Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0848237 (acute stress)
 4,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Groups of female rats were injected daily for 14 days with 10 mg of cortisone acetate subcutaneously, to study the mechanisms of glucocorticoid suppression on the hypothalamic-pituitary-adrenal axis. Pituitary adrenocorticotropic hormone (ACTH) content, plasma ACTH, adrenal venous corticosterone, adrenal weights, and the catabolic effects on body weight were studied simultaneously (under stressful and non-stressful conditions) before, during, and up to six weeks after cortisone. This study confirmed the results of other investigators that cortisone acetate caused catabolic weight loss and adrenal atrophy, but it was noted to persist up to six weeks after the injections. Glucocorticoid acetate was more effective in causing ACTH-axis suppression than succinate or phosphate preparations, and the effects were dose and time related. Significant depletion of pituitary ACTH content, suppression of plasma ACTH, and corticosterone secretion occurred five to seven days after beginning cortisone acetate (p=<0.001); it was continuous throughout the injection schedule (p=<0.001); it remained for two to four weeks after the cortisone was discontinued (p=<0.001). The animals showed minimum plasma ACTH responsiveness to severe acute stress during this two to four-week suppression phase, but rapid recovery occurred thereafter. Plasma ACTH was undetectable up to six weeks post-cortisone when the animals were not under stress. This may be related to residual cortisone acetate found at the injection sites, or to an altered or different ACTH-axis control mechanism. The sequence of events during recovery from cortisone suppression appeared to be (1) repletion of corticotrophin-releasing hormone (by inference), (2) repletion of pituitary ACTH content, (3) secretion of plasma ACTH, (4) reversal of adrenal atrophy, and (5) subsequent secretion of corticosterone.
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PMID:Suppression of the hypothalamic-pituitary-adrenal axis after subcutaneous cortisone acetate administration in rats. 22 95

Glycogen is an essential substrate during myocardial anoxia. Since porpranolol may maintain myocardial glycogen levels after acute stress by blockade of catecholamine-induced glycogenolysis, we evaluated the effect of propranolol treatment in the isolated perfused isovolumic paced rat heart. Forty-one rats were studied after 10 min of ice-water immersion: half were pretreated with propranolol, 20 mg/kg/day x3, and half with saline. Glycogen content of unperfused propranolol-treated hearts exceeded controls by 46% (146 +/- 9 vs. 100 +/- 4 mumoles/g dry wt, p less than 0.02), and this difference persisted during aerobic perfusion. Propranolol did not affect adenine nucleotide concentration or left ventricular hemodynamics. Following 5 min of anoxic perfusion, propranolol hearts showed improved ventricular performance concomitant with enhanced glycogenolytic flux and lactate production. Propranolol augmented high energy phosphate production (ATP/AMP = 5.19 +/- 0.42 vs. 3.39 +/- 0.42, p less than 0.02) and increased coronary flow (22.1 +/- 1.6 vs. 16.6 +/- 1.4 ml/min, p less than 0.02) during anoxia. Thus, propranolol supported glycogen stores following acute stresses, enhanced glycogenolytic energy production, increased coronary flow, and improved ventricular function during subsequent anoxia.
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PMID:Protective role of increased myocardial glycogen stores induced by propranolol. 121 34

Experiments were conducted on rats to study the dynamics of changes of the heart contractile function (CF) and some indices of myocardial energy metabolism during adaptation to moderate continuous 15-day stress. After 24 hours of stress a complex of shifts typical of an acute stress syndrome (mobilization of CF, reduction of the content of glycogen and creatine phosphate, increase of phosphorylase activity) was recorded. After 5 days of stress the absolute CF value reduced, particularly at rest (doubled), as a consequence of which the relative values of the maximally developing CF on the 5th second of an isometric load induced by compression of the aorta were 1.5 times those in the controls. The content of glycogen and creatine phosphate and the activity of phosphorylase were reduced by 25-30%. After 15 days the CF and the values of myocardial energy metabolism were normalized. Exclusion of the vagal tonus by atropine on the 5th day of stress showed that the low level of CF and reduced phosphorylase activity are not consequent upon heart exhaustion but are regulatory mechanisms.
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PMID:[Contractile function and some parameters of energy metabolism of the myocardium in the process of adaptation to the effect of moderate continuous stress]. 188 2

The effect of a single 1 h immobilization or repeated 1 h immobilization for 10 days on the levels of phosphoinositides in rat whole brain was investigated. Immediately after 1 h immobilization the levels of phosphatidylinositol (PI) and phosphatidylinositol 4,5-bisphosphate (PIP2) were decreased by 22 and 31%, respectively, but phosphatidylinositol 4-phosphate (PIP) was not significantly reduced. These changes were restored to normal levels 20 h after the immobilization. After repeated daily immobilizations the effect of stress on phosphoinositides was no longer observed. These results show that acute stress perturbs the concentration of PIP2 (precursor of second messengers) and indicate adaptation to acute stress in animals subjected to repeated stress.
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PMID:Influence of stress on phosphoinositides in rat brain. 215 39

