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At least 829 records · Page 46Linked to original sources
PubMed1996

Pathophysiology and treatment of cocaine toxicity: implications for the heart and cardiovascular system.

OBJECTIVE: To review the data on pharmacology, pathophysiology and treatment of cocaine toxicity, with particular relevance to the heart and cardiovascular system. DATA SOURCE AND STUDY SELECTION: Published epidemiology, laboratory and clinical studies on the pharmacology, electrophysiology and pathophysiology of cocaine toxicity and its treatment. MAIN RESULTS: Cocaine toxicity-related morbidity and mortality are frequent due to the potent pharmacological effects of the drug as an indirect-acting sympathomimetic agent and its class I antiarrhythmic property paradoxically inducing pro-arrhythmia. The cardiac and cardiovascular toxic effects of cocaine include various degrees of myocardial ischemia, cardiac arrhythmias, cardiotoxicity, hypertensive effects, cerebrovascular effects and a hypercoagulable state. Treatment of cocaine toxicity must be based on the multiple factors leading to the toxicity. Sodium bicarbonate appears to have an important role in the acute setting with conduction abnormalities, seizures or acidosis. Unopposed alpha-stimulation provided by beta-blockade should be avoided. Central nervous system hyperexcitability should be treated with diazepam. The use of calcium antagonists appears logical. CONCLUSION: Cocaine is an alkaloid with widespread illicit use. The rationale for treating acute cocaine intoxication has become clearer and more logical with increased knowledge of its mechanisms of action.

Arrhythmias, Cardiac↗
PubMed1987

The acute effects of capsaicin on the cardiovascular system.

Arterial blood pressure and heart rate were recorded from male Wistar rats anaesthetized with urethane. Intravenous injection of capsaicin, 1 microgram, produced a reproducible triphasic effect on blood pressure, comprising an initial fall in blood pressure and heart rate, followed by a transient and then a sustained pressor response. The depressor response and bradycardia were abolished by vagal section. The transient pressor response was altered in shape by hexamethonium. Slow intravenous infusion of capsaicin, 50 micrograms over 12 min, produced only a sustained pressor response accompanied by tachycardia, which was resistant to hexamethonium but abolished by morphine and pithing. Responses to both 1 microgram injection and 50 micrograms infusion of capsaicin were unaffected by the SP antagonist, spantide, but were abolished by capsaicin pretreatment of the rats. Capsaicin induces complex effects on the cardiovascular system, the nature of which varies with the dose and speed of administration.

Animals↗
PubMedDate not supplied

Modifications of the cardiovascular system with aging.

Aging is accompanied by significant cardiovascular modifications, both structural and functional. A slight degree of left ventricular hypertrophy develops, while the resting heart rate and early filling rate are somewhat decreased. In contrast, end-diastolic and end-systolic dimensions, stroke volume, and ejection fraction are largely unchanged. The effort tachycardic and inotropic responses are clearly attenuated, whereas the concomitant increase in end-diastolic diameter is enhanced. Large arterial conduits become less distensible and somewhat hypertrophic. Total blood volume is reduced, whereas total peripheral resistance is moderately increased. Neurohumoral systems relevant to cardiovascular regulation are nonuniformly affected by aging: the sympathetic nervous system is overactive and the circulating levels of vasopressin and atrial natriuretic factor are enhanced, while the activity of the renin-angiotensin system is blunted. Elderly individuals have altered cardiovascular homeostasis, with a typical propensity to postural and postprandial hypotension. "Spontaneous" blood pressure variability is increased, whereas heart rate variability is diminished. Vagally mediated chronotropic responses, including those dependent on baroreflex modulation, are attenuated, although end-organ (cardiac) parasympathetic responsiveness is exaggerated. Arterial baroreceptor control of blood pressure is largely preserved in advanced age, whereas cardiopulmonary-mediated reflex responses are definitely impaired.

Adult↗
PubMed2005

Dysregulation of connexins and inactivation of NFATc1 in the cardiovascular system of Nkx2-5 null mutants.

