteen healthy men. Eight received insulin alone, and eight, including two of the original insulin-only group, were given propranolol and insulin. In the insulin-group the period of hypoglycaemia was associated with an increase in heart-rate and a fall in diastolic blood-pressure. In the propranolol-insulin group there was a significant fall in heart-rate in most subjects and an increase in diastolic pressure. Typical S-T/T changes occurred in the insulin-group but in none of the propranolol-insulin group. Hypertension in diabetics prone to hypoglycaemia attacks should not be treated with beta-blockers because these drugs may cause a sharp rise in blood-pressure in such patients.

Arrhythmia, Sinus↗
PubMedDate not supplied

Cardiovascular effects of fentanyl during enflurane anesthesia in man.

The cardiovascular effects of three doses of intravenous fentanyl (50, 100, and 200 microgram) were determined in 42 adult patients undergoing intraabdominal surgical procedures with enflurane (2--3%) and nitrous oxide (50%) in oxygen. Fentanyl was administered a minimum of 40 minutes after induction of anesthesia and 30 minutes after initiation of the surgical procedure. Stroke volume, heart rate, cardiac output, mean arterial and central venous blood pressures, and peripheral arterial resistance were determined by computer analysis of the central aortic pulse-pressure curve according to the method of Warner. Measurements were made before and 2, 4, 6, 8, and 10 minutes after fentanyl. Fentanyl (50 microgram) produced increases in stroke volume and cardiac output as well as a decrease in peripheral arterial resistance but did not alter heart rate or mean arterial blood pressure. Fentanyl (100 microgram) did not significantly change any variable at any time. Fentanyl (1l (200 microgram) produced sustained decreases in stroke volume, cardiac output and mean arterial blood pressure and increased central venous pressure but did not alter heart rate or peripheral arterial resistance. The data indicate that fentanyl (50--100 microgram) stimulates or has no effect on cardiovascular dynamics during enflurane-nitrous oxide anesthesia but fentanyl (200 microgram) produces significant cardiovascular depression. Our findings suggest that small doses of intravenous fentanyl may be of benefit during enflurane-nitrous oxide but larger doses should probably be avoided.

Adult↗
PubMed1978

Contribution of platelets to the cardiovascular effects of ADP in the rat.

The contribution of platelets to the cardiovascular effects of ADP was investigated in rats in different experimental conditions. Following rapid i.v. bolus injections of ADP (from 0.001 to 0.03 mg/kg b.w.) only a dose-related fall in blood pressure could be detected. Increasing the dose of ADP (up to 1 mg/kg b.w.), platelet fall and changes in cardiac rhythm (bradycardia, A. V. blocks and ectopic beats) became evident. All these phenomena were rapidly reversed. Inhibition of platelet aggregation by a pyrimido-pyrimidine compound (SH 869) or thrombocytopenia induced by Busulfan or antiplatelet antiserum did not significantly protect the animals from the cardiovascular effects of ADP. The fall in blood pressure, however, was reduced. Adenosine, at aquimolar concentrations, caused ECG changes similar to those induced by ADP with no platelet aggregation and a less pronounced blood pressure fall. These results suggest that most of the cardiovascular modifications induced by rapid injection of ADP are largely independent of platelets. Platelets appeared to play a more important role when ADP was given for a longer period of time. A slow i.v. infusion of ADP (6 mg/kg b.w. for 10 min) was accompanied by platelet fall, cardiovascular collapse and ECG alterations typical of myocardial ischaemia. All these effects persisted throughout the ADP infusion but disappeared soon after its termination. They were almost completely inhibited in rats given SH 869 or made thrombocytopenic. In conclusion, platelets seem to contribute to the cardiovascular effects of ADP only in certain experimental conditions. In others, the nucleotide's effects seen more important.

Adenosine Diphosphate↗
PubMed1992

Differential cardiovascular effects of propranolol, atenolol, and pindolol measured by impedance cardiography.

We have evaluated Sramek's method of impedance cardiography as a non-invasive way of detecting the cardiovascular effects of drugs. We made cardiovascular measurements using the method during passive tilting and exercise 2 h after the oral administration of atenolol (50 and 100 mg), propranolol (40 and 80 mg), pindolol (5 and 10 mg), and placebo in seven separate studies involving eight healthy male volunteers. Equivalent doses of the pure antagonists atenolol (beta 1) and propranolol (beta 1, beta 2) produced similar reductions in heart rate, systolic blood pressure, and cardiac index, and increases in stroke volume and total peripheral resistance, particularly during exercise. In contrast the partial agonist pindolol produced increases in heart rate and cardiac index, and reductions in peripheral resistance at rest. During passive tilting and exercise pindolol reduced heart rate, but cardiac output and total peripheral resistance were unchanged except at the highest levels of exercise. The similar cardiovascular effects of atenolol and propranolol, but differing effects of pindolol, are consistent with reports using other methods of measurement. This suggests that impedance cardiography may have a place in the non-invasive assessment of the cardiovascular effects of drugs.

Adult↗
PubMed1992

Cardiovascular effects of intracerebral injection of neuropeptide Y in rats.

