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Query: UMLS:C0848237 (acute stress)
 4,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Evidence is accumulating that acute stress situations such as ischemia, adrenergic dominance, and ouabain intoxication enhance production of endogenous substances (PgI2, adenosine, NO) which may protect the myocardium from harmful consequences of these stress situations. PgI2 and its stable analogue 7-oxo-PgI2 exert an early direct- and induce a delayed indirect antiischemic, antiarrhythmic, and cytoprotective effect. The direct action is shortlasting; it protects from myocardial ischemia and arrhythmias, at least partly, by its vasodilating, antiaggregatory, and "membrane-stabilizing" effects. The delayed, long-lasting PgI2-induced protection from postocclusion, reperfusion- and ouabain-arrhythmias is dose- (optimal 50 micrograms/kg) and time- (optimal 48 h after treatment) dependent. Its mechanism is probably based on a 7-oxo-PgI2 induced increase in the activity of Na/K-ATP-ase, and further, on a reduced sensitivity to beta-adrenergic agonists and to changes at the cardiac membrane level, resulting in a prolongation of the action potential duration and the effective refractory period.
Basic Res Cardiol 1991
PMID:Cardioprotection: endogenous protective mechanisms promoted by prostacyclin. 178 66

Comparative pharmacologic studies have indicated that the cardiac beta 2 adrenoceptors of vertebrate species are "adrenaline" receptors; i.e., the distribution of beta 2 receptors in the heart seems to be related to the amounts of adrenaline in the sympathetic nerves and in the circulation, and the beta 2 receptors seem to be stimulated mainly by adrenaline. In the human right atrium the order of potency for the agonists and the blocking agents indicate a relatively high proportion of active beta 2 receptors. These findings are in agreement with radioligand binding studies demonstrating up to 50% beta 2 receptors in myocardial membrane preparations. The pharmacologic studies thus add support to the assumption that these beta 2 receptors are functionally active and not merely experimental oddities. It is hypothesized that in normal situations the beta 2-receptor effects are additive to the beta 1 effects. However, during acute stress situations the large amounts of released adrenaline are assumed to increase markedly both inotropy and chronotropy in the heart via beta 2 receptors. It is postulated that only unselective beta blockers can abolish all beta-receptor effects in the heart during stress reactions with profound catecholamine stimulation.
Am J Cardiol 1986 Apr 25
PMID:Activation of cardiac beta 2 adrenoceptors in the human heart. 287 46

It is apparent from the above discussion that acute stress, such as ischemia and reperfusion, hypoxia and reoxygenation, hyperthermia and oxidative stress, can rapidly potentiate the induction of genes for certain members of the HSP families and for antioxidants/antioxidant enzymes. Whether the stress response and induction of these genes have a direct role in myocardial protection is not known, but the induction of the expression of these genes are mostly associated with the preservation of myocardial cells from subsequent injury resulting from ischemia, hypoxia and reperfusion. The ubiquitous presence of some of these stress genes, such as for HSP 70 and catalase, in normal unstressed myocardium further suggests a role of these genes in many basic and essential biochemical and metabolic pathways. It is reasonable to speculate that the cells respond to the stress as a consequence of perturbations of one or more of the metabolic pathways by stimulating the induction of the stress genes of that particular pathway in which they participate. Thus, these genes are likely to be involved both in the protection and recovery/repair mechanisms. The precise mechanism by which myocardial cell recognizes and responds to a particular stress agent such as ischemia, hypoxia, hyperthermia or oxidative stress is not clear. While it is tempting to speculate that a generalized mechanism exists, applying to all different modes of stress response and gene induction, whether these agents induce the response via independent pathways or converge within a single point is entirely unclear. However, from the striking resemblance between the pattern of gene expression, especially with regard to HSP and antioxidant genes, it is reasonable to hypothesize the existence of a common and essential pathway of molecular signaling that leads to the expression of these stress genes (Fig. 2). The identification and characterization of the transcription factors that regulate the expression of the genes induced by these forms of stress should greatly facilitate our future understanding of the mechanism of stress response.
J Mol Cell Cardiol 1995 Jan
PMID:Gene expression in acute myocardial stress. Induction by hypoxia, ischemia, reperfusion, hyperthermia and oxidative stress. 776 Mar 41