The purpose of this study was to investigate the kinetic properties of human creatine kinase (CK) isoenzymes partially purified from heart and skeletal muscle. Utilizing the backward CK-catalyzed reaction of creatine phosphate + ADP in equilibrium creatine + ATP, Km values for heart and skeletal muscle CK MM (3.7 mmol/l) were significantly (p less than 0.05) greater than CK MB (2.1 mmol/l) which were significantly (p less than 0.05) greater than mitochondrial CK (1.8 mmol/l) at variable creatine phosphate and fixed ADP concentrations. However, Km values for similar isoenzymes from the two different tissues, i.e., CK MB from heart vs. skeletal muscle, were not different. These results show that kinetic analysis of CK isoenzymes cannot differentiate the tissue source of elevated blood CK isoenzymes after the acute stress of long distance running or after acute myocardial infarction.
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PMID:Kinetic characterization of human heart and skeletal muscle CK isoenzymes. 339 Nov 61

Plasma somatolactin (SL) concentrations in rainbow trout were examined under various physiological and environmental conditions. Background adaptation and feeding did not affect plasma SL levels. There was no consistent change in plasma SL levels during fasting for 21 days, although increased plasma growth hormone levels and decreased condition factor, hepatosomatic index and abdominal fat, occurred. Plasma SL concentrations increased during acute stress and also during exhaustive exercise resulting from being chased in shallow water. Elevation of plasma SL was associated with those of plasma cortisol, Ca2+, phosphate, and glucose levels. On the other hand, plasma level of prolactin was not affected in the stress and exercise experiments, although plasma GH and Na+ were raised in the fish 5 min after the onset of the stress. Our results suggest the involvement of SL in calcium and phosphate metabolism, acid-base regulation, or energy mobilization in the stressed or exercised trout.
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PMID:Effects of feeding, fasting, background adaptation, acute stress, and exhaustive exercise on the plasma somatolactin concentrations in rainbow trout. 763 67

The purpose of this study was to test the hypothesis that energy metabolism is impaired in residual intact myocardium of chronically infarcted rat heart, contributing to contractile dysfunction. Myocardial infarction (MI) was induced in rats by coronary artery ligation. Hearts were isolated 8 wk later and buffer-perfused isovolumically. MI hearts showed reduced left ventricular developed pressure, but oxygen consumption was unchanged. High-energy phosphate contents were measured chemically and by 31P-NMR spectroscopy. In residual intact left ventricular tissue, ATP was unchanged after MI, while creatine phosphate was reduced by 31%. Total creatine kinase (CK) activity was reduced by 17%, the fetal CK isoenzymes BB and MB increased, while the "adult" mitochondrial CK isoenzyme activity decreased by 44%. Total creatine content decreased by 35%. Phosphoryl exchange between ATP and creatine phosphate, measured by 31P-NMR magnetization transfer, fell by 50% in MI hearts. Thus, energy reserve is substantially impaired in residual intact myocardium of chronically infarcted rats. Because phosphoryl exchange was still five times higher than ATP synthesis rates calculated from oxygen consumption, phosphoryl transfer via CK may not limit baseline contractile performance 2 mo after MI. In contrast, when MI hearts were subjected to acute stress (hypoxia), mechanical recovery during reoxygenation was impaired, suggesting that reduced energy reserve contributes to increased susceptibility of MI hearts to acute metabolic stress.
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PMID:Impairment of energy metabolism in intact residual myocardium of rat hearts with chronic myocardial infarction. 788 57

