Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151814 (coronary occlusion)
 3,687 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In previous publications (1,2) the hypothesis was put forward that atheroma is caused by some pathogen or metabolic fault which impairs the transportability of cholesterol in the plasma. The lipoproteins containing the faulty metabolites are assumed to be incapable of traversing the capillary endothelium and continue to circulate uselessly in the blood stream, possibly giving rise to hypercholesterolaemia, until captured by lipophages which, if they can successfully complete their journey, void them into the gall bladder. The present paper takes the argument a step further by pointing out that the types of substances most likely to cause the described impairment are surfactants. A surfactant finding its way into the plasma could separate cholesterol from its carrier protein and itself become its carrier. The complex would still be kept in suspension in the plasma, but unable to cross biological barriers like the capillary endothelium. An important argument in favour of the hypothesis is that it can offer an explanation of the long-standing medical mystery of the connection between atheroma and the hardness or softness of the water supply. Infant deaths from coronary occlusion present a similar enigma. The paper points out that surfactants can conceivably find their way into infants' feeding bottles.
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PMID:Surfactants and atherogenesis. 59 83

To study the action of aspirin upon the myocardium per se, independent of thrombosis, coronary occlusion with a balloon catheter was induced in 53 anesthetized dogs divided into two groups. One group (N = 20) was treated daily with aspirin (600 mg/dog) for seven days and another (N = 33) was untreated. Left ventricular hemodynamics and precordial ECG mapping were used to assess the influence of myocardial ischemia over a four hour period. There were no significant differences in left ventricular function or extent of injury as judged by ECG mapping between the two groups. However, there was a significant decrease in the incidence of ventricular fibrillation in the treated dogs (5% vs 39%). Serial plasma samples for free fatty acid determination showed a significant rise in the untreated group. Aspirin blocked the FFA increment in the treated animals. Tissue samples from the ischemic area of left ventricle exhibited a significant reduction of the sodium and water increments, as well as a lesser potassium loss in the treated animals compared to the controls and may have been the basis for the lower incidence of arrhythmias. Since infusion of 51Cr labelled platelets showed no myocardial accumulation of platelets in either group, microthrombi did not appear to contribute to the observed differences.
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PMID:Antiarrhythmic effects of aspirin during nonthrombotic coronary occlusion. 63 Jun 76

In anesthetized closed-chest dogs, four vasodilators were compared after prolonged coronary occlusion induced by catheter wedging in a coronary branch. With treatment given between 1 hour and 2 hours of occlusion, five groups were studied: no treatment, isosorbide dinitrate, nitroprusside, dipyridamole, and methylprednisolone. Measured were heart rate, cardiac pressures and blood flow (with 85Kr); and cardiac index, left ventricular ejection fraction with vascular resistance, left ventricular minute work index, and an oxygen consumption index were calculated. At sacrifice, ischemic inner/outer wall isotope distribution and myocardial K+, Na+, and H2O were determined. With no treatment, left ventricular end-diastolic pressure and vascular resistances rose while cardiac index, ejection fraction, minute work index, and index of myocardial oxygen consumption fell, with no further change between 1 and 2 hours. Vasodilators did not affect coronary hemodynamics or isotope distribution. Hemodynamic effects of isosorbide dinitrate and nitroprusside differed qualitatively from dipyridamole and methylprednisolone. The latter drugs caused increases in ejection fraction, and dipyridamole also significantly increased cardiac index and minute work index. Only nitroprusside decreased minute work index and O2 consumption index. Only nitroprusside and dipyridamole, despite differing hemodynamics, tended to reduce K+ loss and Na+ and H2O gain in ischemic tissue. Further extended studies with these agents are warranted.
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PMID:A comparison of four potential agents for reducing necrosis after prolonged coronary occlusion. 63 62

The subendocardial to subepicardial gradient in the severity of ischemia following acute coronary occlusion is described. The effects of mild, moderate, and severe ischemia on cell structure and function are compared in summary form, and special attention is given to the effects of severe ischemia on myocardial cells. The characteristics of reversible and irreversible ischemic injury are defined in biologic terms. The failure of cell volume regulation in cells which have entered an irreversible state of ischemic injury is demonstrated by the use of free-hand slices in vitro. Irreversibility is associated with structural defects in the plasma membrane and is reflected in an increased slice inulin-diffusible space, increased slice H2O and Na+ content, and failure of the tissue to maintain the high K+ and Mg2+ levels characteristic of normal left ventricular myocardium. Defective cell membrane function is an early feature of irreversible ischemic injury and may be a primary event in the genesis of the irreversible state.
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PMID:Ischemic tissue injury. 118 Mar 31

