Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thromboxane A2 (TxA2) appears to be an important mediator of ischemia and hypoxia. Despite its short half-life and the fact that it may not circulate in the blood until its values become quite high, TxA2 contributes to the pathogenesis of cardiopulmonary diseases (e.g., sudden death, myocardial ischemia, circulatory shock). It does so because it propagates its own formation by activating platelets and constricting blood vessels, thus activating more TxA2 and trapping it locally within an ischemic or hypoxic region. TxA2 concentrations in the extracellular fluid of lymph of ischemic regions may be much higher than that occurring in nonischemic, normally perfused regions. Specific and potent Tx receptor antagonists (TxRA) have recently become available for study. The TxRA are useful tools in the study of the pathophysiology of Tx-dependent disease processes and have been found to be effective in a variety of ischemic disorders including circulatory shock, myocardial ischemia, and sudden cardiopulmonary death. Moreover, inasmuch as early work indicates that these agents are both safe and effective in humans, Tx receptor antagonists may be employed as therapeutic agents in several cardiovascular disease states. Further investigation is necessary to clarify the role of TxRA as therapeutic agents.
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PMID:A pharmacological approach to thromboxane receptor antagonism. 294 38

Silent myocardial ischemia is undoubtedly the second most prevalent cardiovascular disease after arterial hypertension. Considering its statistical and social importance, the authors, while admitting the less specific coronary character of this entity, do not agree with its being omitted from the last classification of coronary disease (1979), in which especially/angina pectoris and myocardial infarction are emphasized. In the present paper, which opens up an investigation into initially silent ischemia carried out on a great number of cases, the authors discuss the preliminary observations derived from a ten-year (1976-1986) follow up of 56 cases of initially asymptomatic electrocardiographic ischemia with an electric localization suggesting specific coronary territories. It results that the incidence of an unfavourable evolution (myocardial infarction, angina pectoris, onset of arrhythmias or conduction defects) is somewhat higher in males than in females, but not up to 3-4 times as stated in most populational studies on myocardial infarction. The electrocardiographic and clinical improvements are, however, definitely more frequent (4 times) in women than in men (p less than 0.002). Of the 56 cases studied, 26.6% worsened, 23.2% improved, and 21.5% presented no change along the 10 years of follow up (the others showed electrocardiographic evolutions without a clinical expression, while 2 died from a noncardiac cause.
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PMID:Asymptomatic electrocardiographic ischemia and silent myocardial ischemia. 312 9

The hemorheologic changes in three groups of patients suffering from acute and chronic cerebrovascular diseases were studied. Firstly, a horizontal study on 57 patients with definite stroke and on 49 patients with TIA was made. Plasma viscosity, whole blood filtration rate, fibrinogen concentration and hematocrit were evaluated as markers of the rheological property of blood. Blood samples were drawn within 6 h from the onset of vascular syndrome. The findings were compared with values obtained in 112 as controls. At the same time, washed red cell filtration rate, together with lactoferrin, betaglucuronidase and beta-thromboglobulin plasma level were assayed. In both groups the onset of the vascular storm was associated with a marked increase of plasma fibrinogen and of blood and plasma viscosity and a significant decrease of whole blood filterability. Lactoferrin, betaglucuronidase and beta-thromboglobulin levels were also significantly increased. Following this, a longitudinal study was performed on 27 patients with definite stroke and 32 patients with TIA. The clinical regression of acute stroke was associated with the progressive reduction of rheological abnormalities. Finally, 81 patients with clinical diagnosis of cerebrovascular disease due to previous stroke or repeated TIA were studied together. An increase of blood viscosity, of fibrinogen concentration and of hematocrit and a decrease of blood filtration rate together with higher levels of beta-thromboglobulin were registered. These results confirm the existence of an association between CVD and hemorheological alterations and suggest more in depth research directed towards identifying the significance of these alterations in the pathogenesis of tissue ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hemorheological factors in the pathophysiology of acute and chronic cerebrovascular disease. 316 Apr 74