To test the authors' hypothesis that cellular antioxidant enzymes constitute a cellular defense against acute stress, myocardial ischemia reperfusion injury in transgenic mice overexpressing the cellular glutathione peroxidase (GSHPx-1) was studied. Transgenic mice were generated using the entire mouse GSHPx-1 gene including approximately 2.0 kb 5'flanking sequence. A 400% increase of GSHPx activity was found in the hearts of transgenic mice compared with non-transgenic controls. Isolated perfused hearts were prepared from two groups of mice: transgenic overexpressed; non-transgenic controls. Hearts were perfused by Langendorff mode, and after 10 min of stabilization subjected to 30 min of ischemia followed by 20 min of reperfusion. In addition, a group of hearts were perfused for 50 min without subjecting them to ischemia and reperfusion to demonstrate the stability of heart preparation. Transgenic mouse hearts demonstrated significantly improved recovery of contractile force and the rate of contraction, compared to non-transgenic control mouse hearts. The infarct size was also lower in transgenic mouse hearts compared to those of non-transgenic controls. In concert, following ischemia, release of creatine kinase from the transgenic hearts was significantly lower than the control group. The results of this study indicate that increased GSHPx-1 expression renders the heart more resistant to myocardial ischemia reperfusion injury.
J Mol Cell Cardiol 1996 Aug
PMID:Transgenic mice overexpressing glutathione peroxidase are resistant to myocardial ischemia reperfusion injury. 887 85

Social stress is a common occurrence in our society that can negatively impact health. Therefore, we wanted to study the effects of a mild stressor designed to model social stress on seizure susceptibility and GABAA receptors in male and female rats. The mild chronic stress of individual housing consistently decreased bicuculline (but not pentylenetetrazol, PTZ) seizure thresholds by 10-15% in both sexes. Housing conditions did not alter the anticonvulsant activity of diazepam or ethanol, although the anticonvulsant effect of ethanol was significantly greater against PTZ-induced seizures. Experiments testing the addition of an acute restraint stress unmasked sex differences in seizure induction. The acute stress also selectively decreased the potency of GABA to modulate GABAA receptor-mediated chloride uptake in group-housed females. There were additional sex differences by housing condition for GABAA receptor-gated chloride uptake but no differences in [3H]flunitrazepam binding. We also found significant effects of sex and housing on ethanol-induced increases in corticosterone (CORT) levels. In summary, there were complex and sex-selective effects of mild chronic stress on seizure induction and GABAA receptors. Gaining a better understanding of mechanisms underlying interactions between sex and stress has important implications for addressing health concerns about stress in men and women.
 ...
PMID:Sex differences in effects of mild chronic stress on seizure risk and GABAA receptors in rats. 1525 Dec 58

ATP-sensitive potassium (K(ATP)) channels are evolutionarily conserved plasma-membrane protein complexes, widely represented in tissue beds with high metabolic activity. There, they are formed through physical association of the inwardly rectifying potassium channel pore, most typically Kir6.2, and the regulatory sulfonylurea receptor subunit, an ATP-binding cassette protein. Energetic signals, received via tight integration with cellular metabolic pathways, are processed by the sulfonylurea receptor subunit that in turn gates the nucleotide sensitivity of the channel pore thereby controlling membrane potential dependent cellular functions. Recent findings, elicited from genetic disruption of channel proteins, have established in vivo the requirement of intact K(ATP) channels in the proper function of cardiac muscle under stress. In the heart, where K(ATP) channels were originally discovered, channel ablation compromises cardioprotection under ischemic insult. New data implicate the requirement of intact K(ATP) channels for the cardiac adaptive response to acute stress. K(ATP) channels have been further implicated in the adaptive cardiac response to chronic (patho)physiologic hemodynamic load, with K(ATP) channel deficiency affecting structural remodeling, rendering the heart vulnerable to calcium-dependent maladaptation and predisposing to heart failure. These findings are underscored by the identification in humans that defective K(ATP) channels induced by mutations in ABCC9, the gene encoding the cardiac sulfonylurea receptor subunit, confer susceptibility to dilated cardiomyopathy. Thus, in parallel with the developed understanding of the molecular identity and mode of action of K(ATP) channels since their discovery, there is now an expanded understanding of their critical significance in the cardiac stress response in health and disease.
J Mol Cell Cardiol 2005 Jun
PMID:Cardiac KATP channels in health and disease. 1591 Aug 78

