Cardiovascular effects/response

Results of in vitro studies suggest an interaction between calcium ions and cyanide in cardiovascular effects (Allen and Smith 1985 Robinson et al. 1985a). It has been demonstrated that exposure to cyanide in metabolically depleted ferret papillary muscle eventually results in elevated intracellular calcium levels, but only after a substantial contracture develops (Allen and Smith 1985). The authors proposed that intracellular calcium may precipitate cell damage and arrhythmias. The mechanism by which calcium levels are raised was not determined. Franchini and Krieger (1993) produced selective denervation of the aortic and carotid bifurcation areas, and confirmed the carotid body chemoreceptor origin of cardiovascular, respiratory and certain behavioral responses to cyanide in rats. Bradycardia and hyperventilation induced by cyanide are typical responses evoked by carotid body chemoreceptor stimulation (Franchini and Krieger 1993). 

Strassman RJ, Qualls CR. (1994). Dose-response study of N,N-dimethyltryptamine in humans I. Neuroendocrine, autonomic, and cardiovascular effects. Arch Gen Psychiatry. 51(2) 85-97. Strassman RJ, Qualls CR, Uhlenhuth EH, Kellner R. (1994). Dose-response study of N,N-dimethyltryptamine in humans II. Subjective effects and preliminary results of a new rating scale. Arch Gen Psychiatry. 51(2) 98-108. 

Adrenal medulla. On the one hand, release of epinephrine elicits cardiovascular effects, such as increases in heart rate und peripheral vascular resistance. On the other, it evokes metabolic responses, such as glycogenolysis and li-polysis, that generate energy-rich substrates. The sensation of hunger is suppressed. The metabolic state corresponds to that associated with physical exercise - silent stress . 

Cardiovascular Effects. Palpitations, low blood pressure, and tachycardia were described in subjects exposed to 1,3-DNB by the inhalation (Okubo and Shigeta 1982), oral (Kumar et al. 1990), and dermal (White and Hay 1901) routes of exposure. These responses are consistent with effects of organic nitrates. 1,3-DNB is an organic nitrate and shares many of the cardiovascular properties of therapeutic nitrates. Organic nitrates induce relaxation of the vascular smooth muscle which can result in peripheral vasodilation and a fall in blood pressure followed by a compensatory vasoconstriction (Abrams 1980). The general information available on organic nitrates suggests that exposure to 1,3-DNB or 1,3,5-TNB at ammunition waste sites or at work places where these chemicals are used may lead to adverse cardiovascular effects. 

Respiratory and cardiovascular effects of maitotoxin have been studied in pentobarbital anaesthetized cats (21). Sublethal doses of maitotoxin induced an important hyperventilation phase, hypertension and a transitory tachycardia followed by slight bradycardia. Higher dosage caused respiratory depression, cardiac arrhythmias and tachycardia leading to cardiac failure. Artificial respiration did not modify the cardiac responses. 

There is suggestive but inconclusive evidence of adverse cardiovascular effects in humans exposed to relatively high concentrations of CDDs. ° Increased deaths from chronic heart disease were observed in the Seveso cohort, but psychosocial factors could not be ruled out. No clear dose-response relationships were seen among the Ranch Hand cohort. Increased deaths from heart and circulatory disease were reported among German workers exposed to CDDs. No evidence of adverse cardiovascular effects was observed in US workers. 

While the rate limiting step of the cascade is the renin release, the biological active component is the octapeptide angiotensin n. It is an essential regulator of fluid and electrolyte balance as well as blood pressure. It exerts its actions on various structures like blood vessels, adrenal cortex, kidney and central nervous system. Although at least two different receptor subtypes for angiotensin II have been identified (ATi and AT2) the ATi-subtype is responsible for most of the cardiovascular effects of the agonist. 

