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

The effects of repetitive myocardial ischemia on collateral circulation, ST deviation and epicardial wall motion were examined in 12 patients undergoing percutaneous transluminal coronary angioplasty (PTCA) for single left anterior descending artery disease. Rentrop collateral filling grade was assessed using contrast injection to the contralateral artery during the first and final episodes of coronary occlusion. ST deviation was measured by intracoronary electrocardiography. Epicardial wall motion (%pre PTCA) was measured by guide wire motion analysis according to the centerline method. Collateral filling grade was assessed 30 sec after balloon inflation. The ST segment and the epicardial wall motion were measured 60 sec after balloon inflation and deflation, respectively. There was no change in the collateral filling grade between the first and final episode of coronary occlusion. Patients with collateral filling grade I (R-I group, n = 4), II (R-II group, n = 3) and III (R-III group, n = 5) during coronary occlusion showed mean ST segment shifts of 13.2, 9.4, and 0.9 mm, respectively, and mean epicardial wall motion of 41.4%, 67.2%, and 78.5%, respectively. The collateral filling grade correlated with ST deviation and epicardial wall motion, and there was a significant correlation between epicardial wall motion and ST deviation (r = -0.67). Comparison of the R-I group or severe ischemia (n = 4) and the R-III group or slight ischemia (n = 4) during coronary occlusion for the fourth time showed the effect of preconditioning was obtained in R-I group. More R-III group patients than R-I group had hyperkinetic epicardial wall motion during coronary reperfusion. Stunned myocardium was demonstrated in both R-I group and R-III group patients. Epicardial wall motion was poorer in the R-I group than R-III group. We concluded the following: There is no change in the grade of collaterals during repetitive coronary occlusion, and there is a relationship between the grade of collateral and degree of myocardial protection; there is good correlation between ST segment and epicardial wall motion; ischemic preconditioning is obtained during repetitive severe myocardial ischemia; recovery from brief episodes of slight myocardial ischemia is associated with hyperkinesia of epicardial wall motion; the reduction of stunned myocardium is related to the degree of premyocardial ischemia; preconditioning is sufficient to cause myocardial stunning, but myocardial stunning is insufficient to cause preconditioning.
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PMID:[Effects of repetitive myocardial ischemia on collateral circulation, ST deviation and epicardial wall motion]. 912 Jul 96

The findings of troponin I (TnI) proteolysis (in isolated rat hearts) and induction of selected sarcoplasmic reticulum (SR) calcium-regulatory genes (after repetitive total coronary occlusions in swine) have given rise to the hypothesis that the time course of functional recovery of stunned myocardium reflects the resynthesis of reversibly damaged proteins. Although stunning occurs after brief total occlusions and prolonged partial occlusions (ie, short-term hibernation), the time course of functional recovery varies from a few hours to several days, suggesting that the severity of protein damage or mechanisms responsible for the dysfunction may differ. To study this, we examined SR gene expression and TnI degradation in stunned myocardium produced by 10-minute total left anterior descending coronary artery (LAD) occlusions (n=4) or 1-hour partial LAD occlusions, in which flow was reduced to approximately 50% of control values for 60 minutes (n=6) in swine. One hour after reperfusion, LAD wall thickening was severely depressed in both models despite normal perfusion and no triphenyltetrazolium chloride evidence of necrosis. Normal myocardium exhibited TnI immunoreactivity at 31 kDa and a weak secondary band at 27 kDa. Irreversible injury or calpain activation in vitro produced a marked increase in the intensity of the 27-kDa band, consistent with TnI degradation. Stunned myocardium demonstrated no change in the 31- or the 27-kDa band, and the percentage of the 27- to 31-kDa band remained constant after 10-minute total occlusions (LAD, 5.9+/-0.9%; normal, 4.9+/-1.6%) and 1-hour partial occlusions (LAD, 8.5+/-1.9%; normal, 7.3+/-1.4%) and in sham controls (LAD, 10.9+/-1.5%; normal, 9.8+/-1.4%). Northern analysis showed no alterations in TnI or SR gene expression, but the stress protein HSP-70 was variably induced. Thus, stunned myocardium occurs without TnI degradation or altered SR gene expression, indicating that additional mechanisms are responsible for the reversible dysfunction after single episodes of regional ischemia in swine.
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PMID:Absence of troponin I degradation or altered sarcoplasmic reticulum uptake protein expression after reversible ischemia in swine. 1047 76

