Cardiovascular system ischemia

Ca2+ is an important intracellular second messenger that controls cellular functions including muscle contraction in smooth and cardiac muscle. Ca2+ channel blockers inhibit depolarization-induced Ca2+ entry into muscle cells in the cardiovascular system causing a decrease in blood pressure, decreased cardiac contractility, and antiarrhythmic effects. Therefore, these drugs are used clinically to treat hypertension, myocardial ischemia, and cardiac arrhythmias. 

As for the cardiovascular system, the cardioprotective effects of selective H3-receptor agonists, demonstrated in models of protracted myocardial ischemia (Imamura et al., 1994, 1995, 1996a Hatta et al., 1996, 1997), could be predictive of beneficial effects in coronaropatic patients. Hence, the attenuation of carrier-mediated noradrenaline release in hypoxic and/or ischemic myocardium by H3-agonists would limit the sympathetic overactivity and the associated incidence of ventricular arrhythmias and angina, as well as the increase of metabolic demand by the myocardium, thus preventing further damage and cardiac failure. 

Cocaine also blocks the reuptake of norepinephrine in the PNS the combination of central and peripheral actions leads to a high probability of toxicity. The cardiovascular system is particularly sensitive to the actions of cocaine, and cardiac arrhythmias, marked increases in blood pressure, cerebral hemorrhage, myocardial ischemia, and outright heart failure are not uncommon with cocaine use. Even young, otherwise healthy individuals with normal coronary and cerebral arteries have died suddenly after cocaine use from cerebral hemorrhage or ventricular fibrillation. There have been several deaths of famous athletes attributed to cocaine cardiotoxicity. These cardiotoxic effects may be related to increased intracellular calcium levels and involve both cardiac and vascular actions of the drug. 

Toxicity primarily involves the CNS and cardiovascular system. CNS effects include increased alertness, restlessness, decreased appetite, irritability, stereotyped repetitive behavior, and insomnia with low doses. With larger exposures confusion, panic reactions, aggressive behavior, hallucinations, seizures, delirium, coma, and death can occur. Intracranial bleeding can result from untreated hypertension. Trauma is common secondary to the changes in behavior and decreased judgment. Frequent use results in fatigue, paranoia, and depression. Cardiovascular effects include increased heart rate and blood pressure, chest pain, myocardial ischemia or... 

Cocaine can have marked effects on the heart and cardiovascular system. Adverse actions may include myocardial ischemia, cardiac arrhythmias, cardiotoxicity, hypertensive effects, cerebrovascular events, and a hyperco-agulable state (24,40). By 1997 more than 250 cases of myocardial infarction related to the recreational use of cocaine had been documented in the literature (41). Although less common, aortic dissection related to use of cocaine-free base ("crackcocaine") has also been documented (42). Seizures also can be associated with cocaine use (43). 

Reimer KA, Jennings RB (1992) Myocardial ischemia, hypoxia, and infarction. In Fozzard HA, Haber E, Jennings RB (eds) The heart and cardiovascular system, 2nd edn. Raven Press, New York, NY, pp 1875-1953... 

CARDIOVASCULAR SYSTEM The major therapeutic effects of receptor antagonists are on the cardiovascular system. It is important to distinguish these effects in normal subjects from those in subjects with cardiovascular disease such as hypertension or myocardial ischemia. 

Cardiovascular System The hypotensive effect of sevoflurane primarily is due to systemic vasodilation, although sevoflurane also produces a concentration-dependent decrease in cardiac output. Unlike isoflurane or desflurane, sevoflurane does not produce tachycardia and thus may be a preferable agent in patients prone to myocardial ischemia. 

AVP is synthesized in the fetal hypothalamus. In addition to its role in altering gene expression (e.g., POMC), plasma AVP levels also increase in response to fetal hypoxia-ischemia (30,70,71). The release of AVP is not mediated by peripheral chemoreceptor mechanisms and therefore is unlikely to contribute to the rapid cardiovascular changes at the onset of hypoxia (see above) (30). Exogenously administered AVP produces hypertension, peripheral vasoconstriction, and bradycardia (71-73), although the contribution of hypoxia-stimulated increases in AVP to the redistribution of fetal CVO is uncertain (74,75). Endothehal VI receptors mediate an AVP vasodUatory effect, which means that the net effect of AVP on the cardiovascular system is likely to reflect an integrated picture of vasoconstriction from a number of vascular beds, modulated by endothelium-dependent vasodUatory mechanisms (76). 

The main effect of hawthorn is on the cardiovascular system. Pharmacological studies report enhanced coronary blood flow and myocardial perfusion improvement of cardiac muscle contractility increased left ventrical output velocity lowering of blood pressure " an antiarrhythmic effect increased myocardium tolerance to oxygen deprivation under hypoxic conditions cardioprotective effect against myocardial infarc-tion and stimulation of revascularization after myocardial ischemia (escop 1) Various clinical studies reveal efficacy in congestive heart failure increased cardiac performance decrease in peripheral vascular... 

Like the examples cited above, there are several current hot topics of research in photosensitization, including the use of photodynamic therapy for malignancies, the use of photosensitizers as model systems for studying physiological and pathological processes involving reactive oxygen species, the development of model systems to produce cerebral ischemia, the use as antimicrobials and to treat blood and blood products, and photosensitization in the cardiovascular system, the main topic area of this review. 

Adverse cardiovascular effects seen with intravenously infused pressor agents include marked elevations in blood pressure that cause increased cardiac work, which may precipitate cardiac ischemia and failure. Systemically administered Preceptor-stimulant drugs may cause sinus... 

The clinical manifestations of PAD are associated with reduction in functional capacity and quality of life, but because of the systemic nature of the atherosclerotic process there is a strong association with coronary and carotid artery disease. Consequently, patients with PAD have an increased risk of cardiovascular and cerebrovascular ischemic events [myocardial infarction (Ml), ischemic stroke, and death] compared to the general population (4,5). In addition, these cardiovascular ischemic events are more frequent than ischemic limb events in any lower extremity PAD cohort, whether individuals present without symptoms or with atypical leg pain, classic claudication, or critical limb ischemia (6). Therefore, aggressive treatment of known risk factors for progression of atherosclerosis is warranted. In addition to tobacco cessation, encouragement of daily exercise and use of a low cholesterol, low salt diet, PAD patients should be offered therapies to reduce lipid levels, control blood pressure, control blood glucose in patients with diabetes mellitus, and offer other effective antiatherosclerotic strategies. A recent position paper... 

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