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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A transient forebrain ischemia produced a delayed neuronal death of the hippocampus pyramidal cells in stroke-prone spontaneously hypertensive rats (SHRSP). Long term exposure of rats to stress has been reported to induce deleterious effects on the brain including morphological neuronal degeneration in the hippocampus. The present study was designed to examine the effects of psychological and physical stress on the ischemia-related neuronal death and the effects of 5-hydroxytryptamine(4) (5-HT(4)) receptor antagonist. SHRSP were exposed to the psychological or physical stress for 60 min in the communication box once or repeatedly for 3 days and occluded. SB204070, a 5-HT(4) receptor antagonist was injected before the occlusion. Seven days after the occlusion, the number of the neurons damaged morphologically was examined. A transient bilateral carotid occlusion produced a neuronal death of the CA1 subfield of the hippocampus in a time-dependent manner between 3 and 10 min. A 4 min occlusion induced very little morphological damage and a 5 min one produced a significant neuronal death. Exposure of rats to the psychological stress during 60 min for 3 days before the ischemic insults damaged the pyramidal cells by 4 min ischemia much more than without stress. Physical stress daily for 3 times also increased the damaged neurons. Pretreatment of SB204070 0.1 mg/kg after the stress exposure for 3 days significantly decreased the neuronal damage exacerbated by the stress exposure; however, it did not alter the damage induced by 4 or 10 min occlusion without stress. These results suggest that the repeated exposure of animals to the stress dramatically exacerbates the neuronal death by a transient ischemia and the 5-HT(4) receptor may be involved in the stress-induced exacerbating mechanism of the neuronal damage.
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PMID:Involvement of 5-hydroxytryptamine4 receptor in the exacerbation of neuronal loss by psychological stress in the hippocampus of SHRSP with a transient ischemia. 1272 57

This brief review highlights human studies on the role of nitric oxide (NO) and limb vasodilation conducted at the Mayo Clinic over the last 10 years. These studies have attempted to determine whether NO is responsible for the "unexplained" limb vasodilation seen with body heating, limb ischemia, exercise, and mental stress. Our findings are placed in context with data from others, and possible future areas of study are identified.
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PMID:Nitric oxide and physiologic vasodilation in human limbs: where do we go from here? 1295 73

Fear, anger, and grief may precipitate myocardial ischemia and infarction. The prognosis of patients with inducible ischemia during mental stress is worse than in those without inducible ischemia. The sympathetic nervous system plays an important role in stress-associated changes in cardiovascular regulation and contributes to cardiovascular morbidity and mortality by inducing vasoconstriction and tachycardia, as well as arrhythmia. Hostility--previously termed type A personality--is often associated with sympathetic hyperreactivity to mental stress and carries an increased risk for atherosclerotic vascular disease. As endothelial dysfunction is an early manifestation of atherosclerosis, the impact of mental stress on endothelial function is also important. Acute mental stress induces prolonged endothelial dysfunction in healthy volunteers, which is prevented by selective endothelin A receptor antagonism. This represents an important link between mental stress and atherosclerotic vascular disease. In addition, patients with depression show hypercortisolemia, and changes in platelet function leading to a prothrombotic state. These findings help to explain the increased cardiovascular risk in patients with depression.
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PMID:[Pathophysiologic cardiovascular changes in stress and depression]. 1466 4

Panic disorder serves as a clinical model for testing whether mental stress can cause heart disease. Our own cardiologic management of panic disorder provides case material of recurrent emergency room attendances with angina and electrocardiogram ischemia, triggered arrhythmias (atrial fibrillation, ventricular fibrillation), and documented coronary artery spasm, in some cases with coronary spasm being complicated by coronary thrombosis. Application of radiotracer catecholamine kinetics and clinical microneurography methodology suggests there is a genetic predisposition to panic disorder that involves faulty neuronal norepinephrine uptake, possibly sensitizing the heart to symptom generation. During panic attacks there are large sympathetic bursts, recorded by clinical microneurography in the muscle sympathetic nerve neurogram, and large increases in cardiac norepinephrine spillover, accompanied by surges of adrenal medullary epinephrine secretion. In other conditions such as heart failure and presumably here also, a high level of sympathetic nervous activation can mediate increased cardiac risk. The sympathetic nerve cotransmitter, neuropeptide Y (NPY), is released from the cardiac sympathetics during panic attacks, an intriguing finding given that NPY can cause coronary artery spasm. There is ongoing, continuous release of epinephrine from the heart in panic sufferers, perhaps attributable to epinephrine loading of cardiac sympathetic nerves by uptake from plasma during panic attacks, or possibly to in situ synthesis of epinephrine through the action of intracardiac phenylethanolamine-N-methytransferase (PNMT) activated by repeated cortisol responses. We have used internal jugular venous sampling and measurement of overflowing lipophilic brain monoamine metabolites to quantify brain norepinephrine and serotonin turnover in untreated patients with panic disorder. We find normal norepinephrine turnover but a marked increase in brain serotonin turnover in patients with panic disorder, in the absence of a panic attack, which presumably represents an underlying neurotransmitter substrate for the condition.
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PMID:Cardiac sympathetic nerve biology and brain monoamine turnover in panic disorder. 1524 Apr 8