In humans, mutations of the gene encoding the transcription factor Nkx2-5 result in the heart in electrical conduction defects and morphological abnormalities. In this organ Nkx2-5 is expressed in both the myocardium and the endocardium. Connexins (Cxs) are gap junction channel proteins that have been shown to be involved in both heart development and cardiac electrical conduction, suggesting a possible correlation between expression of Cxs and Nkx2-5. To evaluate this correlation, the expression of Cxs has been investigated in the cardiovascular system of wild-type and Nkx2-5-/- 9.2 days post-conception (dpc) mouse embryos. The disruption of the Nkx2-5 gene results in the loss of Cx43 in the heart, due in part to the poor development of the ventricular trabecular network, as well as specific downregulation of Cx45 gene expression. In addition, the nuclear translocation of NFATc1 in the endocardial endothelial cells is inhibited in the Nkx2-5-/- embryos. These results indicate for the first time that Nkx2-5 is involved in the transcriptional regulation of the Cx45 gene expression. In the mutant embryos the aorta is collapsed, and the vascular endothelial Cxs, Cx40 and Cx37, are no longer expressed in its posterior region. Poor development of the trabeculae and downregulation of Cx45 may contribute both to failure of the myocardial function and to hemodynamic insufficiency. The latter, in turn, may result in the dysregulation of Cx40 and -37 expressions along the whole length of the aorta. Direct or indirect effects of Nkx2-5 inactivation on the Cx45 gene expression could explain the absence of the endocardial cushions in the heart of Nkx2-5-/- embryos.

Animals↗
PubMed1981

[The influence on the cardiovascular system of etomidate infusion anaesthesia combined with fentanyl/nitrous oxide (author's transl)].

Blood pressure and heart rate after the application of etomidate, soluble in alcohol 70% (a ml approximately or equal to 125 mg) and supplemented by fentanyl under controlled respiration with N2O/O2 as an continuous infusion for anaesthesia has been investigated during surgery. After the administration of fentanyl/etomidate (Hypnomidate)/succinylcholine the patients were intubated. Then the infusion of etomidate began with 1.5-2 mg/min for ten minutes, whereafter the dose was reduced to 0.15-0.25 mg/min. The continuous infusion of etomidate was stopped about 20 minutes before the end of the operation. The influence on the cardiovascular system during the whole operation was very minimal. The anaesthesia could be handled without any problems. Therefore the application of etomidate as a continuous infusion in combination with fentanyl and nitrous oxide 66% seems to be an effective technique of intravenous anaesthesia.

Adult↗
PubMed1991

Dose-dependent effects of angiotensin II on the ovine fetal cardiovascular system.

The purpose of this experiment was to establish dose-response relationships for the effects of angiotensin II on arterial pressure, venous pressure, heart rate, and blood volume in the ovine fetus. Chronically catheterized fetal sheep at 132 +/- 1 (SE) days' gestational age were infused with angiotensin II at 4.8 +/- 1.1 (n = 7), 27.7 +/- 4.6 (n = 7), 102.2 +/- 16.7 (n = 6), or 239.0 +/- 30.9 (n = 4) ng/min/kg fetal body weight for 30 minutes. Fetal arterial pressure increased at the three highest doses. Fetal venous pressure, heart rate, and blood volume responded only at 102.2 and 239.0 ng/min/kg. At 239.0 ng/min/kg, arterial pressure increased by 17.7 +/- 1.6 mm Hg (p less than 0.00001), venous pressure increased by 1.5 +/- 0.3 mm Hg (p less than 0.0005), blood volume decreased by 7.8 +/- 2.2% (p less than 0.0001), and heart rate initially decreased by 14 +/- 4 beats/min, followed by an increase of 52 +/- 17 beats/min from control (p less than 0.0005) at the end of angiotensin II infusion. Thus this study shows that angiotensin II affected multiple fetal cardiovascular variables in a dose-dependent manner, suggesting that it is an important regulatory hormone for the entire fetal cardiovascular system.

Angiotensin II↗
PubMed1978

Sympathomimetic effects of pancuronium bromide on the cardiovascular system of the pithed rat: a comparison with the effects of drugs blocking the neuronal uptake of noradrenaline.

1. The effects of pancuronium bromide on the cardiovascular system of the pithed rat were examined. Pancuronium had two effects, a short-lasting cardiovascular stimulation following injection and a longer-lasting potentiation of responses to sympathetic nerve stimulation. 2 The initial effect of pancuronium was compared with that of tyramine. The cardioaccelerator but not the pressor responses to both pancuronium and tyramine were significantly reduced following sympathectomy with 6-hydroxydopamine (6-OHDA). 3 The action of pancuronium in potentiating sympathetic nerve responses was compared with that of known blockers of the neuronal uptake of noradrenaline (NA). Pancuronium (1 mg/kg) and cocaine (0.5 mg/kg) potentiated cardioaccelerator and pressor responses to sympathetic stimulation. These effects of pancuronium could be obtained following adrenalectomy and during neuromuscular blockade with gallamine. Pancuronium and uptake blockers potentiated the cardioaccelerator response to NA, reduced the response to tyramine, but did not affect the response to isoprenaline. Pancuronium and uptake blockers potentiated the pressor response to NA, but did not affect the response to tyramine or clonidine. 4 Following sympathectomy with 6-OHDA, pancuronium failed to potentiate cardioaccelerator and pressor responses to NA. 5 These results are discussed in relation to two main cardiovascular effects of pancuronium; an indirect sympathomimetic action and blockade of the neuronal uptake of NA.