PAP of harvested livers is routinely used to minimize parenchymal anoxia during storage. PP is compared with PAP to evaluate the relative reliability of PAP. Sixty female Landrace pigs were used for 30 OLTs. Group 1 livers underwent PP, whereas group 2 livers were treated with PAP. The cold ischemic time was less than 120 minutes for both groups, with no warm ischemia. Intraoperative and 24-hour postoperative biochemical, coagulation, and histocytological data were analyzed. Morphological studies of cellular damage were based on the percentage of CVD and KP and classified as light, moderate, and severe damage. Data, at closing, were compared by using Fisher's test (group 1 v group 2,P = 0.003 for light damage and P = .04 for severe damage; first postoperative day for group 1 v group 2, P = .133 for light damage and P = .25 for severe damage. Blood samples at closing and 24 hours postoperatively showed significant differences between groups 1 and 2: At closing for groups 1 and 2, respectively: AST, 968.9 +/- 742.7 and 327.4 +/- 174.7 IU/L (P less than .001); ALT, 63.1 +/- 40.3 and 20.3 +/- 5.3 IU/L (P less than .001); AP, 292.2 +/- 107.1 and 139.5 +/- 45.3 IU/L (P less than .001); and 24 hours postoperatively for groups 1 and 2, respectively: AST, 1,664.9 +/- 917.8 and 419.3 +/- 230.9 IU/L (P less than .001): ALT. 180.4 +/- 28.9 and 66.4 +/- 17.5 IU/L (P less than .001); AP, 602.1 +/- 153.3 and 255.7 +/- 116.3 IU/L (P less than .01). Comprehensively, the results reflect a better perfusate distribution of the PAP livers compared with PP ones: uniform organ preservation, faster metabolic recovery, and reduced postoperative mortality.
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PMID:Comparison of combined portal-arterial versus portal perfusion during liver procurement. 327 50

Atherogenic traits, living habits, signs of preclinical disease, and susceptibility all contribute to cardiovascular disease. High low-density lipoprotein is positively related to coronary heart disease, and high high-density lipoprotein is inversely related. Systolic or diastolic hypertension at any age in either sex contributes powerfully. The impact of diabetes is greater for women and varies with the number of accompanying risk factors. High-normal fibrinogen values further escalate risk of these atherogenic factors. An atherogenic life-style is typified by a diet excessive in fat, calories, and salt; sedentary habits; unrestrained weight gain; and cigarette smoking. Moderate alcohol use may be beneficial. Use of oral contraceptives beyond age 35 years and in conjunction with cigarette smoking predisposes one to thromboembolism. Type A behavior carries an increased risk, and men married to more highly educated women and to women in white-collar jobs are more vulnerable. Signs of preclinical ischemia include silent myocardial infarction, left ventricular hypertrophy on ECG, blocked intraventricular conduction, and repolarization abnormalities. Measures of innate susceptibility include a family history of early cardiovascular disease. Quantitative combination of risk factors provides optimal prediction, including persons with multiple marginal abnormalities. Preventive management should also be multifactorial and requires a commitment to behavior modification and alteration in life-style.
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PMID:New perspectives on cardiovascular risk factors. 330 Feb 33

