Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Circulating prolactin levels were monitored in nonarteriosclerotic, arteriosclerotic, and hormonally sterilized male and female Sprague-Dawley rats during the acute necrosis and repair phases of myocardial infarction induced by isoproterenol. Male rats are particularly prone to succumb to acute myocardial ischemia but reduction of androgen levels by neonatal sterilization improved survival considerably. Circulating prolactin levels are greatly increased, particularly in females, during acute myocardial ischemia. Since androgens suppress the hypothalamic center for prolactin release, prolactin levels were delayed and transitory in males. It is suggested that the superior survival of female rats may be related to their greater production of prolactin during acute stages of myocardial ischemia, which would dampen the tachycardia-inducing effects of the potent beta-adrenergic stimulating agent, isoproterenol.
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PMID:Serum prolactin levels in rats following isoproterenol-induced myocardial infarction. 120 95

Cardiac pains related to estrogen therapy for prostatic cancer (PC) emerged in 53% of treated patients with ischemic heart disease (IHD). The pain complaints were associated with impairment of coronary circulation in 48% of cases. This clinical condition is attributed to elevated STH levels and a trend to hypercorticism. In hypertensive PC patients estrogens provoked more frequent and severe headaches which occurred at initial stages of the treatment in 23% and after 1-year administration of hormones in 44% of patients. Hypertensive reactions may be caused by aldosterone and prolactin hyperproduction. Observation of the therapist and endocrinologist can help to prevent complications in IHD patients with PC.
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PMID:[Changes in hormonal homeostasis and development of disorders of the cardiovascular system in patients with prostatic cancer on estrogen therapy]. 172 22

Hemostatic changes and hyperestrogenemia have been reported in men during myocardial ischemia and acute myocardial infarction. Because marked augmentation of Hageman factor (factor XII) titer is induced by estrogen intake in humans, we studied the factors participating in the surface-mediated reactions of clotting in patients with documented acute myocardial infarction. We report lower coagulant titers of Hageman factor, prekallikrein, high molecular weight kininogen, and plasma thromboplastin antecedent (factor XI) in the plasma samples of patients with acute myocardial infarction than in control samples. Further, the plasma estradiol titers of patients with acute myocardial infarction were not significantly different from those of controls. In contrast, the prolactin concentration of patients with acute myocardial infarction was elevated. These data suggest that other nonhormonal factors such as excessive consumption may influence the observed reduction in the titers of surface-mediated clotting factors in acute myocardial infarction.
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PMID:Hyperprolactinemia and reduction in plasma titers of Hageman factor, prekallikrein, and high molecular weight kininogen in patients with acute myocardial infarction. 364 93

Relevance of IHD risk factors and hormone concentrations (insulin, estradiol, testosterone, prolactin, LH, FSH, TTH and hydrocortisone) to IHD incidence was studied in 1200 men. Multivariate statistical analysis demonstrated that only a small number of hormonal indices are associated with main lipid and nonlipid risk factors. The relationships exist between systolic arterial pressure (SAP) and hydrocortisone, between TTH and total cholesterol, SAP and age, estradiol, testosterone and age. Significant independent associations were found between IHD prevalence and age (R = 0.140, 3 = 0.000), SAP (R = 0.130, P.0.001), HDLP cholesterol (R = -0.082, P = 0.007), height (R = -0.078, P = 0.010), insulin (R = 0.067, P = 0.035), standard deviation of estradiol from median value (R = 0.083, P = 0.017). The findings confirm a great role of high SAP in the development of IHD, a significant and independent association of high insulin levels with IHD prevalence, the presence of nonlinear relation of estradiol concentration to IHD occurrence in males.
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PMID:[The relation of a number of hormonal indices to risk factors for IHD and its prevalence based on the data from a large population study]. 749 32

The term ''adrenergic'' originates from ''adrenaline'' and describes hormones or drugs whose effects are similar to those of epinephrine. Adrenergic stress is mediated by stimulation of adrenergic receptors and activation of post-receptor pathways. Critical illness is a potent stimulus of the sympathetic nervous system. It is undisputable that the adrenergic-driven ''fight-flight response'' is a physiologically meaningful reaction allowing humans to survive during evolution. However, in critical illness an overshooting stimulation of the sympathetic nervous system may well exceed in time and scope its beneficial effects. Comparable to the overwhelming immune response during sepsis, adrenergic stress in critical illness may get out of control and cause adverse effects. Several organ systems may be affected. The heart seems to be most susceptible to sympathetic overstimulation. Detrimental effects include impaired diastolic function, tachycardia and tachyarrhythmia, myocardial ischemia, stunning, apoptosis and necrosis. Adverse catecholamine effects have been observed in other organs such as the lungs (pulmonary edema, elevated pulmonary arterial pressures), the coagulation (hypercoagulability, thrombus formation), gastrointestinal (hypoperfusion, inhibition of peristalsis), endocrinologic (decreased prolactin, thyroid and growth hormone secretion) and immune systems (immunomodulation, stimulation of bacterial growth), and metabolism (increase in cell energy expenditure, hyperglycemia, catabolism, lipolysis, hyperlactatemia, electrolyte changes), bone marrow (anemia), and skeletal muscles (apoptosis). Potential therapeutic options to reduce excessive adrenergic stress comprise temperature and heart rate control, adequate use of sedative/analgesic drugs, and aiming for reasonable cardiovascular targets, adequate fluid therapy, use of levosimendan, hydrocortisone or supplementary arginine vasopressin.
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PMID:Sympathetic overstimulation during critical illness: adverse effects of adrenergic stress. 2750 1