Adrenalectomy↗
PubMed1999

Desensitization of G-protein-coupled receptors in the cardiovascular system.

Multiple mechanisms exist to control the signaling and density of G-protein-coupled receptors (GPRs). Upon agonist binding and receptor activation, a series of reactions participate in the turn off or desensitization of GPRs. Many GPRs are phosphorylated by protein kinases and consequently uncoupled from G proteins. In addition, many GPRs are sequestered from the cell surface and become inaccessible to their activating ligands. Both receptor:G protein uncoupling and receptor sequestration may involve the participation of arrestins or other proteins. A model for receptor regulation has been developed from studies of the beta-adrenergic receptor. However, recent studies suggest that other GPRs important in the cardiovascular system, such as the muscarinic cholinergic receptors that regulate heart rate, might be regulated by mechanisms other than those that regulate the beta-adrenergic receptors. This review summarizes our current understanding of the processes involved in the desensitization of GPRs.

Animals↗
PubMed1994

The effect of C-terminal fragment of ANF-ANF(24-28)OH on the cardiovascular system in rat.

1. The effect of C-terminal fragment of ANF-ANF(24-28)OH on the cardiovascular system was investigated in rats. 2. In vivo this pentapeptide caused the fall of systolic and diastolic blood pressure. 3. ANF(24-28)OH increased cardiac contraction amplitude and changed coronary outflow in vitro. 4. These experiments showed that the shorter fragment of ANF containing five amino acids: Asn24-Ser25-Phe26-Arg27-Tyr28-COOH is a bioactive substance.

Amino Acid Sequence↗
PubMed1991

[Characteristics of the cardiovascular system in children with primary arterial hypotension].

Overall 120 children aged 12 to 15 years with primary arterial hypotension and different variants of the disease course (grave, of medium gravity or mild) were examined. The control group was made up to 50 normal children. The program of the examination included electrocardiography, echocardiography, tetrapolar chest rheography and bicycle ergometry. It has been established that in children with arterial hypotension, the intracardiac hemodynamics undergoes compensatory adaptive reconstruction characterized by the enhancement of contractile and pump functions of the myocardium combined with the increased relaxation capacity. The central hemodynamics is characterized by the lowering of the general peripheral vascular resistance. The functional potentialities of the cardiovascular system decline, manifesting in the form of a decrease of exercise tolerance in association with energy losses necessary for its performance. The use of bicycle ergometry made it possible to delineate dysadaptation reactions of arterial pressure to exercise, modified by hereditary factors.

Adolescent↗
PubMed1985

Distribution and function of peripheral alpha-adrenoceptors in the cardiovascular system.

alpha-Adrenoceptors may be subdivided based on their anatomical distribution within the synapse. Presynaptic alpha-adrenoceptors are generally of the alpha 2-subtype and modulate neurotransmitter liberation via a negative feedback mechanism. Postsynaptic alpha-adrenoceptors are usually of the alpha 1-subtype and mediate the response of the effector organ. Although this "anatomical" subclassification is generally applicable, many exceptions exist. A more useful classification of alpha-adrenoceptor subtypes is based on a pharmacological characterization in which selective agonists and antagonists are used. Peripheral alpha-adrenoceptors are critical in the regulation of the cardiovascular system. Postsynaptic alpha-adrenoceptors in arteries and veins represent a mixed population of alpha 1/alpha 2-adrenoceptors, with both subtypes mediating vasoconstriction. In the peripheral arterial circulation, postsynaptic vascular alpha 1-adrenoceptors are found in the adrenergic neuroeffector junction, whereas postsynaptic vascular alpha 2-adrenoceptors are located extrajunctionally. In the venous circulation, it appears that alpha 2-adrenoceptors may be predominantly junctional, whereas alpha 1-adrenoceptors may be predominantly extrajunctional. It has been proposed that junctional alpha-adrenoceptors will respond predominantly to norepinephrine liberated from sympathetic neurons, whereas extrajunctional alpha-adrenoceptors likely respond to circulating catecholamines. The functional role of extrajunctional alpha-adrenoceptors may be more important in disease states such as hypertension and congestive heart failure where circulating levels of catecholamines may be high and contribute to the maintenance of elevated vascular resistance. alpha 2-Adrenoceptors are also associated with the intima and may play a role in the release of an endogenous relaxing factor from the endothelium.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1996

Protein families that mediate Ca2+ signaling in the cardiovascular system.

