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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Alterations in cation homeostasis during and after recovery from myocardial ischemia may account for some of the reversible and irreversible components of myocardial cell injury. To investigate possible mechanisms involved, we exposed cultured layers of spontaneously contracting chick embryo ventricular cells to media containing 1 mM cyanide (CN) and 20 mM 2-deoxyglucose (2-DG), and zero glucose for up to 6 h, and then allowed cultured cells to recover in serum-free culture medium for 24 h. Changes in Na, K, and Ca contents, 42K uptake and efflux, ATP content, cell water content, and lactate dehydrogenase (LDH) release were measured, and compared with changes produced by exposure to 10(-3) M ouabain and severe hypoxia. Exposure to CN and 2-DG caused marked increase in cell Na (sevenfold) and Ca (fivefold) contents, and a decrease in K content (one-fifth normal), coincident with ATP depletion to one-tenth normal levels. This produced only slight cell injury, evidenced by increased LDH release. Recovery for 24 h resulted in return to near normal values (expressed in nanomoles per milligram of protein) of Na, Ca, and ATP contents. However, there was failure of cell K content to return to normal, associated with a persistent reduced net uptake of 42K, and an increase in the rate of 42K efflux. These abnormalities in K homeostasis were associated with a decrease in cell volume and water content per milligram of protein. More marked ATP depletion (to 1/100 normal values) was produced by hypoxia plus 2-DG and zero glucose, and was associated with much more severe cell injury manifested by LDH loss. Ouabain exposure resulted in a much greater Ca gain (20-30-fold), relative to increase in Na content, than did either CN and 2-DG or hypoxia; and ouabain effects were not reversible (after a 15-fold or greater increase in Ca content was produced) and were associated with significant LDH release. We conclude that these cells are resistant to cell injury caused by moderately severe Ca overload and ATP depletion produced by exposure to CN and 2-DG. However, metabolic inhibition of ATP production produces persistent abnormalities in K homeostasis, associated with functional abnormalities.
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PMID:Alterations in cation homeostasis in cultured chick ventricular cells during and after recovery from adenosine triphosphate depletion. 335 Sep 67

Present-time Greenlanders are living a stressful 'westernized life' complete with an elevated consumption of tobacco and alcohol. The drinking water in Greenland is extremely soft and the diet is very low in calcium (and probably magnesium) and rich in carbohydrate and fat. Despite these different predisposing factors, death from ischemic heart disease is 3-6 times less frequent than in Denmark. The serum calcium/magnesium ratio in Greenlanders is significantly lower than in Danes. Magnesium deficits in patients with acute myocardial infarction, as well as epidemiologically positive correlations between dietary calcium/magnesium ratios and ischemic heart death, are the basis for attributing the low incidence of ischemic heart death in Greenland to the low Greenlandic calcium/magnesium ratio in diet and blood serum. Other characteristics of the Greenlandic disease pattern include a low incidence of stones in kidney and urinary tract, few cases of diabetes mellitus, prolonged bleeding time, increased atrioventricular block and osteoporosis, all of which may also be related to a low calcium and high magnesium metabolic status.
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PMID:Greenland, a soft-water area with a low incidence of ischemic heart death. 344 6

During acute myocardial ischemia, granulocytes accumulate and obstruct the microcirculation. Granulocytes remain plugged in individual myocardial capillaries on reperfusion and are the major cause of the no-reflow phenomenon. During 3 h of ischemia, the granulocyte content of myocardium measured by 111In labeling increases from 1.0 X 10(6) to 1.5 X 10(6) cells/g, and after 5 min of reperfusion increases to 2.4 X 10(6) cells/g. The effects of granulocytes during 1 h of acute ischemia were determined by comparing agranulocytic to whole blood perfusion. With whole blood collateral flow decreased, water content increased (edema), ventricular fibrillation was common, and 27% of capillaries had no-reflow, whereas in the absence of granulocytes, collateral flow increased, there was no edema, arrhythmias were rare, and the no-reflow phenomenon was completely prevented. It is unfortunate that the inflammatory signals triggered by ischemia remain active on acute reperfusion, limit tissue salvage, and perhaps cause reperfusion injury. Several activating stimuli for granulocytes are known, but what inhibits them? Adenosine is known to inhibit superoxide radical formation by granulocytes, and 5-amino-4-imidazole carboxamide-riboside (AICA-riboside) augments adenosine release from energy-deprived cells. In dogs subjected to 1 h of ischemia, AICA-riboside pretreatment augmented adenosine release by nearly 10-fold, which was accompanied by a significant increase in collateral blood flow and decreased arrhythmias. We propose a new hypothesis: adenosine acts as a natural antiinflammatory autacoid during transient injury linking the ability to catabolize ATP (an indicator of viability) to granulocyte inhibition, thus preventing premature activation of the inflammatory response to cell death. Granulocytes are active participants in acute myocardial ischemia and means to prevent their activation, remove them from the reperfusate, or inhibit them will be necessary for optimum reperfusion salvage.
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PMID:Consequences of activation and adenosine-mediated inhibition of granulocytes during myocardial ischemia. 356 43

