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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↗
PubMed1988

Lethal effects and cardiovascular effects of purified alpha- and theta-toxins from Clostridium perfringens.

Shock, a common and frequently fatal manifestation of gas gangrene caused by Clostridium perfringens, is probably mediated by extracellular toxins. Previous studies implicating alpha-toxin as the major lethal factor were frequently done with preparations contaminated with a second lethal factor, theta-toxin. We purified alpha- and theta-toxins from C. perfringens and demonstrated that both were lethal to mice. We investigated the effects of these purified toxins on cardiovascular function in intact rabbits; both toxins caused profound hypotension and bradycardia within 40 min. Reduced cardiac output preceded the development of hypotension and bradycardia. Purified alpha-toxin produced a dose-dependent reduction in myocardial function in isolated rabbit atrial preparations. Purified theta-toxin did not directly inhibit myocardial function. Shock induced by alpha-toxin may be partly mediated by direct depression of myocardial function. theta-Toxin reduced cardiac output in intact animals but had no direct effects on isolated heart preparations at concentrations that induced shock in intact animals. These data suggest that theta-toxin-induced shock could be mediated by an endogenous myocardial depressant factor.

Animals↗
PubMed1999

Investigation on SCH00013, a novel cardiotonic agent with Ca++ sensitizing action. 3rd communication: stereoselectivity of the enantiomers in cardiovascular effects.

The cardiovascular effects of the enantiomers, (+)-SCH00013 and (-)-SCH00013, of a novel cardiotonic agent 4,5-dihydro-6-[1-[2-hydroxy-2-(4-cyanophenyl)ethyl]- 1,2,5,6-tetrahydropyrido-4-yl]pyridazin-3(2H)-one (SCH00013) were investigated in vitro and in vivo. The enantiomers of SCH00013 elicited an equipotent positive inotropic effect in isolated guinea-pig papillary muscles. Both of the enantiomers had a modest negative chronotropic effect in isolated guinea-pig right atria and the difference in the chronotropic effects of the enantiomers was not significant. In anesthetized dogs, both enantiomers increased LVdP/dtmax without change in heart rate and slightly decreased blood pressure. These hemodynamic effects of the enantiomers were not significantly different from each other. (+)-SCH00013 and (-)-SCH00013 increased the extent of cell shortening in association with only a small increase in the Ca++ transients in indo-1-loaded rabbit cardiomyocytes, and both the increases in cell shortening and Ca++ transients were not significantly different between the enantiomers. Both isomers equally shifted the relationships between the increases in the cell shortening and Ca++ transients to the left and upward as compared with the relationships for the elevation of extracellular Ca++ concentration and isoproterenol, which indicates that the effectiveness of the Ca++ sensitizing effects of the enantiomers are almost equivalent. The enantiomers of SCH00013 showed equipotent inhibitory effect on the phosphodiesterase (PDE) III activity. The maximal extent and the potency of prolonging effect of the two enantiomers on the effective refractory period were also the same. Thus, the efficacy and potency of the effects on the cardiovascular parameters such as myofibrillar Ca++ sensitivity, PDE III activity and the effective refractory period for the both enantiomers of SCH00013 are equivalent, indicating that the cardiovascular effects of SCH00013 may be due to equal contribution of both enantiomers.

Anesthesia↗
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↗
PubMed1986

Monoamine oxidase inhibitors and tricyclic antidepressants: comparison of their cardiovascular effects.

The cardiovascular effects of monoamine oxidase inhibitors (MAOIs) are contrasted with those of the tricyclic antidepressants (TCAs). At therapeutic doses, MAOIs lower supine blood pressure and increase the postural fall in blood pressure, whereas TCAs have only the latter effect. MAOIs have little effect on heart rate and do not prolong cardiac conduction; TCAs increase heart rate and prolong cardiac conduction. Neither class of drugs appears to impair cardiac mechanical functioning. For patients with certain cardiac problems, MAOIs may have an advantage over TCAs.

Angina Pectoris↗
PubMed2001

[Cardiovascular effects of doping].

Cardiovascular effects of doping drugs are numerous, with different mechanisms: vasoconstriction of amphetamines, erythropoietin and cocaine; sodium water retention of anabolic steroids and corticosteroids; elevation in blood viscosity of erythropoietin, perflurocarbon emulsion, recombinant hemoglobin and anabolic steroids; sympathetic nervous system activation of amphetamines, beta 2 agonists and clenbuterol; lipids profile disorder of anabolic steroids. Physical activity consequences, particularly bradycardia and dehydration, are worsening. Thrombosis and arrythmogenic effects, with possibility of sudden death, are the severe immediate events. Hypertension and coronary diseases are medium-term effects; acute myocardial infarction is frequent. Heart failure can be secondary to cardiac muscle direct fibrosis, like with anabolic steroids. These cardiovascular effects are serious and it is necessary to early detect the doping drugs use in sporstmen; all prescribing physician should be aware of existing drugs and their clinical events.