Cardiovascular effects of microinjection of neuropeptide Y (NPY) (25, 50, and 100 pmol/site) into field CA3 of hippocampus (CA3), lateral septal nuclei (LSN) and substantia nigra (SN) were investigated in urethane-anesthetized rats. NPY administered into CA3 produced a dose-dependent hypotension and bradycardia. Maximal changes of mean arterial blood pressure (MAP) were -1.5 +/- 0.7, -2.0 +/- 0.4, and -4.2 +/- 1.6 kPa, respectively; maximal changes of heart rate (HR) were -7 +/- 14, -23 +/- 24, and -64 +/- 50 bpm, respectively. NPY microinjection into LSN produced a dose-dependent increase in MAP (0.9 +/- 0.8, 1.3 +/- 0.5, and 3.1 +/- 0.5 kPa, respectively) and a prominent increase in HR (14 +/- 15, 41 +/- 28, and 42 +/- 31 bpm, respectively), but the tachycardia was not dose-dependent. NPY applied into SN elicited a dose-dependent decrease in MAP (-1.0 +/- 0.5, -2.2 +/- 0.9, and -4.3 +/- 2.0 kPa, respectively), but no statistically significant change in HR. The results showed that exogenously applied NPY has distinct cardiovascular effects in CA3, LSN, and SN.

Animals↗
PubMedDate not supplied

Cardiovascular effects of carbachol and other cholinomimetics administered into the cerebral ventricles of conscious cats.

1. The cholinomimetic substances acetylcholine, nicotine, tetramethylammonium chloride and carbachol were infused intracerebroventricularly (i.c.v.) into conscious, normotensive cats and their effects on behaviour, blood pressure and heart rate recorded. 2. Intracerebroventricular acetylcholine, nicotine and tetramethylammonium chloride each produced small, mainly stimulant, effects on the cardiovascular system which were not accompanied by any marked behavioural effects. 3. Intracerebroventricular carbachol at a dose of 30 microgram produced marked and persistent cardiovascular stimulant effects accompanied by a striking rage/fear reaction. When the dose of carbachol was reduced to 7.5 microgram the behavioural effects were no longer seen but marked cardiovascular stimulant effects remained. 4. The cardiovascular stimulant effects of i.c.v. carbachol were apparently mediated via the peripheral sympathetic system since they were abolished by peripheral adrenergic neurone blockade. 5. The blood pressure and heart rate increases produced by i.c.v. carbachol were blocked by prior i.c.v. treatment with atropine, hexamethonium, guanethidine, bethanidine or propranolol. 6. The data are consistent with an interaction between central cholinergic and catecholaminergic neural pathways involved in central regulation of blood pressure and further suggest the involvement of beta-adrenoreceptors in the responses to centrally-administered cholinomimetics.

Acetylcholine↗
PubMed1991

Cardiovascular effects of bupropion in depressed patients with heart disease.

OBJECTIVE: The cardiovascular effects of therapeutic plasma levels of tricyclic antidepressants in depressed patients with and without preexisting cardiac disease have been well characterized and include orthostatic hypotension and conduction delay. Bupropion, structurally unrelated to tricyclic antidepressants, is relatively free of cardiac side effects in depressed patients without cardiac disease. However, it is unknown whether bupropion is safe for depressed patients with preexisting heart disease, so the authors studied the cardiovascular effects of bupropion in such patients. METHOD: The subjects were 36 inpatients with DSM-III major depression and preexisting left ventricular impairment (N = 15), ventricular arrhythmias (N = 15), and/or conduction disease (N = 21). The patients continued their cardiac drug regimens and received bupropion for 3 weeks (mean +/- SD dose = 442 +/- 47 mg/day). Cardiovascular functioning was measured by pulse, blood pressure, high-speed ECG, 24-hour portable ECG, and radionuclide angiography. RESULTS: Although bupropion caused a rise in supine blood pressure, it did not cause significant conduction complications, did not exacerbate ventricular arrhythmias, had a low rate of orthostatic hypotension, and had no effect on pulse rate. However, bupropion treatment was discontinued for 14% of the patients because of adverse effects, including exacerbation of baseline hypertension in two patients. CONCLUSIONS: The cardiovascular profile of bupropion may make this drug a useful agent in the treatment of the depressed patient with preexisting cardiovascular disease. Further studies, with longer durations of bupropion treatment and more subjects, are needed to confirm these findings.

Aged↗
PubMed1991

Role of peripheral and central catecholaminergic and cholinergic mechanisms in the cardiovascular effects of thyrotropin-releasing hormone.

The mechanisms of the cardiovascular effects of i.c.v. administered thyrotropin-releasing hormone (TRH) were studied in anesthetized rats. The pressor response to TRH was blocked after depletion of catecholamines by i.p. reserpine whereas vagotomy or i.v. methylatropine reduced the TRH-induced tachycardia. Centrally administered catecholaminergic or cholinergic receptor antagonists failed to block the cardiovascular effects of TRH. However, centrally administered reserpine reduced the pressor response to TRH and the affinity of its specific binding in brain homogenates. Similar reduction in the affinity of TRH binding was observed after depletion of brain serotonin with p-chlorophenylalanine (PCPA), which was earlier shown to antagonize the TRH-induced pressor effect. It was concluded that TRH acts through a central mechanism to enhance the sympathetic outflow and to attenuate the vagal cardiac activity which leads to hypertension and tachycardia. Central serotonergic mechanisms rather than those related to catecholamines appear to be involved in the pressor response to TRH.

Animals↗
PubMed1977

Cardiovascular effects of fever in the ewe and fetal lamb.

Ewes carrying fetuses with permanently implanted cannulas developed fevers following intravenous injections of bacterial pyrogen (1 microng). During the rising phase of the fever, maternal heart rate increased, but no consistent changes in mean arterial blood pressure (MABP), arterial pH, PO2, or PCO2 were observed during the course of the fever. Fetal temperature, which was initially 0.3 to 0.8 degrees C. higher than maternal temperature rose in parallel with the ewe's temperature. During the maternal fever, fetal MABP, pH, PO2, and PCO2 remained unchanged, but on several occasions the fetal heart rate developed irregularities that persisted after the fever had subsided. These observations suggest that maternal fever does not appear to have adverse effects on fetal oxygenation but has a variable effect on cardiovascular function.

Animals↗