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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Intravenous infusions of lipid-free albumin were used to lower the arterial non-esterified fatty acids (NEFA)/albumin ratio during coronary occlusion in dogs. 2. Reduction of the NEFA/albumin ratio was accompanied by proportionate reductions in myocardical uptake of NEFA and the degree of ST segment elevation in epicardial electrocardiographic recordings from the ischaemic zone. Aortic pressure and heart rate were unchanged. 3. Infusions of control albumin preparations had no effect on the NEFA/albumin ratio or ST segment elevation. 4. These observations support the proposition that the disturbance of cellular function during myocardial ischaemia is influenced by the degree of saturation of albumin-binding sites with NEFA and by their availability.
Clin Sci Mol Med 1976 Aug
PMID:Relationship of epicardial ST segment elevation to the plasma free fatty acid/albumin ratio during coronary occlusion in dogs. 95 68

1. This study includes 1038 patients (325 men and 713 women) who consulted the medical out-patient clinic, Rigshospitalet, Copenhagen, during the years 1932-38. All these patients had a blood pressure of 160/100 mmHg or 180 mmHg or more. 2. The average age at the first examination was 54 years; 97% were followed at intervals of 10 years until 1975, when sixty patients were still alive. Treatment was minimal until 1970. 3. Sixty percent of the men and 76% of the women reached an age of 65 years or more. Nine percent of the total patients lived to 85 years or more. Excess mortality was far higher in men than in women. 4. Causes of death were stroke in 17%, heart failure in 24%, coronary occlusion in 16%, uraemia in 4% and other diseases in 39%. At the first examination, thirteen cases of malignant hypertension were registered, none at later sessions.
Clin Sci Mol Med Suppl 1976 Dec
PMID:A 40 years' follow-up study of 1000 untreated hypertensive patients. 107 6

1. Peak blood flow acceleration measured in the common carotid artery was compared with peak flow acceleration measured in the ascending aorta of three baboons. 2. The response to occlusion for 60s of the circumflex branch or the anterior descending branch of the left coronary artery was investigated. 3. Both accelerations decreased approximately to the same extent. Peak aortic flow velocity, stroke volume and cardiac output also decreased but to a smaller extent. 4. It is concluded that peak aortic flow acceleration is a sensitive index of myocardial function during acute coronary occlusion in conscious primates and that peak carotid flow acceleration is an indirect measure of myocardial performance under the same conditions.
Clin Sci Mol Med 1975 Apr
PMID:Correlation of peak aortic and carotid flow acceleration during coronary occlusion in conscious baboons. 112 18

Moderate and severe stages of congestive heart failure due to the loss of myocardium upon coronary occlusion in rats was associated with an increase in alpha-adrenergic receptors and a decrease in beta-adrenergic receptors in the viable left ventricle. However, at early stages of heart failure the number of beta-adrenergic receptors was decreased without any changes in the number of alpha-adrenergic receptors. The affinities of these receptors to alpha receptor antagonist (3H-prazosin) and beta receptor antagonist (3H-dihydroalprenolol) were not altered in the failing hearts. On the other hand, the pattern of changes in both alpha- and beta-adrenergic receptors in heart membranes treated with oxygen free radical generating system was different from that seen in the failing hearts. In particular, the affinities for these receptors were decreased whereas the number of beta-receptors was increased and the number of alpha-receptors was decreased or unchanged. These results indicate that alterations in the adrenergic receptors in heart failure are not due to the formation of oxygen free radicals.
Mol Cell Biochem 1992 Sep 08
PMID:Changes in adrenergic receptors during the development of heart failure. 146 Dec 61