Exaggerated blood pressure (BP) reactivity to stress may contribute to left ventricular (LV) hypertrophy, a major risk factor for cardiovascular morbidity. This study examined the extent to which BP responses to acute stress are associated with LV mass and relative wall thickness in a community sample of African-American and white men and women. BP was measured at rest and in response to 2 acute challenges (mental arithmetic and handgrip). Systolic BP at rest was positively associated with LV mass and relative wall thickness (p < 0.001). The associations between the responses to the stressors and LV mass were not significant. African-American and white men who exhibited high BP responses to the arithmetic stressor had greater relative wall thickness than those with low reactivity (p < 0.05). In conclusion, BP reactivity is not related to LV mass, but may be related to concentric remodeling.
Am J Cardiol 2006 Jan 15
PMID:Blood pressure stress reactivity and left ventricular mass in a random community sample of African-American and caucasian men and women. 1644 70

Acute stress-induced cardiomyopathy is a syndrome originally described in Japan but increasingly recognized all over the world. Patients typically present with chest pain triggered by an intense emotional or physiological stressor, electrocardiographic changes, and mild cardiac enzyme elevation. Patients typically return to normal cardiac function within 1 month. A retrospective review was conducted of all acute stress-induced cardiomyopathy cases at the University of Maryland Medical Center between May 2006 and May 2007. Six patients fulfilled the criteria and were included in the study. The main clinical features of the syndrome were statistically analyzed. Most patients were post-menopausal women presenting with chest pain. An emotional or physiological stressor was identified in 3 of the 6 patients. Electrocardiographic changes (ST segment elevation or T wave inversion) were present in 3 patients. All patients had left ventricular apical hypokinesis with basal hyperkinesis and elevated cardiac enzymes. The 3 patients receiving a follow up echocardiogram had improved left ventricular contractility and reduced mitral regurgitation within 1 month. Two of the patients had complete resolution in 3-4 days. Stress-induced cardiomyopathy is an important syndrome which mimics an acute myocardial infarction. It is typically self-limiting but can result in ventricular arrhythmias and cardiogenic shock. Our findings should caution clinicians that an identifiable stressor and electrocardiographic changes are not always present. In addition, our observation suggests that patients may regain normal cardiac function in less than 4 days.
Int J Cardiol 2009 May 15
PMID:Acute stress-induced cardiomyopathy: a brief observation. 1840 80

We present our observations on 2 cases of stress cardiomyopathy in which, for the first time, wall motion and myocardial deformation analysis were performed by 2D-strain imaging. Strikingly, in both patients, serial 2D-strain wall motion analysis revealed always synergic and synchronic longitudinal strain and strain-rate patterns, even during the acute stress-induced episodes of left ventricular (LV) dysfunction, indicating uniform myocardial shortening, despite akinetic appearance of the LV apex in both conventional echocardiography and ventriculography. Another important observation was that during the acute stress-induced episodes of severe LV dysfunction the end-systolic LV circumferential wall stress became in both patients several times higher in apical regions than at the LV base. These data suggest that the akinetic appearance of the apex can be related to the high systolic circumferential wall stress in this region, which opposes circumferential fiber shortening and thus apical akinesia and ballooning could be mainly the consequences of LV geometry-induced regional differences in wall stress, rather than a result of severely impaired myocardial contractility in apical regions.
Int J Cardiol 2009 Jun 26
PMID:Left ventricular wall motion abnormality and myocardial dysfunction in stress cardiomyopathy: new pathophysiological aspects suggested by echocardiography. 2023 Oct 38

Takotsubo cardiomyopathy is a syndrome characterized by acute regional systolic dysfunction of the left ventricle, frequently related to psycho-physical acute stress, and usually reversible. This rare syndrome involves more often the female sex with the highest frequency of occurrence between the seventh and eighth decade of life. Etiology has not been clarified yet and several hypotheses have been postulated: multiple epicardial coronary artery damage, abnormal coronary microcirculation, catecholamine-mediated cardiac toxicity, and neurogenic stunning. Clinical presentation is not easy to distinguish from an acute coronary syndrome: chest pain at rest or dyspnea, new-onset electrocardiographic changes, characterized by ST-segment elevation or T-wave inversion. Coronary angiography, which should be performed within 48 h of symptom onset in order to be diagnostic, excludes the presence of significant atherosclerotic stenosis or plaque rupture. Ventricular angiography shows the typical regional wall motion abnormalities (apical akinesia and hyperkinesia of the mid-basal segments) that give to the syndrome its name (takotsubo is a traditional Japanese octopus trap or pot). Echocardiography performed in the acute phase also evidences wall motion abnormalities that characteristically regress in the following days. There is no specific treatment for this syndrome, but supportive and symptomatic therapy is usually administered.
G Ital Cardiol (Rome) 2008 Nov
PMID:[Takotsubo cardiomyopathy: a consensus document]. 2010 3


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