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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↗

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↗

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↗

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↗

PubMed1988

Peripheral opiate receptors are not involved in the naloxone-sensitive cardiovascular effects of clonidine in rats.

The cardiovascular effects of clonidine and their inhibition by naloxone or naloxone methylbromide were tested in urethane-anesthetized, normotensive Sprague-Dawley rats. Clonidine administered intravenously (5 micrograms/kg) or directly into the nucleus tractus solitarii (NTS, 5 nmol) caused hypotension and bradycardia. The effects of intra-NTS clonidine were dose-dependently inhibited by intra-NTS administration of either antagonist, naloxone being 10 times more potent than naloxone methylbromide. The effects of i.v. clonidine were significantly inhibited by 2 mg/kg of i.v. naloxone, but were unaffected by 20 mg/kg of i.v. naloxone methylbromide. Naloxone alone had no effect on blood pressure or heart rate when given either centrally or systemically, whereas naloxone methylbromide given i.v., but not intra-NTS, caused transient hypotension and tachycardia. It is concluded that central but not peripheral opiate receptors are involved in the cardiovascular effects of clonidine.

Animals↗

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↗

PubMedDate not supplied

Cardiovascular effects of social support in the work place: twenty-four-hour ECG monitoring of men and women.

Psychosocial work characteristics, such as work demand, work control, and social support at work, have been shown to be related to the development of coronary heart disease in epidemiological studies. However, the mechanisms which mediate the social and psychological effects on the cardiovascular system are not known. We have studied the direct cardiovascular effects of psychosocial work environment characteristics in 148 working men and women, representing seven different occupational groups (physicians, teachers, musicians, policemen, train engineers, prison personnel, and saw mill workers). Besides standardized measures of work demand, work control, and social support, ambulatory 24-hour monitoring of electrocardiograms in the customary work and home environment was performed. Systolic and diastolic blood pressure were measured as well as other standard physiologic risk factors for coronary heart disease. Mean heart rates were found to be significantly higher in persons reporting low social support at work. This effect was maintained during working hours as well as during leisure time and rest. Of the other related physiologic risk factors, systolic, but not diastolic blood pressure was found to be higher in persons reporting low social support. Smoking, alcohol consumption and relative body mass index were not related to social support at work. Controlling for age, sex and physical strain at work, strengthened the association of low social support with elevated heart rates.

Adult↗

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↗

PubMed1989

Cardiovascular effects from stimulation of 5-hydroxytryptamine receptors.

The cardiovascular effects of 5-hydroxytryptamine (5-HT), consisting of bradycardia or tachycardia, hypotension or hypertension, and vasodilatation or vasoconstriction, are mediated by three main types of receptors called 5-HT1-like, 5-HT2, and 5-HT3. In intact animals 5-HT elicits a short-lasting bradycardia, accompanied by hypotension, via stimulation of 5-HT3 receptors located on sensory vagal nerve endings in the heart (Bezold-Jarisch reflex). The nature of 5-HT receptors mediating tachycardiac responses is species-dependent. Myocardial 5-HT1-like and 5-HT2 receptors subserve tachycardia in the cat and rat, respectively. Tachycardia in the dog and rabbit is due to a release of catecholamines effected via the 5-HT2 receptors on the adrenal medulla and the 5-HT3 receptors on postganglionic cardiac sympathetic nerve fibres, respectively. The receptors mediating tachycardia in the pig are unique as they do not resemble any of the three 5-HT receptors characterized so far. The blood pressure response to 5-HT is usually triphasic: initial short-lasting hypotension due to reflex bradycardia (via 5-HT3 receptors), a middle pressor phase (via 5-HT2 receptors), and a longer-lasting hypotension (via 5-HT1-like receptors). Vascular contraction by 5-HT is generally mediated by 5-HT2 receptors (located primarily on the large conducting vessels), though in some instances (e.g., dog saphenous vein, dog and human basilar artery, and porcine arteriovenous anastomoses) the contractile response is (also) mediated via 5-HT1-like receptors. Venous dilatation and arteriolar dilatation (leading to increased capillary ['nutrient'] blood flow) occur via 5-HT1-like receptors located mainly on the vascular smooth muscles but also on the endothelium; the smooth muscle and endothelial 5-HT1-like receptors seem to be heterogeneous. In addition, 5-HT can elicit vasodilatation and hypotension as a result of decreased sympathetic nervous tone by acting within the central nervous system and by inhibiting noradrenaline release by a presynaptic action. Both these effects also involve 5-HT1-like receptors that do not appear to be identical. Last, knowledge of the cardiovascular effects of 5-HT and the nature of the receptors involved should be helpful in developing 5-HT-related compounds that may be useful in the treatment of hypertension, migraine, and peripheral vascular diseases.