Radiolabeled deoxyglucose (FDG) has been advocated as a marker of viability of reperfused myocardium during acute infarction. However, data for such recommendation are few. We investigated cardiac deposition of C-14 deoxyglucose (C-14 DG) and of Thallium -201 (Tl-201) in rabbits subjected to coronary occlusion (15, 30, 60 or greater than 100 min) and reperfusion (75 min and 24 h). Measured myocardial concentrations of C-14 DG and Tl-201 in macroautoradiograms were quantitatively correlated in a 24 h reperfusion group with presence of myocardial necrosis evaluated by light microscopy. The major finding in this investigation was that with 30 min or 60 min of ischemia followed by reperfusion there were myocardial regions with significant hypoperfusion (Tl-201) and histologic necrosis. However, in the same myocardial areas, the deposition of C-14 DG was not correlated with the extent of necrosis (r = 0.27). Also, the deposition of C-14 DG in acute myocardial infarction was higher than that of Tl-201 (P = 0.05 by paired T test and by nonparametric Wilcoxon's test). It was also demonstrated that when the occlusion time was varied (15-130 min) and early reperfusion was provided for 75 min or omitted altogether, the myocardial accumulation of Tl-201 was variable and that myocardial sequestration of C-14 DG was higher than perfusion in central and peripheral portions of the area-at-risk. These observations do not support a role for the use of radiolabeled deoxyglucose for the detection of myocardial viability in recently infarcted cardiac muscle.
J Mol Cell Cardiol 1991 May
PMID:Discordance between accumulation of C-14 deoxyglucose and Tl-201 in reperfused myocardium. 188 39

We tested whether recombinant human superoxide dismutase conjugated to polyethylene glycol (PEG-SOD) to prolong its plasma retention time could limit myocardial infarct size in an ischemia-reperfusion model in the rabbit. One group of animals received 1000 units/kg of PEG-SOD as an intravenous bolus 15 min before coronary occlusion. A second group received saline only and served as controls. Under pentobarbital anesthesia, a left coronary branch was occluded for 30 min and then reperfused. The surgical wounds were repaired and the animals were allowed to recover. Seventy-two hours after the coronary occlusion, the heart was excised and the size of the area at risk (ischemic vascular bed) was assessed with fluorescent particles and the infarct size was determined by histology (Hematoxylin-eosin, Azan stain). Infarct size as a percentage of the area at risk was similar between the groups, 46.5 + 2.7 in the PEG-SOD group (n = 8) and 48.9 + 3.1 in the control group (n = 8). There were no significant differences between the groups indicating that PEG-SOD did not limit infarct size in this model.
J Mol Cell Cardiol 1991 Feb
PMID:Superoxide dismutase conjugated to polyethylene glycol fails to limit myocardial infarct size after 30 min ischemia followed by 72 h of reperfusion in the rabbit. 206 22

The protective effect of angiotensin-converting enzyme inhibitors (ACEI) on myocardial ischemia and reperfusion damage was estimated in rat hearts, both in vivo and in vitro. Enalapril 2.5 mg/kg ip pretreatment at 24 and 5 h before coronary occlusion, significantly blunted the rise of CPK (445 +/- 151 vs 649 +/- 244 mu/ml, P less than 0.05) and improved electrocardiogram (ECG) 8 h after coronary occlusion. In global ischemia and reperfusion ex vivo, enalapril improved contractility (0.9 +/- 0.2 vs 0.3 +/- 0.3 g, P less than 0.05) and coronary flow (15.6 +/- 3.3 vs 11.9 +/- 3.1 ml/min/g, P less than 0.05), shortened significantly the duration of reperfusion arrhythmia (3.1 +/- 2.7 vs 9.7 +/- 8.1 min, P less than 0.05). In Langendorffs heart, captopril remarkably preserved force of contraction (2.1 +/- 0.4 vs 1.4 +/- 0.4 g, P less than 0.01) and coronary flow (2.7 +/- 0.5 vs 3.6 +/- 0.9 ml/min/g, P less than 0.05) in segmental infarction deteriorated by angiotensin I. Captopril 10(-5) M infusion reduced the release of CPK (435 +/- 112 vs 640 +/- 123 mu/min coronary flow, P less than 0.05). This action was almost completely abolished by pretreating and infusing with indomethacin. As a positive control, prostacyclin 5 X 10(-7) M infusion further reduced the release of CPK to 330 +/- 77 mu/min. It is concluded that angiotensin-converting enzyme inhibitor can protect both myocardial ischemia and reperfusion damage in rat hearts. The mechanism of protection was ascribed to reduced production of angiotensin II by ACE inhibition and increased prostacyclin release in the myocardium.
J Mol Cell Cardiol 1987 Sep
PMID:Protective effects of captopril and enalapril on myocardial ischemia and reperfusion damage of rat. 282 45

