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)

The effect of halothane on net myocardial oxygen balance of ischemic myocardium was studied in the non-failing canine heart. Myocardial ischemia was produced by repeated reversible occlusions of a coronary artery; the severity of ischemia was estimated by summating ST-segment elevations (sigma ST) obtained by epicardial ECG mapping at 15 to 18 sites. Control measurements were obtained before and after administration of halothane (0.75 per cent) to six dogs with chloralose-urethane basal anesthesia. Halothane was associated with significant decreases of systemic arterial pressure (P less than .001), heart rate (P less than .01), and the product of systolic arterial pressure X heart rate (P less than .01), an indirect index of myocardial oxygen consumption, while left atrial pressure remained unchanged at normal levels. sigmaST during occlusion was less (P less .001) during halothane (26.5 +/- 7.4 (SD) mv) than before (36.6 +/- 5.4 mv) or after (34.4 +/- 8.2 mv) its administration. Thus, halothane decreased the severity of experimentally-induced myocardial ischemia in the non-failing canine heart. The data suggest that, in the absence of ventricular failure, halothane influences the relationship between myocardial oxygen supply and demand in a favorable direction when coronary blood flow is limited.
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PMID:Halothane-induced decrease in experimental myocardial ischemia in the non-failing canine heart. 96 78

The effect of ischemia on synthesis of myocardial proteins was investigated using a model of perfusion in which low levels of coronary flow were provided to paced hearts worked against a closed aortic outflow tract. These conditions rapidly produced ischemia and ventricular failure, as evidence by reduced coronary flow, increased left atrial pressure, and decreased pressure development. Protein synthesis was inhibited in a subsequent 1-hour period, during which a minimal coronary flow was maintained by retrograde perfusion. ATP, GTP, and creatinine phosphate were depleted in ischemic hearts and AMP accumulated. Production and accumulation of lactate within the tissue increased, whereas palmitate uptake was inhibited. The inhibition of protein synthesis was not associated with reduced levels of intracellular amino acids. During ischemia, decreased levels of ribosomal subunits as compared to paced or unpaced aerobic hearts suggested that peptide chain elongation was slow relative to initiation. Provision of insulin further reduced subunit levels but did not increase protein synthesis, suggesting that the hormone did not prevent inhibition of peptide chain elongation in energy-poor hearts.
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PMID:Effects of anoxia and ischemia on protein synthesis in perfused rat hearts. 126 87

Regional wall motion abnormalities (RWMA) detected by intraoperative transesophageal echocardiography (TEE) are thought to be sensitive markers of myocardial ischemia. To assess the prognostic significance of RWMA as compared with other less costly technologies such as electrocardiography (ECG) and hemodynamic measurements [blood pressure (BP) and pulmonary artery (PA) pressure], 50 patients were prospectively studied who were undergoing elective coronary artery bypass graft (CABG) surgery using continuous TEE, ECG (Holter), and hemodynamic measurements during the prebypass, postbypass, and early postoperative intensive care unit (ICU) periods (first 4 h). Echocardiographic and ECG evidence of ischemia was characterized during each of these three periods and related to adverse clinical outcomes (postoperative myocardial infarction, ventricular failure, and cardiac death). Clinicians were blinded to the TEE and ECG information. The prevalence of myocardial ischemia during the perioperative periods was as follows: prebypass, 20% (TEE) versus 7% (ECG); postbypass, 36% (TEE) versus 25% (ECG); ICU 25% (TEE) versus 16% (ECG). Neither prebypass TEE ischemia nor ECG ischemia occurring in any of the three periods predicted adverse outcome. In contrast, postbypass TEE ischemia was predictive of outcome: six of 18 patients with postbypass TEE ischemia had adverse outcomes versus 0 of 32 without TEE ischemia (P = 0.001). Seventy-three percent of the echocardiographic ischemic episodes occurred without acute change (+/- 20% of control) in heart rate, BP, or PA pressure. The authors conclude that: 1) prebypass myocardial ischemia was relatively uncommon, 2) the incidence of ECG and TEE ischemia was highest in the postbypass period, and 3) postbypass RWMA were related to adverse clinical outcome.
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PMID:Prognostic importance of postbypass regional wall-motion abnormalities in patients undergoing coronary artery bypass graft surgery. SPI Research Group. 278 9