Repeated CBF-measurements can be performed after inhalation or intravenous injection of 133Xe. After the development of a bicompartmental model by Obrist et al. in 1975 atraumatic CBF-measurements became widely used but there were still some difficulties concerning the sensitivity of different flow-indices towards CBF changes in normals under test conditions or ischemia in stroke patients. Due to the "slippage phenomenon" mostly noncompartmental flow-indices are used for the detection of ischemic brain areas. In this study a scintillation camera, that is usually available in every nuclear medicine department, was used for atraumatic CBF-studies. A collimator consisting of hexagonal lead tubes (septa 0.2 mm thick; FWHM 1.7 cm in 10 cm) was constructed for this purpose. The obtained counting rate varied between 2432 and 9081 cps over the whole hemisphere and 116-1094 cps in regions of approximately 2.5 X 2.5 cm. In 31 patients with CVD CBF was measured with the intracarotid (i.c.) technique and 1 hour later after i.v. 133Xe-injection. Intravenous flow values were comparable to those obtained after i.c. 133Xe injection (fB X MFr = 0.904; p less than 0.001). In 12 of the used 13 regions also significant correlation coefficients were found. In order to estimate the reproducibility of the intravenous injection method CBF-measurements were performed in both hemispheres of 10 patients on two consecutive days. Highly significant correlation coefficients were found for hemispheric blood flow (r = 0.933; p less than 0.001) and temporal, frontotemporal, temporoparietal and praecentral regions, while in the high parietal, frontal and occipital region lower reporducibility was found. Normal CBF-values were obtained from 12 healthy volunteers (MF right hemisphere: 50.7 +/- 4.6 ml/100 g/min; MF left hemisphere: 50.6 +/- 4.6 ml/100 g/min). MF did not show any hyperfrontality, while F1 and the ISI gave highest flow values in frontal regions. The clinical status of 76 patients suffering from cerebral ischemia (68 with flow disturbances in one hemisphere, 8 with vertebrobasilar insufficiency) was estimated by a semiquantitative scorescale at time of admission and after an observation period lasting from 6 to 35 months. In each case CBF was measured twice: once in the subacute stage after onset of symptoms and once after the observation period. The duration of neurologic symptoms (TIA, RIND, CS) was compared to the obtained flow values. A significant relationship was found between the duration of symptoms and impairment of CBF, thus showing the prognostic value of intravenous CBF measurements.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Noninvasive measurement of cerebrovascular circulation with the scintillation camera. A neurologic nuclear medicine study]. 659 71

A double-blind study comparing electrocardiographic (ECG) abnormalities induced by methyglucamine iodamide and methylglucamine/sodium diatrizoate was conducted in 189 patients. The media were each administered by both bolus and infusion. Iodamide caused fewer ECG changes both by injection and infusion. This contrast medium also resulted in fewer ECG changes in the patient groups with known prior ECG abnormalities, cardiovascular disease, arrhythmias, ischemia, or renal impairment and in those over 50 years of age. Digitalis did not increase the frequency of ECG abnormalities with either medium. With diatrizoate, the lower bolus dose produced as many major ECG changes in the presence of preexisting ECG abnormalities (arrhythmias, ischemia) or prior cardiovascular disease as the three-times-larger infusion dose more slowly administered; conversely, the opposite was found when renal insufficiency or older age existed. The conclusion is that iodamide media caused fewer ECG abnormalities and may be less hazardous.
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PMID:Contrast-medium-induced electrocardiographic abnormalities: comparison of bolus and infusion of methylglucamine iodamide and methylglucamine/sodium diatrizoate. 660 Mar 6

Persistence of impaired ventricular function after repair of cyanotic congenital heart defects may be due to previous exposure to chronic hypoxemia or to perioperative ischemic injury. Clarification of this phenomenon was sought in a canine model of cyanotic cardiovascular disease (Group I), in which the left atrium was anastomosed proximal to the banded pulmonary artery. Animals that had pulmonary artery banding alone (Group II) or no prior surgical intervention (Group III) served as controls. All Group I animals became cyanotic during the study period (arterial oxygen tension, 38 +/- 4 mm Hg; hematocrit, 55 +/- 5%). Radionuclide-determined ejection fractions performed three months after operation showed significant depression of global biventricular function by 16 to 29% (p less than 0.05) compared with groups II and III. On cardiopulmonary bypass, all hearts were subjected to 4 degrees C potassium cardioplegic arrest and reperfusion with serial assays for myocardial adenosine triphosphate (ATP) and creatine phosphate (CP) levels. The ATP and CP stores in each ventricle were similar at all sampling intervals, and preischemic levels were comparable in cyanotic and control groups. However, ATP levels were significantly depressed 37 to 43% from preischemic levels (p less than 0.02) after arrest and reperfusion in cyanotic dogs, but they were preserved in Groups II and III. During ischemia, CP stores were depleted to 27% of preischemic values in Group I but only to 46 to 63% of preischemic levels in the control groups (p less than 0.05). These data indicate that chronic hypoxemia impairs global ventricular function and predisposes to the accelerated depletion of high-energy phosphates during cardioplegic arrest.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chronic hypoxemia depresses global ventricular function and predisposes to the depletion of high-energy phosphates during cardioplegic arrest: implications for surgical repair of cyanotic congenital heart defects. 671 31