Krypton-81m, a radionuclide emitting a 190 kev gamma ray, has a half-life of 13 seconds. It is a radioisotope of an inert water-soluble noble gas and is produced at a constant rate by spontaneous decay of rubidium-81 in an 81Rb-81mKr generator-delivery system. Delivery is through a minibore Teflon catheter that can be threaded through a standard no. 7 or 8F angiographic catheter. The generator is eluted by 5 percent dextrose-in-water, delivered by infusion pump at 1.5 ml/min, and the eluate is infused intraarterially directly into any organ. Delivery and decay reach equilibrium within 2 minutes, producing a heterogeneous distribution that is proportional to the perfusibility of the tissue concerned and the time required to reach it. The ultrashort halflife of the radionuclide rapidly eliminates activity when delivery ceases; thus, experiments can be sequentially repeated at brief intervals. The radiation hazard for easily imaged doses is negligible. Preliminary studies in open chest dogs were visualized by scintillation camera, stored on digital data disk, processed, and displayed in dual channel, dual color mode on a video system. Images of myocardial perfusion defined relative levels of perfusion, collateral circulation between coronary arterial branches, equilibrium time of diffusible perfusion of the myocardium, focal defects in induced occlusion, collateral circulation to occlusion, and reactive hyperemia after release of induced coronary occlusion. The system and technique appear applicable to human subjects.
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PMID:Definition of myocardial perfusion by continuous infusion of krypton-81m. 126 54

Myocardial protection by the water-soluble vitamin E analogue, Trolox, was investigated in 18 regionally ischemic, reperfused porcine hearts. The left anterior descending coronary artery was distally ligated for 45 min and was reperfused for three days. Five grams of Trolox (n = 9) were infused intravenously before coronary occlusion. Treatment was continued with an intravenous dose of 5 grams Trolox/24 hours until the end of the experiment. Infarct size was determined as the ratio of infarcted (tetrazolium stain) to ischemic myocardium (dye technique). Regional systolic shortening was assessed by sonomicrometry. Generation of free radicals by stimulated neutrophils was evaluated by luminol-enhanced chemiluminescence. Plasma concentrations of Trolox were measured by high-performance liquid chromatography. Aside from heart rate before ischemia, global hemodynamic values including calculated left ventricular oxygen consumption did not differ significantly between the two groups. Plasma concentrations of Trolox measured 1.8 +/- 0.3 mmol/l (before ischemia), 0.96 +/- 0.13 mmol/l (before reperfusion), 0.77 +/- 0.1 mmol/l (40 min of reperfusion), and 0.08 mmol/l (end of the experiment). Generation of free radicals by stimulated neutrophils was reduced by about 30% in the treatment group before ischemia and immediately before reperfusion, but was not reduced at the end of the experiment. Risk regions (control group 19.4 +/- 6 g, treatment group 19.3 +/- 7 g) and infarct sizes (control group 69.3 +/- 8%, treatment group 69.3 +/- 12%) were almost identical. Regional systolic shortening of a control segment and of the risk region were similar in both groups before ischemia, before reperfusion, and after 45 min of reperfusion. After 3 days of reperfusion, regional systolic shortening of the reperfused myocardium of the treated group had recovered to a significantly greater extent (P = 0.027). This parameter amounted to 9 +/- 6% in the treated group and to 3 +/- 3% in the control group. Improved functional recovery was not accompanied by higher tissue concentrations of adenosine triphosphate. It is concluded that the chosen treatment with Trolox does not reduce infarct size but accelerates functional recovery. This finding suggests that the mechanisms resulting in myocardial necrosis during ischemia/reperfusion and in post-ischemic myocardial dysfunction may differ.
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PMID:The effects of Trolox, a water-soluble vitamin E analogue, in regionally ischemic, reperfused porcine hearts. 179 Oct 83

The effects of the dihydropyridine calcium channel blocker amlodipine on subendocardial segment shortening (%SS), regional myocardial blood flow, myocardial high-energy phosphate levels and tissue water content were compared with those of a saline-treated group of barbital-anesthetized dogs subjected to a 45-minute coronary artery occlusion followed by 60 minutes of reperfusion. Saline or amlodipine (200 micrograms/kg administered intravenously) was given 15 minutes before coronary occlusion. There were no significant differences between groups in ischemic bed size or hemodynamics although dP/dt was higher after amlodipine administration. Subepicardial collateral blood flow was higher in the amlodipine group during coronary occlusion. After occlusion, %SS in the ischemic region was markedly decreased in both series and passive systolic lengthening resulted. Despite similar decreases in %SS during occlusion, the amlodipine-treated dogs showed a marked improvement in myocardial segment function of the ischemic reperfused region throughout 60 minutes of reperfusion compared with saline-treated dogs. In addition, amlodipine prevented the rebound increase in phosphocreatine and attenuated the loss of adenine nucleotides and increase in tissue water in the ischemic reperfused area at 60 minutes of reperfusion. These results suggest that amlodipine has a favorable effect on the functional and metabolic recovery of the ischemic reperfused myocardium and may have potential as a therapeutic agent for the treatment of coronary artery disease. The mechanism of action of amlodipine in this model is unknown but may be partially related to a drug-induced increase in coronary collateral blood flow or a decrease in afterload.
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PMID:Effects of amlodipine on myocardial ischemia-reperfusion injury in dogs. 253 Aug 91