Blood Viscosity↗
PubMed2002

[Effects of bradykinin in the cardiovascular effects of angiotensin-converting enzyme inhibitors].

The role of bradykinin in the cardiovascular effects of angiotensin converting enzyme inhibitors remains difficult to establish. On their haemodynamic effects, bradykinin acts during their acute administration, participating in their vasodilatation action, while during their chronic administration they act slightly or not at all. On their trophic effects, the action of the tissue kallikrein-kinin system, suggested by the results of animal experimentation, is yet to be demonstrated in man. For their effects on cardiovascular morbidity and mortality the role of bradykinin remains under discussion. Nevertheless, besides ACE inhibitors, the other therapeutic agents which increase the levels of bradykinin, such as neutral endopeptidase inhibitors, have a significant field of development in the course of cardiovascular pathologies.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2006

Cardiovascular effects of felypressin.

Cardiovascular effects of felypressin (FEL) were studied in Wistar rats. Heart rate and mean arterial pressure measurements were taken in awake rats treated with vasopressin (AVP), FEL, or epinephrine (EPI). Each group received either an intravenous (IV) or an intracerebroventricular V1 receptor antagonist, saline, area postrema removal, or sham surgery. Analysis of variance and Student-Newman-Keuls (P < .05) were applied. Felypressin and AVP induced a pressor effect, and bradycardia was inhibited by IV V1 antagonist. Intracerebroventricular V1 antagonist and area postrema removal enhanced their pressor effects. Epinephrine induced a higher pressor effect and a similar bradycardia that was not affected by the treatments. It was concluded that FEL depends on V1 receptors to induce pressor and bradycardic effects, and that it produces a high relationship between bradycardia and mean arterial pressure variation depending on area postrema and central V1 receptors. These effects are potentially less harmful to the cardiovascular system than the effects of EPI.

Animals↗
PubMed1987

Paradoxical effect of calcium on some cardiovascular effects of verapamil in the rat.

The ability of calcium infusions to reverse some cardiovascular effects of verapamil was tested in anesthetized rats and on isolated rat atria. Intravenous infusions of 1.88 mg/kg verapamil increased the cycle length (CL), lengthened the PR interval (PRi), and decreased the mean arterial pressure (Pa). After these effects were stabilized, a series of infusions of calcium chloride (338 mumol/kg each) were performed. Calcium on the one hand promoted the return of Pa to its basal value; on the other hand, it failed to reverse the effect of verapamil on AV conduction and the first infusion of calcium produced an additional increase in CL of 55 +/- 16 ms. This paradoxical effect of calcium was prevented by previous infusion of atropine (0.2 mg/kg). On isolated atria, the increase of calcium concentration in the media ([Ca2+]0) from 1.0 to 6.0 mM increased the concentration frequency by approximately 40 beats/min, both in atropinized and in nonatropinized preparations. After verapamil, however, the same increase in [Ca2+]0 decreased atrial rate in 50 +/- 15 beats/min in nonatropinized atria. The results obtained indicate that extra calcium can overcome the hypotensive effect of verapamil, whereas it paradoxically increases its negative chronotropic effect and fails to reverse its effect on AV conduction. This paradoxical effect of calcium can be prevented, both in vivo and in vitro, by atropine blockade of muscarinic receptors.

Animals↗
PubMed1990

Cardiovascular effects of caffeine therapy in preterm infants.

Theophylline therapy increases left ventricular output in preterm infants by a combination of positive inotropic and chronotropic effects. The cardiovascular effects of caffeine were evaluated in 20 clinically stable preterm infants. Ten infants received intravenous caffeine citrate with a loading dose of 20 mg/kg and a maintenance dose of 5 mg/kg every 24 hours, and 10 infants were control subjects. Left ventricular output, stroke volume, and heart rate were measured by using a combination of two-dimensional and pulsed Doppler echocardiography and mean arterial blood pressure by oscillometry (Dinamap, Critikon, Division of McNeil Laboratories, Irvine, Calif) before the start and on days 1, 2, 3, and 7 of caffeine therapy and 7 days after discontinuation of therapy. Compared with controls, left ventricular output and stroke volume were significantly increased on days 1 to 7 of caffeine therapy. Caffeine led to an increase in the mean arterial blood pressure on the first 3 days of therapy, but the heart rate did not change. These data indicated that caffeine administration leads to a significant increase in left ventricular output in preterm infants and that this inotropic effect is accompanied by a pressor effect.