Left ventricular filling dynamics were examined at rest and during supine bicycle exercise in 33 patients at cardiac catheterization; 23 had coronary artery disease (ischemia group), five with prior infarction had an akinetic area at rest (scar group), and five had minimal cardiovascular disease (control). Peak filling rate and mean filling rate during the first half and second half of diastole were assessed by biplane angiography. Simultaneous micromanometer pressures were used to compute the time constant of isovolumic pressure decay (T). Peak filling rate and mean filling rate during the first half of diastole increased with exercise in all groups (from 615 to 1050 and 358 to 681 ml/sec in controls and comparably in the scar group and from 697 to 1035 and 347 to 768 ml/sec in the ischemia group). However, T was greater (reduced rate of pressure decay) with exercise in the ischemia group (38 vs 26 msec in controls; p less than .05). Changes in the atrial driving pressure for filling appeared to counterbalance the difference in T. Mean filling rate during the second half of diastole increased with exercise in controls and in the scar group but only modestly in the ischemia group (from 202 to 349 ml/sec). The reduction in late diastolic filling during exercise-induced ischemia was associated with increased filling in early diastole, with a middiastolic volume increase from 160 to 186 ml and an upward shift in the diastolic pressure-volume relation. Thus left ventricular filling is not impaired at rest in patients with coronary artery disease who have normal ejection fractions. Furthermore, the augmentation of early filling induced by exercise is not blunted but is maintained during ischemia, apparently at the expense of elevated left atrial pressure. However, late filling is restricted with ischemia by an increase in impedance.
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PMID:Dynamics of left ventricular filling at rest and during exercise. 685 Oct 55

Global and regional systolic function during exercise were studied at cardiac catheterization with biplane cineangiography and micromanometer pressures in three groups of patients: an ischemia group (n = 22) with exercise-induced asynergy from coronary artery disease, a control group with no or minimal cardiovascular disease (n = 5) and a "scar" group (n = 5) with prior infarction and no new asynergy with exercise. Ventricular emptying curves at rest did not distinguish patients with coronary artery disease from control subjects. During exercise, end-systolic volume increased in all patients in the ischemia group; ejection fraction decreased from 62 to 51% p less than 0.001) despite an increased end-diastolic volume. Stroke volume decreased from 65 to 58 ml/m2 (p less than 0.001) and limited the average increase in cardiac index to 65%. The scar group had no decrease in stroke volume, but end-systolic volume failed to decrease during exercise, as it did in all control subjects (35 to 28 ml/m2, p less than 0.05). An exercise-induced decrease in peak left ventricular pressure in five patients (23%) in the ischemia group was not accompanied by more severe or extensive ischemia as judged by ejection phase indexes. There was a tendency for maximal positive first derivative of left ventricular pressure (dP/dt) to be less (1,912 versus 2,446 mm Hg/s, difference not significant), suggesting an abnormality of pressure generation, not shortening. Global function during exercise in the ischemia group was determined, in part, by the extent of regional dysfunction. Those in whom between three and five regions of eight regions studied had abnormal fractional shortening during exercise had a 6% decrease in ejection fraction, while those with six to eight abnormal regions had a decrease in ejection fraction of 15% (p less than 0.05). In addition, function of nonischemic, noninfarcted myocardium was studied at the base of the left ventricle in those with exercise-induced anteroapical ischemia (n = 4) and those with anteroapical infarction (n = 4). Base fractional shortening and shortening velocity were greater at rest in those with infarction (39% and 1.6 circ/s, respectively) than in control subjects (31% and 1.0 circ/s, respectively, p less than 0.01), indicating a chronic augmentation of shortening. Base shortening velocity during exercise in those developing anteroapical ischemia increased from 1.1 to 1.4 circ/s (p less than 0.005), suggesting an acute augmentation of function balancing the deterioration of anteroapical function. Systolic function in coronary artery disease is determined by acute and chronic alterations in regional function. During exercise, there is an interplay between regional dysfunction from ischemia or infarction and regional hyperfunction of nonischemic myocardium which determines global performance.
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PMID:Systolic function during exercise in patients with coronary artery disease. 686 58


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