Cardiovascular effect. [6]-shogaol, administered intravenously to rats at a dose of 0.5 mg/kg, produced a rapid fall in blood pressure, bradycardia, and apnea. There was a marked pressure pressor response in blood pressure that occurred after the rapid fall. A dose of 3.6 pM produced inotropic and chronotropic actions on isolated atria in rats. The effect disappeared by repeated injections or pretreatment of 100 mg/kg administered subcutaneously ° k Intravenous doses of 0.1 to 0.5 pg produced a pressor response in a dose dependent manner. The response was markedly reduced by spinal destruction at the sacral cord level. Norepinephrine (10 pg/kg, intravenously) induced pressor response that was not affected by spinal destruction. In rats in which the spinal cord was destroyed at the thoracic cord level, [6]-shogaol-induced pressor response was reduced by hexamethonium (10 mg/kg, intravenously) and phentolamine (10 mg/ kg, intravenously). When the spinal cord was destroyed at the sacral level, the pressor response was not affected by these blockades. In the hindquarters of rats that were perfused with rat s blood, [6]-shogaol produced two pressor responses on the perfusion pressure. The first was accompanied by a rise in systemic blood pressure, was re-... 

Donnelly, M., Zametkln, A.J., Rapoport, J.L., Ismond, D.R., Wein-gartner, H., Lane, E., Oliver, J., Linnoila, M., and Potter, W.Z. (1986) Treatment of childhood hyperactivity with deslpramlne plasma drug concentration, cardiovascular effects, plasma and urinary catecholamine levels, and clinical response. Clin Pharmacol Ther 39 72-81. 

Most of the important effects of histamine in allergic diseases, including bronchoconstriction and contraction of the gut, are mediated through HI receptors. Other effects, including the cardiovascular responses, involve both HI and H2 receptors. In man the predominant cardiovascular effect is vasodilatation and a lowering of blood pressure. This response is also responsible for the cutaneous flushing commonly observed with histamine release. The... 

Effects of autonomic blockade on the response to phenylephrine (Phe) in a human subject. Left The cardiovascular effect of the selective K-agonist phenylephrine when given as an intravenous bolus to a subject with intact autonomic baroreflex function. Note that the increase in blood pressure (BP) is associated with a baroreflex-mediated compensatory decrease in heart rate (HR). Right The response in the same subject after autonomic reflexes were abolished by the ganglionic blocker trimethaphan. Note that resting blood pressure is decreased and heart rate is increased by trimethaphan because of sympathetic and parasympathetic withdrawal. In the absence of baroreflex buffering, approximately a tenfold lower dose of phenylephrine is required to produce a similar increase in blood pressure. Note also the lack of compensatory decrease in heart rate. 

Estrogens have a number of important metabolic and cardiovascular effects. They seem to be partially responsible for maintenance of the normal structure and function of the skin and blood vessels in women. Estrogens also decrease the rate of resorption of bone by promoting the apoptosis of osteoclasts and by antagonizing the osteoclastogenic and pro-osteoclastic effects of parathyroid hormone and interleukin-... 

There has been considerable controversy over the dangerousness of ecstasy. Some researchers, based on animal studies or positron emission tomography (PET) scans of users brains, believe the drug causes a destruction of the brain cells responsible for producing serotonin, an important neurotransmitter. However, it is unclear how lasting or dangerous these effects are in humans. Ecstasy can also cause severe dehydration and unpredictable cardiovascular effects. 

No cardiovascular effects were observed in a group of Air Force veterans exposed to 2,3,7,8-TCDD-contaminated herbicides during the Vietnam war and examined several years post-exposure (Wolfe et al. 1985). However, a follow-up study of the Ranch Hand cohort reported increased mean diastolic blood pressure in those with current serum lipid 2,3,7,8-TCDD levels from 15 to 33.3 ppt, but not in subjects with higher 2,3,7,8-TCDD serum levels (USAF 1991). In addition, the proportion of abnormally low peripheral pulses in all Ranch Hand veterans, regardless of serum levels, was elevated relative to a comparison group. Also, arrhythmias detected on the electrocardiogram were significantly associated with 2,3,7,8-TCDD exposure, but there was no consistent dose-response relationship. 

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