In man, electrocardiographic changes typical of transient myocardial ischemic episodes can be accompanied by increases in arterial pressure and heart rate or, at the opposite side of the spectrum, by decreases in arterial pressure and heart rate. It has been clearly proved that all of these changes can occur independently of the perception of pain. Transient ischemic episodes associated with hypotension and bradycardia or hypotension without the tachycardia that could be expected from a baroreceptive mechanism, are likely to reflect a depressor reflex mediated by cardiac vagal afferent fibers. It is a clinical and experimental working hypothesis that these depressor reflexes would characterise more severe episodes of ischemia: in clinics, those accompanied by signs of acute ventricular failure; in the laboratory, those induced by "global" ischemia. On the other hand, ischemic episodes associated with hypertension and tachycardia, usually thought to depend on a pain mechanism, are likely to reflect a pressor reflex mediated by cardiac sympathetic afferent fibers. It is our hypothesis that these pressor reflexes from the heart are the most frequent companions of less severe ischemic episodes, whether or not signalled by anginal pain. In the laboratory, a pressor reflex can be constantly obtained with a limited "regional" ischemia. These neural mechanisms, that should be analyzed independently of any teleologic reasoning, may be of paramount importance not only in determining the hemodynamic profile accompanying ischemic episodes, but in inducing those local changes in visceral neural activity that an increasing evidence indicates as crucial factors in arrhythmias and coronary death.
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PMID:Circulatory markers of nervous activation during myocardial ischemia. 375 96

Isolated working rat heart preparations were used to ascertain whether the addition of adenosine and prevention of its catabolism could aid in the functional recovery of hearts following global ischemia. Hearts were infused with either 80 micro M EHNA (an adenosine deaminase inhibitor) or 20 micro M adenosine and EHNA in either normal (2.4 mM) or low (0.05 mM) calcium-containing buffer prior to clamping of the aorta for 30 minutes. In one series of hearts, postischemic concentrations (mumoles/gram wet weight) of adenosine triphosphate (ATP), diphosphate (ADP), and monophosphate (AMP), adenosine, inosine, and hypoxanthine were measured; in another series, the recovery of aortic flow rate was used as a measure of functional recovery of ventricular muscle. With normal electrolyte balance, EHNA was unable to protect hearts against ATP loss and ventricular failure. Hearts with EHNA + adenosine recovered 14% of preischemic aortic output and ATP levels were slightly elevated at 0.93 mumole/gm. Those treated with either EHNA or EHNA + adenosine in low-calcium buffer recoverd 100% of their original aortic output. However, EHNA + adenosine maintained considerably higher ATP levels (1.57 mumoles/gm) than did EHNA alone (1.14 mumoles/gm) and was associated with faster initial recovery of aortic output. Thus the prevention of adenosine catabolism was insufficient for adequate ventricular recovery unless the tissue ATP was maintained above about 1.0 mumole/gm. EHNA + adenosine in a 0.05 mM Ca++ infusion solution conserved ATP, markedly improved the functional recovery of hearts, and thus may have a role to play in myocardial preservation during elective cardiac arrest.
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PMID:Improved functional recovery of ischemic myocardium by suppression of adenosine catabolism. 708 38