The aging heart has an impaired response to many kinds of stress. In clinical practice, there is a need for senescence-specific therapies to protect against stress and for biochemical markers of senescence to identify those patients most in need of therapy. In isolated rat hearts, in human tissues, and in a clinical trial, we have shown previously that coenzyme Q(10) has the ability to protect the heart against stress especially in senescence. We recently have devised a regimen of therapy to protect the senescent heart against stress, combining metabolic therapy (coenzyme Q(10), alpha lipoic acid, magnesium orotate, and omega 3 polyunsaturated fatty acids) with physical exercise and mental stress reduction. The preliminary results of this program are promising. In an endeavor to predict the likely response of individual senescent hearts to stress, we correlated the tissue load of mitochondrial DNA deletions and total cellular mitochondrial DNA copy number in human cardiac tissue with recovery of the same tissue from ischemia/reperfusion stress. We found that these mitochondrial markers actually were less predictive of impaired response to stress than age alone. We conclude that the aging heart has a diminished capacity to recover from stress that is not readily predictable by cardiac content of intact mitochondrial DNA and that this recovery can be improved by metabolic therapy combined with physical exercise and mental stress reduction.
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PMID:Response of the senescent heart to stress: clinical therapeutic strategies and quest for mitochondrial predictors of biological age. 1524 98