Global ischemia in guinea-pig hearts for 60 to 90 min depressed microsomal and mitochondrial Ca2+ uptake activities. Reperfusion of the 60 min ischemic hearts resulted in incomplete recovery of contractile function and calcium uptake activities of both mitochondrial and microsomal fractions. On the other hand, reperfusion of the 90 min ischemic hearts further depressed the microsomal Ca2+ uptake activity. Coronary occlusion for 90 min in dog hearts was found to decrease microsomal Ca2+-pump and sarcolemmal Na+-K+ ATPase activities. Reperfusion of these regional ischemic hearts further depressed the microsomal Ca2+ uptake and Ca2+-stimulated ATPase as well as sarcolemmal Na+-K+ ATPase activities whereas mitochondrial Ca2+ uptake was increased. Perfusion of rat hearts for 60 min with hypoxic medium resulted in depression of the sarcolemmal Na+-dependent Ca2+ uptake and ATP-dependent Ca2+ uptake activities. Reperfusion of these hypoxic hearts failed to recover the sarcolemmal Na+-Ca2+ exchange and Ca2+-pump activities. These results demonstrate that membrane defects with respect to Ca2+ transport processes in ischemic/hypoxic hearts may be associated with irreversible injury.
J Mol Cell Cardiol 1988 Mar
PMID:Alterations in heart membrane calcium transport during the development of ischemia-reperfusion injury. 284 10

To assess the effect of Fluosol-DA treatment on infarct morphology, detailed histologic examination was performed in 17 dogs with permanent proximal left anterior descending coronary artery occlusion. Two of the three groups of dogs received an equal blood volume exchange (40 ml/kg i.v.) with either Fluosol-DA (F) or heparinized autologous blood (H) 30 min post occlusion while being ventilated with 100% oxygen. A third group received no therapy (C). Animals were sacrificed 3 days post occlusion and sections were obtained for light and electron microscopy. Histologic studies showed that infarct size was statistically smaller in dogs treated with F 54 +/- 7% versus heparin 64 +/- 10% treatment or no therapy 79 +/- 6%. Fluosol-DA animals demonstrated decreased inflammatory infiltrate, larger viable subepicardial zones and greater endocardial sparing in the area surrounding the central zone of necrosis. By electron microscopy, perfluorochemical particles were found within endothelial and inflammatory cells in subepicardial zones of infarction. In midmyocardial zones, Fluosol-DA particles were present in capillaries, extracellular spaces and necrotic myocytes. In the normal myocardium Fluosol-DA particles were rarely seen within endothelial cells and never within the interstitium or myocytes. Thus, Fluosol-DA reduces infarct size and alters infarct morphology in the 3 day post permanent coronary occlusion model.
Virchows Arch B Cell Pathol Incl Mol Pathol 1985
PMID:Effect of perfluorochemical (Fluosol-DA) on infarct morphology in dogs. 286 60

The hypothesis that prostacyclin (PGI2) might have a direct cytoprotective action in ischaemic cardiac tissue was investigated. Myocardial ischaemia was induced in perfused rabbit hearts by ligating the left main coronary artery. Coronary flow, oxygen uptake, and turnover of lactate and purines were measured before and up to 120 min after coronary occlusion. After this, ischaemic tissue was separated from perfused myocardium, and levels of lactate, adenine nucleotides and creatine phosphate were determined in specimens from non ischaemic, ischaemic and border zones. PGI2 (final conc. 10(-7) M) was infused before or 30 min after ligation and the results were compared to those in control hearts. Coronary ligation reduced coronary flow and oxygen consumption by about 50%. The fractional extraction of lactate decreased from 20% to close to zero and purine release increased 5-fold. In the non-ischaemic area the tissue levels of ATP and creatine phosphate were high, with a low content of lactate, but in the ischaemic area the levels of ATP and creatine phosphate were considerably reduced and the content of lactate was high. Although coronary flow and oxygen uptake were elevated after treatment with PGI2, no change in lactate or purine turnover was observed. Neither the weight of the non-perfused myocardium nor the tissue levels of the adenine nucleotides, creatine phosphate and lactate were affected by PGI2 treatment. The data indicate that in this model, in which effects on cardiac work, collateral flow and platelets are eliminated, PGI2 does not limit ischaemic myocardial injury. Hence, the hypothesis of a direct cytoprotective action of PGI2 in ischaemic myocardial tissue was not supported.
J Mol Cell Cardiol 1986 Oct
PMID:Effect of prostacyclin on the severity of ischaemic injury in rabbit hearts subjected to coronary ligation. 353 19


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