The arrival of a patient with chest pain syndrome (precordial) to the emergency represents a diagnostic challenge for the physician. Around 6 million persons are seen each year at the Emergency units in the USA. More than half of the patients are admitted for their cardiac evaluation. Its cardiac origin is confirmed in 10 to 15%, and about 15% of them develop myocardial infarction. However, 5 to 10% of patients are dismissed and develop myocardial infarction during the next 48 h. The diagnosis of the infarct is inadvertent and/or patients is not hospitalized in 2 to 8%. The mortality rate is duplicated in none hospitalized patients. Frequently, a conservative observation conduct and/or diagnostic expectation is taken, with the consequent saturation of the intensive care unit that looses its critical character and avoids quick mobilization of the patient with an increase in costs. The clinical judgment, a meticulous clinical history, and careful physical examination play a key role in the differential diagnosis of the precordial pain syndrome; however, pain can be atypical, absent or manifest as an equivalent of pain, which does not exclude the diagnosis of myocardial infarction or ischemia. Likewise, chest pain in the presence of a normal conventional ECG at rest, non-diagnostic or with minimal variations, does not rule out the possibility of a coronary obstruction and does not mean that the pain is not of coronary origin. Other characteristics of the ECG, such as T wave and ST segment alterations, bundle branch block (BBB), LV hypertrophy, interpretation discrepancies, can pose doubts or mistakes in the diagnosis. Although its diagnostic information is essential, other non-invasive laboratory tests are needed, such as the treadmill stress ECG, serial bioenzymatic markers, and myocardial perfusion scintigraphy (SPECT and Gated-SPECT) at rest or under physical or pharmacologic stress. The advantages and disadvantages of the stress ECG, the echocardiography, magnetic resonance and PET are mentioned. The advantages of the SPECT and Gated-SPECT in the diagnosis and prognosis are: 1) great diagnostic objectivity; 2) high sensitivity and specificity; 3) diagnosis does not depend on evolution time of the ischemia and/or infarction, since SPECT diagnoses the initial primary modifications of ischemia; 4) diagnosis is achieved within the established limit of time, in less than 4 to 6 hours. The designed protocols allow to obtain the diagnosis between 30 min and 1:30 h; 5) assesses the myocardium at risk; 6) stratifies the risk and prognosis; 7) defines the site and 8) the involved coronary artery(les); 9) provides the functional significance of the anatomic obstruction; 10) quantifies the ventricular function, i.e., ejection fraction, systolic and diastolic volumes, systolic thickening, ventricular failure signs; 11) provides three-dimensional visualization of the mobility of the left ventricular wall; 12) diagnoses simultaneously the associated presence of ischemia and/or infarction of the right ventricle; 13) its high negative predictive value allows to dismiss immediately and with a great safety margin those patients in whom SPECT revealed normal perfusion; 14) costs are reduced without adversely compromising the safety of the patients. We describe the algorithm used as guideline for the early diagnosis in the presence or absence of ischemic heart disease in the patient with precordial or chest pain syndrome with normal or non-diagnostic ECG at arrival to the emergency ward. It is necessary to modified the clinical educational patterns and to revaluate the advantages and limitations of the clinical history, physical exploration, as well as of the conventional ECG at rest and other diagnostic methods used specifically in relation to the chest pain syndrome with a normal or non diagnostic conventional ECG. SPECT and Gated-SPECT scintigraphy is considered as the best individual and isolated non-invasive test for the diagnostic solution of the precordial syndrome at the Emergency Unit.
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PMID:[Chest pain syndrome in normal or non-diagnostic conventional ECG at the emergency service. Assessment with myocardial perfusion (SPECT) and ventricular function (Gated-SPECT)]. 1521 44

Cardiac remodeling occurs frequently in chronic kidney disease patients and affects quality of life and survival. Current treatment options are highly inadequate. As kidney function declines, numerous metabolic pathways are disturbed. Kidney and heart functions are highly connected by organ crosstalk. Among others, altered volume and pressure status, ischemia, accelerated atherosclerosis and arteriosclerosis, disturbed mineral metabolism, renal anemia, activation of the renin-angiotensin system, uremic toxins, oxidative stress and upregulation of cytokines stress the sensitive interplay between different cardiac cell types. The fatal consequences are left-ventricular hypertrophy, fibrosis and capillary rarefaction, which lead to systolic and/or diastolic left-ventricular failure. Furthermore, fibrosis triggers electric instability and sudden cardiac death. This review focuses on established and potential pathophysiological cardiorenal crosstalk mechanisms that drive uremia-induced senescence and disease progression, including potential known targets and animal models that might help us to better understand the disease and to identify novel therapeutics.
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PMID:Cardiac Remodeling in Chronic Kidney Disease. 3215 Aug 64