In the field of forensic medicine, shock has been identified as a cause of death owing to various kinds of exogenous insults. The etiology and pathogenesis of shock cannot be explained well by the usual gross appearance in medicolegal autopsies, because it is now generally established that the shock is a functional reaction of the vascular system to bodily injury, and that several organs are secondarily impaired during shock. Thus it seemed to forensic pathologists that these morphological changes in several organs after shock did not reveal any significant differences among the causes of death. We approached to the induction mechanism of shock, and we investigated what etiology induced these morphological changes after shock in order to identify shock as the cause of death. It is now generally accepted that the kidney is a target organ of shock, so we mainly investigated the cause of kidney disorder in a case of burn shock and hemorrhagic shock. 1. Consequences of bacterial translocation (BT) in the shock. The concept of BT indicates that the beginning of shock is induced by the loss of gut barrier function and consequent translocation of bacteria. In general, impaired gut barrier function can be caused either during the shock period by decreased intestinal blood flow and reduced oxygen delivery, resulting during reperfusion in a stage of increased intestinal blood flow, or at a later stage again by reduced flow. A variety of physiological stresses, such as trauma, hemorrhage, thermal injury, surgical operation, various kinds of drags and mental stress, have been shown to cause failure of the gut mucosal barrier, with translocation of bacteria/endotoxin from the gastrointestinal into the mesenteric lymph nodes, and translocation into remote organs and systemic circulation. 2. Burn shock. We designed to evaluate the BT in a burn shock rat model (following 20% full-thickness scald injury). The p38 MAPK pathway is an important stress-responsive signal molecule pathway, and it is responsible for the production and signal transduction of cytokines. This pathway is activated by the bacterial LPS or ischemia, so we examined the effects of FR167653, a specific inhibitor of p38 MAPK, on the development of renal failure after the burn-induced intestinal barrier damage. Our study demonstrated that viable bacteria reached the remote organs after burn by quantitative bacterial culture data and FR167653 blocked the burn-induced intestinal barrier damage, and the immunohistochemical data showed that FR167653 prevented the accumulation of polymorphonuclear leukocytes (PMNs) in the glomerular capillaries after burn, and blockaded the burn-induced renal failure by serum UN assay. FR167653 especially decreased the phosphorylation levels of p38 MAPK in the infant kidney after burn, and TNF-alpha and IL-1beta mRNA decreased through the p38 MAPK pathway. The above-mentioned facts do provide additional support for the hypothesis that postburn renal failure is mediated by endotoxin associated with the bacterial translocation, and we identified the pathophysiologic role of p38 MAPK pathway in the development of renal failure after the burn-induced intestinal barrier damage. 3. Hemorrhagic shock. We evaluated the role of endogenous TNF-alpha in the renal failure and gut bacterial translocation induced by mild hemorrhagic shock (16.7% bleeding of total body blood via a common carotid catheter without fluid resuscitation). FR167653, a potent inhibitor of TNF-alpha up regulation through p38 MAPK pathway, significantly inhibited these increases of TNF-alpha. Adding to this, our study demonstrated that FR167653 prevented renal failure, such as the infiltration of inflammatory cells and tubular cell necrosis after hemorrhage, and the intestinal barrier damage was also dramatically improved by FR167653 treatment. These results show that derived endogenous TNF-alpha plays a key role in renal failure through p38 MAPK activation during the early phase of mild hemorrhagic shock, including the possible participation of BT. According to these results, we hypothesized that the invading leukocytes induced these organs failures after hemorrhagic shock, so we examined the appearances of leukocytes by the immunohistochemical myeloperoxidase (MPO) staining (marker staining for PMNs). The incidences of PMNs in these organs after mild hemorrhagic shock increased significantly, and FR157653 prevented the appearance of PMNs. These results showed the possible effective role of the PMNs on the occurrence of organ failure caused by mild hemorrhagic shock. 4. Forensic practice. Six hundred and seven forensic autopsy cases in our department of forensic medicine during the past 11 years between 1992 and 2002 were analyzed with regard to the cause of death. Shock cases accounted for 18% of all forensic autopsy cases, and among them 65% of cases identified hemorrhagic shock as the cause of death. So we investigated what good grounds to clearly identify the cause of death induced by hemorrhagic shock. Our experimental hemorrhagic shock data showed PMNs activation and priming during hemorrhagic shock, and it might be closely related to BT and remote organ failure. Consequently, we used the MPO staining method, and we immunohistochemically investigated several organs of our practical autopsy cases to detect the appearance of PMNs as a marker of shock induction. We compared the hemorrhagic shock with other causes of death, such as blood loss, asphyxia, drawing and head injury (intracranial hemorrhage). In every organ, a significant appearance of PMNs was observed in the hemorrhagic shock compared to the other causes of death. Especially, the appearance of PMNs in the heart was clear than that of the other organs in the hemorrhagic shock cases. Therefore, detecting the appearance of PMNs as a marker of shock induction is a very useful and significant method forjudging the cause of death in forensic practice.
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PMID:[Induction mechanism of shock: applying the etiology in judgment of the cause of death in forensic practice]. 1552 67

To examine the susceptibility to myocardial ischemia with mental stress in patients who have coronary artery disease and normal left ventricular (LV) function versus those who have impaired LV function, we examined 58 patients who had coronary artery disease, including 22 who had normal LV function (ejection fraction >/=50%), 16 who had mild to moderate LV dysfunction (ejection fraction 30% to 50%), and 20 who had severe LV dysfunction (ejection fraction </=30%) and underwent bicycle and mental stress testing with myocardial perfusion scintigraphy on consecutive days in random order. Ischemia was assessed based on summed difference scores in regional rest versus stress myocardial perfusion and defined as a summed difference score >3. At comparable double products across the 3 groups, ischemia was induced with mental stress more frequently in patients who had severe LV dysfunction (50%) than in those who had normal LV function (9%; p <0.01). The frequency of exercise-induced ischemia was different only between those who had mild/moderate LV dysfunction and those who had normal LV function (56% vs 18%, respectively, p <0.05). The pattern of mental stress versus exercise ischemia differed between groups (p <0.02): there was a higher prevalence of mental stress ischemia versus exercise ischemia in patients who had severe LV dysfunction (p = 0.06), a marginally higher prevalence of exercise versus mental stress ischemia in those who had moderate LV dysfunction (p = 0.07), and no difference in mental stress versus exercise ischemia in those who had normal LV function. Thus, at comparable double products during mental stress and similar extent of coronary artery disease, ischemia with mental stress was induced more frequently in patients who had severe LV dysfunction than in those who had normal LV function. These data suggest that mental stress ischemia may be of particular clinical importance in patients who have coronary artery disease and LV dysfunction.
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PMID:Comparison of mental stress-induced myocardial ischemia in coronary artery disease patients with versus without left ventricular dysfunction. 1567 May 38