Apnea↗
PubMed2000

Cardiovascular effects of combination of perindopril, candesartan, and amlodipine in hypertensive rats.

The combination therapy with ACE inhibitors, angiotensin II type 1 (AT(1)) receptor antagonists, or calcium channel antagonists may exert more beneficial effects on cardiovascular diseases than monotherapy. Perindopril, candesartan cilexetil, or amlodipine alone or the combination of low doses of each agent was administered orally to stroke-prone spontaneously hypertensive rats (SHRSP) for 4 weeks to compare the hypotensive or cardiovascular effects. Although perindopril (2 mg/kg), candesartan cilexetil (2 mg/kg), or amlodipine (3 mg/kg) alone caused comparable hypotensive effects in SHRSP, monotherapy with perindopril or candesartan decreased left ventricular (LV) weight; mRNA levels for atrial natriuretic factor, skeletal alpha-actin, and collagen types I and III; and aortic weight and platelet-derived growth factor-beta receptor tyrosine phosphorylation to a greater extent than monotherapy with amlodipine. Although monotherapy with a low dose (0.2 mg/kg) of perindopril or candesartan cilexetil did not significantly reduce the LV mRNA levels and aortic platelet-derived growth factor-beta receptor phosphorylation of the SHRSP, combination therapy at such a low dose normalized these parameters more potently than the use of amlodipine (3 mg/kg) alone. Although perindopril or candesartan cilexetil alone at 0.05 mg/kg did not decrease the blood pressure of the SHRSP, such a low dose of combination therapy decreased LV weight and atrial natriuretic factor mRNA levels of the SHRSP to a greater extent than amlodipine alone or amlodipine combined with perindopril or candesartan cilexetil. Our results provide evidence that suggests the combination of an ACE inhibitor and an AT(1) receptor antagonist may be more effective in the treatment of cardiac and vascular diseases than the combination of a calcium channel blocker with an ACE inhibitor or an AT(1) receptor antagonist or monotherapy with each agent.

Adrenergic beta-Antagonists↗
PubMed1986

Cardiovascular effects of the new positive inotropic agent denopamine with special reference to species difference and the effect on failing heart.

Cardiovascular effects of (-)-(R)-1-(p-hydroxyphenyl)-2-[(3,4-dimethoxyphenethyl)amino]ethanol (denopamine, TA-064) were investigated in various experimental animals. An intravenous bolus injection of denopamine dose-dependently increased the contractile force or the maximum rate of rise of left ventricular pressure (LV dp/dtmax in cynomolgus monkeys, miniature pigs, cats and rats. In these animals, the doses of denopamine which increased the contractile force by 30% of the control (ED30) were found to be 2-3 micrograms/kg. On the other hand, ED30 values for dl-isoprenaline ranged from 0.005 to 0.04 micrograms/kg. Thus, the potency of denopamine for increasing the contractility was approximately 1/60-1/300 that of dl-isoprenaline. It is noteworthy that the positive inotropic effect of denopamine was more pronounced than the positive chronotropic effect compared with those of isoprenaline, as estimated at ED30 for positive inotropy. In general, denopamine produced little effect on the blood pressure, and only a slight increase or an increasing tendency was observed in all of these animals. An intravenous continuous infusion of denopamine to monkeys or pigs produced qualitatively similar cardiovascular effects to those following intravenous bolus injection. When examined with monkeys, the positive inotropic effect and plasma levels of denopamine were closely related. Denopamine increased cardiac output, and reduced total peripheral resistance in pigs and dogs. In dogs, common carotid, superior mesenteric and femoral arterial blood flow were increased concomitant with the increase in cardiac output, while the vascular resistance of the corresponding vascular bed was reduced. Denopamine had no significant influence on central venous pressure in monkeys and pulmonary arterial pressure in dogs.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Central cardiovascular effects of kappa agonists dynorphin-(1-13) and ethylketocyclazocine in the anaesthetized rat.

Opiate kappa agonists were administered into the cisterna magna of normotensive urethane-anaesthetized artificially ventilated rats: ethylketocyclazocine (78.7 nM) (EKC) and dynorphin-(1-13) (62.3 nM) produced significant and long-lasting decreases in both blood pressure and heart rate. High doses of naloxone (1 mg/kg i.v.) were required to partially antagonize these effects. The central cardiovascular effects of EKC and dynorphin-(1-13) were compared to those of fentanyl (3 nM), [D-Ala2,Met5]enkephalinamide (17 nM) and beta-endorphin (2.9 nM) which induced increases in blood pressure and heart rate. These results suggest that opposite central cardiovascular effects could be induced by activation of various opiate receptors.

Animals↗