The effects of the dihydropyridine calcium-channel blocker, amlodipine, on subendocardial segment shortening (%SS), regional myocardial blood flow, myocardial high-energy phosphate levels and tissue water content were compared to those of a saline-treated group of barbital-anesthetized dogs subjected to a 45-minute coronary artery occlusion followed by 60 minutes of reperfusion. Saline or amlodipine (200 micrograms/kg, IV) were administered 15 minutes prior to coronary occlusion. There were no significant differences between groups in ischemic bed size or hemodynamics, although dP/dt was higher following amlodipine. Subepicardial collateral blood flow was higher in the amlodipine group during coronary occlusion. Following occlusion, %SS in the ischemic region was markedly decreased in both series and passive systolic lengthening resulted. In spite of similar decreases in %SS during occlusion, the amlodipine- treated dogs showed a marked improvement in myocardial segment function (%SS) of the ischemic-reperfused region throughout 60 minutes of reperfusion as compared to saline-treated animals. In addition, amlodipine prevented the rebound increase in phosphocreatine and attenuated the loss of adenine nucleotides and the increase in tissue water in the ischemic-reperfused area at 60 minutes of reperfusion. These results suggest that amlodipine has a favorable effect on the functional and metabolic recovery of the ischemic-reperfused myocardium, and may have potential as a therapeutic agent for the treatment of coronary artery disease. The mechanism of action of amlodipine in this model is unknown but may be partially related to a drug-induced increase in coronary collateral blood flow.
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PMID:Effect of amlodipine on myocardial functional and metabolic recovery following coronary occlusion and reperfusion in dogs. 253 1

Midazolam is gradually replacing diazepam in neuroleptanalgesia with fentanyl and sufentanil because of its greater water solubility, greater hypnotic potency, shorter half-life, lack of pharmacologically active metabolites and low incidence of thrombophlebitis. In order to substantiate midazolam as being as safe and effective as diazepam in cardiac patients with severe coronary occlusion, hemodynamic measurements were made before and 10 min after completion of intravenous injection of 0.2 mg/kg i.v. midazolam (n = 45) and 0.4 mg/kg i.v. diazepam (n = 30), the doses which are identical to those used in patients undergoing cardiac catheterization. All 75 patients were spontaneously breathing 40% O2 in air. No positional changes or stimulation of patients were allowed before and during the study. Of hemodynamic variables, systemic systolic blood pressure was significantly reduced by both midazolam and diazepam. Midazolam also caused significant reduction in systemic vascular resistance with reduction in diastolic pressure and left ventricular stroke work index. No changes in heart rate, systolic and diastolic pulmonary artery pressures, cardiac output and index, stroke volume and index, pulmonary vascular resistance, right ventricular stroke work index and rate pressure product were observed following either midazolam or diazepam. No statistically significant differences were observed in any hemodynamic variable between those patients receiving midazolam or diazepam. It is concluded that midazolam is as safe as diazepam in cardiac patients with coronary obstruction.
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PMID:Comparison of the hemodynamic effects of midazolam and diazepam in patients with coronary occlusion. 278 97

This study tests the hypothesis that irreversible muscle damage does not occur after as long as 6 hours of ischemia before reperfusion, immediate functional recovery is possible by controlling the conditions of reperfusion during total vented bypass and the composition of the reperfusate with substrate-enriched blood cardioplegic solution, and such control can be accomplished without thoracotomy. Of 43 dogs undergoing 2 to 6 hours of left anterior descending coronary occlusion, seven were studied by ultrastructural and mitochondrial analyses after 6 hours of regional coronary occlusion without reperfusion. Sixteen other dogs were reperfused with normal blood, with the heart in the beating state after 2 to 4 hours of ischemia, and 20 dogs received regional substrate-enriched blood cardioplegic reperfusion after 2 to 6 hours of ischemia for 20 minutes during total vented bypass accomplished through the femoral artery, femoral vein, and transaortic left ventricular venting. Six hours of ischemia without reperfusion caused minimal changes in mitochondrial structure and retained mitochondrial adenosine triphosphate production capacity at 64% of control values despite complete depletion of tissue adenosine triphosphate. Reperfusion with normal blood in the beating, working hearts caused extensive structural damage, reduced reflow, and failed to restore contractility in any instance (-27% systolic shortening, p less than 0.05). In contrast, regional cardioplegic reperfusion during total vented bypass at 2, 4, and 6 hours caused 52 +/- 3%, 41 +/- 7%, and 21 +/- 6% immediate recovery of regional contractile function. The seven hearts reperfused at 6 hours of ischemia had more segmental shortening (21% versus -27%, p less than 0.05), less edema (81% versus 83% water content, p less than 0.05), and more postischemic flow (57 versus 18 ml/100 gm/min in subendocardial muscle, p less than 0.05) than did 2-hour controls, and postischemic ultrastructure was not altered by reperfusion. Six hours of ischemia does not produce irreversible damage, and immediate recovery of contractile function is possible if the conditions of reperfusion are controlled with total vented bypass and a regional substrate-enriched blood cardioplegic solution is administered. Such control can be obtained by the peripheral cannulation technique.
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PMID:Immediate functional recovery after six hours of regional ischemia by careful control of conditions of reperfusion and composition of reperfusate. 287 24


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