From the epidemiological view point, chronic Mg intake deficiency could play a role of the onset of ischemic heart disease. Mg intake deficiency increases not only vaso-spasmobility of coronary artery, but also exacerbates several coronary risk factors such as hypertension, diabetes mellitus, and mental stress. We have previously reported that blood concentrations of Mg(2+) in patients with ischemic heart disease, especially acute coronary syndrome, was lower than that of healthy subjects. The lower blood concentrations of Mg(2+) may be a result of serious cardiac ischemia. According to the large-scale clinical trials, the efficacy of Mg administration to the patients with acute myocardial infarction has not been established, however, supplementary Mg may keep blood Mg(2+) level adequately and protect cardiac injury from cardiac ischemia.
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PMID:[Magnesium and ischemic heart disease]. 1569 54

This study examined gender differences in smoking-related analgesia and stress-induced analgesia (SIA), as a function of pain modality. Forty men (20 smokers, 20 nonsmokers) and 37 women (17 smokers) were tested twice for pain sensitivity to tourniquet ischemia, thermal heat, and cold pressor tests; once following mental stress and once following rest control, counterbalancing order. Cardiovascular and neuroendocrine responses to mental stress were also examined. While expected gender differences in pain sensitivity were observed, women smokers had greater threshold and tolerance times to ischemic pain than women nonsmokers (P<0.05) when pain testing followed rest. Male smokers had greater threshold and tolerance to cold pressor pain than male nonsmokers (P<0.05) after both rest and stress. Only women showed evidence for SIA, since women nonsmokers demonstrated greater ischemic pain threshold and tolerance following mental stress versus rest (P<0.05), and all women reported lower thermal heat pain unpleasantness after stress versus rest (P=0.05). Only nonsmokers showed expected inverse relationships between sympathetic and hypothalamic-pituitary-adrenal (HPA) axis reactivity measures and sensitivity to pain. Smokers showed evidence for blunted HPA-axis function at rest and stress. These results indicate that analgesia related to both being a smoker and stress is influenced by gender and pain modality. The reduced pain perception in smokers and absence of relationships between endogenous pain regulatory mechanisms and pain sensitivity may reflect a maladaptive response to chronic smoking.
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PMID:Cigarette smoking, stress-induced analgesia and pain perception in men and women. 1577 63

Reactive oxygen species (ROS) cause damage to the structure and function of tissues. Therefore tissues have systems that eliminate ROS. Bilirubin is one antioxidant that reacts with ROS to produce oxidative metabolites. Biopyrrins are one of the metabolites, the level of which in urine reflects oxidative stress. They are measured by non-competitive inhibition ELISA that employs anti-bilirubin antibody (24G7) and the results are corrected for the urinary concentration of cereatinine. Some reports suggested that psychological stress increased oxidative stress markers. Urinary biopyrrins were also elevated by speech stress, and the subjective stress score recorded by the speakers correlated with the level. The result suggests that bilirubin might eliminate ROS generated by psychological stress. From the beginning of the study of biopyrrins, their urinary level has been known to be increased by surgical stress. Furthermore, it was significantly higher in a major operation patient group than in a minor one, and correlated with operation duration. Sepsis increased the level in surgical patients. Ischemia-reperfusion elevates ROS and, as a result, biopyrrin production. An increase in urinary biopyrrins was observed in a coronary spastic angina group after a spasm provocation test, and the level in myocardial infarction patients with NYHA (New York Heart Association) classification became higher. Correlation between urinary biopyrrins and plasma B-type natriuretic peptide (BNP) was also reported. Research that determines the structures of biopyrrins and their clinical application are in progress.
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PMID:[Oxidative stress related diseases and biopyrrins]. 1579 50


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