The effects of tetrandrine (Tet) on the contractile function and microvascular permeability in stunned rat myocardium in vivo were studied. Stunned myocardium was induced by 15 (MS(15) group) or 20 (MS(20) group) min of myocardial ischemia plus 60 min of reperfusion. The following was shown. (1) FITC-BSA concentration was 166.0 +/- 7. 9 microg/g myocardium in the control group. The concentrations in ischemic myocardium increased by 35.4 and 45.6% in MS(15) and MS(20) groups respectively (p<0.05). (2) Administration of Tet (64.2 and 96. 3 micromol/kg, I.P.) 20 min before ischemia not only ameliorated the contractile function, but also reduced the FITC-BSA concentrations in ischemic myocardium. At 60 min after reperfusion, the contractile function parameters in Tet-treated groups were significantly superior to those in corresponding stunning groups. FITC-BSA concentrations in Tet-treated groups were lower than those in stunning groups. Then, there was already no significant difference in FITC-BSA concentrations between Tet-treated groups and the control group. The FITC-BSA concentrations at the end of experiments were correlated negatively with dp/dt(max) (r = -0.83, p<0.01). (3) Tet inhibited KCl-induced calcium influx in isolated cardiomyocytes. The results suggest that Tet given before ischemia may be involved in the reduction of microvascular permeability in stunned myocardium, which might be associated with its calcium channel blocking effect.
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PMID:The effects of tetrandrine on the contractile function and microvascular permeability in the stunned myocardium of rats. 1060 35

The identification of myocardial viability in patients with coronary artery disease and left ventricular dysfunction (LVD) has important clinical and prognostic implications. Two terms commonly used to define clinical conditions of potentially reversible contractile dysfunction are stunned myocardium and hibernating myocardium. Stunned myocardium refers to transient depression of contractile function secondary to an acute ischemic insult. Hibernating myocardium is a form of contractile dysfunction of living myocytes in the setting of chronic ischemia or chronically reduced flow reserve. Numerous observational studies have shown improved clinical outcomes after revascularization of patients with LVD and evidence of myocardial viability, although patients with nonviable myocardium have not been shown to have the same benefits. The use of noninvasive techniques to determine myocardial viability provides important information to guide clinicians in deciding which patients with LVD are likely to receive benefit from a revascularization procedure. Positron emission tomography, single-photon emission computed tomography, dobutamine echocardiography, and cardiac magnetic resonance imaging each have advantages and limitations.
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PMID:Assessment of myocardial viability: review of the clinical significance. 1912 80

Recovery of Contractile Function of Stunned Myocardium in Chronically Instrumented Dogs Is Enhanced by Halothane or Isoflurane. By Warltier DC, al-Wathiqui MH, Kampine JP, and Schmeling WT. ANESTHESIOLOGY 1988; 69:552-65. Reprinted with permission.Following brief periods (5-15 min) of total coronary artery occlusion and subsequent reperfusion, despite an absence of tissue necrosis, a decrement in contractile function of the postischemic myocardium may nevertheless be present for prolonged periods. This has been termed "stunned" myocardium to differentiate the condition from ischemia or infarction. Because the influence of volatile anesthetics on the recovery of postischemic, reperfused myocardium has yet to be studied, the purpose of this investigation was to compare the effects of halothane and isoflurane on systemic and regional hemodynamics following a brief coronary artery occlusion and reperfusion. Nine groups comprising 79 experiments were completed in 42 chronically instrumented dogs. In awake, unsedated dogs a 15-min coronary artery occlusion resulted in paradoxical systolic lengthening in the ischemic zone. Following reperfusion active systolic shortening slowly returned toward control levels but remained approximately 50% depressed from control at 5 h. In contrast, dogs anesthetized with halothane or isoflurane (2% inspired concentration) demonstrated complete recovery of function 3-5 h following reperfusion. Because the anesthetics directly depressed contractile function, additional experiments were conducted in which a 15-minute coronary artery occlusion was produced during volatile anesthesia; however, each animal was allowed to emerge from the anesthetized state at the onset of reperfusion. Similar results were obtained in these experiments, demonstrating total recovery of contractile function within 3-5 h following reperfusion. Thus, despite comparable degrees of contractile dysfunction during coronary artery occlusion in awake and anesthetized dogs, the present results demonstrate that halothane and isoflurane produce marked improvement in the recovery of segment function following a transient ischemic episode. Therefore, volatile anesthetics may attenuate postischemic left ventricular dysfunction occurring intraoperatively and enhance recovery of regional wall motion abnormalities during reperfusion.
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PMID:Classic Papers Revisited: An Early Study of Cardioprotection by Volatile Anesthetics: A Behind-the-scenes Look. 2998 98


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