Five protein families are known to participate in the signaling cascades that enable calcium ions (Ca2+) to regulate functions in the cardiovascular system. Ca2+ signaling is involved in muscle contraction, pacemaking, and perhaps cell growth and differentiation. Recent evidence about the molecular properties of Ca2+ regulatory proteins has suggested possibilities for new therapeutic agents, including T-type Ca2+ channel blockers for patients with cardiovascular disease. This article reviews new information about Ca2+ signaling in the heart, vascular smooth muscle, and other tissues.

Calcium↗
PubMed1970

The effect of progressive hypoxia on the respiratory and cardiovascular systems of the pigeon and duck.

1. During the initial stages of progressive hypoxia in ducks and pigeons (P(a, O2) 100 --> 60 mm Hg) there were no significant changes in heart rate, blood pressure or oxygen uptake, but respiratory frequency increased.2. As hypoxia became more profound (P(a, O2) 60 --> 30 mm Hg), there was a significant tachycardia, and blood pressure fell slightly in both animals. Respiratory frequency continued to increase in both species, and ducks were able to maintain their oxygen uptake at control levels at a lower P(a, O2) than pigeons.3. The response to progressive hypoxia of pigeons and ducks was compared with that of the domestic fowl. The former two birds could maintain control of their cardiovascular system at a lower environmental oxygen concentration than the latter. Arterial P(O2) followed a similar course in all three birds in relation to environmental oxygen content. Pigeons and ducks were therefore able to endure a lower arterial P(O2) than chickens.

Animals↗
PubMedDate not supplied

[The effect of gidazepam on the cardiovascular system function in patients with neurotic reactions and in healthy subjects under aggravated conditions].

Administration of 0.05 g gidazepam once or twice daily for 7 days increased the stroke volume (SV) and circulation volume (CV) and reduced total peripheral resistance in neurotic patients. In healthy individuals 0.05 g gidazepam administered 60 min before an important examination stabilized CV. In subjects kept for 60 min in a microclimate with increasing temperature (55 +/- 2 degrees C, relative humidity 75-80%, rate of movement 1.5 m/min, rectal temperature at the end of exposure 39 degrees C) 0.05 g gidazepam administered 60 min before overheating optimally reorganized the reaction of the cardiovascular system, stabilized the SV at the initial level, which together with the growing heart rate increased the CV and provided sufficient perfusion of the vital organs. In healthy subjects working as operators for 4 h under conditions of hypercapnia (1.5% CO2), a single administration of 0.05 g gidazepam one hour before the beginning of work reduced the pulse pressure and increased the SV. The results obtained are evidence of the safety of using gidazepam as a corrector of emotion-induced disorders in operator performance under extreme conditions.

Adolescent↗
PubMed1998

A novel, nongenomic action of estrogen on the cardiovascular system.

To examine the time course and mechanisms of action of single doses of estrogen on the skin microvasculature, two double-blind placebo-controlled cross-over studies were conducted in healthy young men using the noninvasive technique of laser Doppler velocimetry with iontophoretic application of vasodilator substances. Estradiol (2 mg sublingually) produced a significant increase in the response to the endothelial vasodilator acetylcholine (ACh) after 15 min, but not after 20 or 30 min. The mean plasma estradiol concentration increased from 89.4 +/- 9 pmol/L at baseline to 486.6 +/- 218 pmol/L at 15 min. An i.v. bolus of 25 mg conjugated equine estrogens produced significant increases in the responses to ACh at 15 and 20 min but not at 30 min. There was no change in responses to the nonendothelial vasodilators sodium nitroprusside or nicotine, and administration of placebo produced no change in ACh responses at any time point. These experiments show that, at plasma estradiol concentrations within the physiological range for premenopausal women, estrogens act directly on the cutaneous microvasculature through a rapid onset, rapid offset, nongenomic mechanism that is specific to the endothelium; in addition, it supports the view that estrogens can act on the male cardiovascular system in a manner that is potentially clinically beneficial.

Acetylcholine↗