Previous studies have shown a parallel relationship between pituitary vasopressin (VP) receptor content and responsiveness of the corticotroph during chronic stress. The regulation of pituitary VP receptors was further studied by analysis of V1b VP receptor mRNA levels in pituitaries of rats subjected to chronic immobilization, i.p. hypertonic saline injection (physical stress paradigms associated with increased pituitary responsiveness), and water deprivation, or to 2% saline in the drinking water (osmotic stress paradigms associated with decreased pituitary responsiveness). Northern blot hybridization with a 363 bp 32P-labelled fragment of the rV1b receptor cDNA coding sequence revealed two bands of about 3.7 and 3.2 Kb, whereas a probe directed to the 5' untranslated region recognized only the 3.7 Kb band. Repeated i.p. hypertonic saline injection, 3 times in 24 h at 8 h intervals, or daily for 8 days, increased the intensity of the 3.7 Kb band by 155 +/- 17.5% (P < 0.01) and 118 +/- 14.6% (P < 0.01), respectively, while the 3.2 Kb band increased by 122 +/- 39.3% (P < 0.01) only after 3 times injection. Smaller increases of 39 +/- 11 and 33 +/- 9% (P < 0.05) in the 3.7 Kb band were found after repeated immobilization 3 times in 24 h and 2 h for 8 days respectively. In situ hybridization studies confirmed significant increases (P < 0.05) in V1b receptor mRNA levels after 8 and 14 days repeated immobilization (63 +/- 19% and 83 +/- 10%) or i.p. hypertonic saline injection (110 +/- 13% and 73 +/- 20%). In response to acute stress, V1b receptor mRNA increased by 77 +/- 5% (3.7 Kb band) after 4 h immobilization for 1 h, whereas both bands were reduced by 49 +/- 5% and 45 +/- 5%, 4 h after a single i.p. hypertonic saline injection. The decrease in V1b receptor mRNA following a single i.p. hypertonic saline injection was prevented by pretreatment with a V1 receptor antagonist, suggesting that increased VP secretion may account for this effect. In spite of the decrease in V1b receptor mRNA following i.p. hypertonic saline injection, VP binding in pituitary membrane rich fractions, and VP-stimulated inositol phosphate formation in quartered hemipituitaries were increased by 24 and 39%, respectively. V1b receptor mRNA levels were unchanged or decreased following prolonged osmotic stimulation. These studies suggest that increased V1b receptor mRNA levels contribute to the VP receptor upregulation observed during repeated immobilization and i.p. hypertonic saline injection, whereas the lack of parallelism between V1b receptor mRNA and VP binding indicates that regulation of steady-state levels of V1b receptor mRNA is not a primary determinant in the control of pituitary VP receptor concentration during stress.
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PMID:Regulation of pituitary vasopressin V1b receptor mRNA during stress in the rat. 874 67

Nongenomic in vitro effects of aldosterone on the sodium-proton antiport and intracellular second messengers have been described in human mononuclear leukocytes, vascular smooth muscle cells, and endothelial cells. To test the potential physiological relevance of these effects, an in vivo 31P magnetic resonance spectroscopy study on the human calf at rest and during exercise was performed in 10 healthy volunteers receiving either 1 mg aldosterone or placebo iv in a double blind, randomized, cross-over trial. Spectra were analyzed for phosphocreatine, ATP, phosphomonoesters, inorganic intracellular phosphate, and intracellular pH. Resting values remained unchanged by aldosterone. After isometric contraction of the calf (50% body weight for 3 min), phosphocreatine recovered to significantly higher levels after application of aldosterone compared with placebo. Other parameters were not significantly changed by aldosterone. Effects appeared immediately after isometric contraction and, thus, occurred within 8 min of aldosterone administration. They are, therefore, likely to represent the first contemporary evidence of nongenomic in vivo effects of aldosterone in man. These findings also point to an involvement of aldosteron in the acute stress adaptation of cellular oxidative metabolism in human muscle physiology.
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PMID:Nongenomic effects of aldosterone on phosphocreatine levels in human calf muscle during recovery from exercise. 895 30

The creatine kinase (CK) system is involved in the rapid transport of high-energy phosphates from the mitochondria to the sites of maximal energy requirements such as myofibrils and sarcolemmal ion pumps. Hearts of mice with a combined knockout of cytosolic M-CK and mitochondrial CK (M/Mito-CK(-/-)) show unchanged basal left ventricular (LV) performance but reduced myocardial high-energy phosphate concentrations. Moreover, skeletal muscle from M/Mito-CK(-/-) mice demonstrates altered Ca2+ homeostasis. Our hypothesis was that in CK-deficient hearts, a cardiac phenotype can be unmasked during acute stress conditions and that susceptibility to ischemia-reperfusion injury is increased because of altered Ca2+ homeostasis. We simultaneously studied LV performance and myocardial Ca2+ metabolism in isolated, perfused hearts of M/Mito-CK(-/-) (n = 6) and wild-type (WT, n = 8) mice during baseline, 20 min of no-flow ischemia, and recovery. Whereas LV performance was not different during baseline conditions, LV contracture during ischemia developed significantly earlier (408 +/- 72 vs. 678 +/- 54 s) and to a greater extent (50 +/- 2 vs. 36 +/- 3 mmHg) in M/Mito-CK(-/-) mice. During reperfusion, recovery of diastolic function was impaired (LV end-diastolic pressure: 22 +/- 3 vs. 10 +/- 2 mmHg), whereas recovery of systolic performance was delayed, in M/Mito-CK(-/-) mice. In parallel, Ca2+ transients were similar during baseline conditions; however, M/Mito-CK(-/-) mice showed a greater increase in diastolic Ca2+ concentration ([Ca2+]) during ischemia (237 +/- 54% vs. 167 +/- 25% of basal [Ca2+]) compared with WT mice. In conclusion, CK-deficient hearts show an increased susceptibility of LV performance and Ca2+ homeostasis to ischemic injury, associated with a blunted postischemic recovery. This demonstrates a key function of an intact CK system for maintenance of Ca2+ homeostasis and LV mechanics under metabolic stress conditions.
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PMID:Creatine kinase-deficient hearts exhibit increased susceptibility to ischemia-reperfusion injury and impaired calcium homeostasis. 1510 71


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