Animals↗

PubMed1988

Cardiovascular effects of leukotrienes in the bullfrog.

While the cardiovascular effects of the sulfidopeptide leukotrienes (LTs) have been well studied in mammals, their effects are not well known in lower vertebrates. American bullfrogs (Rana catesbeiana) were cannulated in the right sciatic artery and left sciatic vein. In some studies an additional ventricular cannula was implanted. LTC4, LTD4, and LTE4 were compared for their cardiovascular actions by infusion via the sciatic vein into the unanesthetized animals. While all three leukotrienes decreased mean arterial pressure (MAP) and increased heart rate (HR), LTC4 was found to be more potent than the other leukotrienes. In bullfrogs with ventricular cannulae to measure ventricular pressure (VP) and its derivative (+ dP/dt), LTC4 had negative inotropic effects which were blunted by indomethacin (4 mg/kg-bw). 3H-LTC4 metabolism studies were carried out using blood and plasma to examine conversion to other products. Following incubation for 12 min and extraction by C18 Sep-Pak cartridges, samples were analyzed by high performance liquid chromatography. In whole blood, but not in plasma, 3H-LTC4 was rapidly converted to a compound with the retention time of the LTD4 standard. Little conversion to LTE4 was observed within the time course of the experiment. The data suggest that cardiovascular effects of LTC4 may be greater than those observed, since LTC4 is rapidly metabolized to a less active compound. The effects of LTC4 may, in part, be due to stimulation of synthesis of cyclooxygenase metabolites. The ability to record the effects of leukotrienes uncomplicated by effects on coronary arteries make the bullfrog an excellent model for comparative studies on the cardiovascular effects of leukotrienes.

Animals↗

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↗

PubMed1990

Cardiovascular effects of microinjection of angiotensin II in the brainstem of renal hypertensive rats.

The cardiovascular effects of microinjection of angiotensin II (AII) into the area postrema (AP), nucleus of the solitary tract (NTS) and rostroventrolateral medulla were studied in urethane anesthetized sham-normotensive (NT) and two-kidney, one-clip renal hypertensive rats. Microinjection of AII (2-2000 ng) in the AP of renal hypertensive rats elicited a dose-dependent decrease in blood pressure, heart rate and renal sympathetic nerve activity. Similar effects were observed in the NTS. In the NT rats, low doses of AII (2 and 20 ng), either in the AP or NTS, were also depressor. High doses of AII (200-2000 ng) were needed to observe a modest pressor effect in the NT animals. A decrease in heart rate and renal sympathetic activity was observed with the pressor effect. The AII-antagonist, [Sar1,Val5,Ala8]-AII, into the NTS or AP increased blood pressure and heart rate and inhibited the cardiovascular effects of low doses of AII in both group of rats. In contrast, [Sar1,Val5,Ala8]AII did not affect the pressor action of high doses of AII in the NT group. While the microinjection of AII into the rostroventrolateral medulla did not produce any significant cardiovascular effect in the renal hypertensive group, it resulted in a modest pressor effect in the NT rats. These results indicate that acute activation of AII receptors in the AP or NTS does not contribute to the pressor effect of AII in renal hypertensive rats.

Angiotensin II↗

PubMed1991

Methodological problems in evaluation of cardiovascular effects of stress in humans.

Cardiovascular effects of stress in humans are often assessed by application of physical or emotional stimuli in a laboratory environment. Although this method provides important information, these procedures have several limitations. First, blood pressure and heart rate responses to laboratory stressors are characterized by a limited within-subject reproducibility. Second, there is poor correlation between blood pressure and heart rate responses to different stressors, which implies that individual reaction to stress may be estimated differently according to the test used. Finally, these responses bear only a limited relation to 24-hour or daytime blood pressure variability, that is, they reflect to only a limited extent the tendency of blood pressure to vary during daily activities. If assessed by techniques that allow blood pressure to be continuously recorded for 24 hours in ambulatory subjects, blood pressure variability represents a possible approach to observation of cardiovascular reactivity away from an artificial laboratory environment. However, whether blood pressure variability should be expressed as a percentage or in absolute values is controversial. Furthermore, although naturally occurring stress may markedly increase blood pressure, 24-hour blood pressure variations also depend on factors that are not related to emotional stimuli. Thus, the study of cardiovascular responses to stress in humans encounters several problems, regardless of the method used.

Blood Pressure↗

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↗