Hemofiltration has been suggested as a new therapeutic tool in refractory heart failure. In this study, 11 patients with primary or ischemic heart disease in New York Heart Association class IV, in whom there was no response to medical treatment, were subjected to hemofiltration. The pathophysiologic adjustments promoted by subtraction of plasma water were investigated, and guidelines for an appropriate use of this procedure in heart failure are provided. Fluid was removed from plasma at a rate of 500 ml/hour until either normalization of the right atrial pressure (which was increased in all cases) was achieved or the hematocrit exceeded 50 percent. According to these criteria, the duration of treatment ranged from four to six hours and the total amount of fluid removed was 2,000 to 3,000 ml. In each case, hemofiltration promoted relief of dyspnea and of clinical and radiographic evidence of lung congestion and pleural effusion, and substantially reduced the dependent edema and abdominal girth. These effects were paralleled by progressive decrease of the right (-70 percent) and left (-45 percent) ventricular filling pressures and of the pulmonary arterial pressure and arteriolar resistance, without significant variations in heart rate, aortic pressure, cardiac index, and systemic vascular resistance. Changes in the right atrial and wedge pulmonary pressures are interpreted as reflecting a combined effect of a decrease in pressure on the outside of the heart due to fluid reabsorption (from lung interstitial spaces and pericardial, pleural and abdominal cavities) and of intravascular volume subtraction. The arterial partial pressure of oxygen was raised, the partial pressure of carbon dioxide and pH were unchanged, and urinary output was substantially enhanced by the procedure. The study indicates that: hemofiltration may be a short-term treatment for refractory cardiac insufficiency with overhydration; a filtration rate of 500 ml/hour is effective and safe; and the central venous pressure may be a reliable guide to volume subtraction.
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PMID:Hemofiltration as short-term treatment for refractory congestive heart failure. 360 81

The authors investigated the effect of ethanol on platelet impedance aggregation in whole blood (WB-PIA). Healthy moderate drinkers were given ethanol, 1 mL/kg body weight, to drink. Thirty minutes after ingestion of ethanol, WB-PIA was significantly inhibited when compared with baseline values. There was no significant inhibition when the same volunteers ingested water instead of ethanol. These observations suggest that WB-PIA is a sensitive technic for the detection of the effect of ethanol on platelets. These findings also support the view that blood ethanol levels achievable during social drinking impair platelet function, thus possibly accounting, at least in part, for the reported "protection" from ischemic heart disease in moderate drinkers. The sensitivity of human platelets to the inhibitory effect of ethanol suggests that continued drinking will adversely influence the incidence of initial bleeds and of rebleeding in gastrointestinal hemorrhage associated with alcoholism.
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PMID:Ethanol ingestion inhibits human whole blood platelet impedance aggregation. 363 Sep 75

Mortality rates for acute myocardial infarction and ischaemic heart disease (IHD) of white males and females in South Africa are much higher than those in the USA, Australia, England and Wales when individuals in the 15- to 64-year age group are considered. Magnesium levels in the drinking water of 12 South African districts and deaths due to IHD assessed on the basis of corrected statistics for deaths apparently due to IHD in white residents were studied and a significant negative correlation was found between these two variables. No such correlation has been demonstrated in blacks.
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PMID:Content of magnesium in drinking water and deaths from ischaemic heart disease in white South Africans. 372 39

Recent evidence indicates that leukocytes (LEU) are large, stiff, viscous cells that naturally adhere to vascular endothelium. Their broad role in the early myocardial microvascular response to acute ischemia was suggested by 1) the role of leukocyte capillary plugging in the no-reflow phenomenon, 2) resistance increases in skeletal muscle with LEU infusions, and 3) salvage of ischemic myocardium by anti-LEU agents. We perfused the coronary circulation under matched, controlled conditions with whole blood or granulocyte-depleted whole blood. During 1 h of ischemia (left anterior descending occlusion) circumflex perfusion pressure was servocontrolled to a constant value. In whole blood-perfused hearts, flow measured by the radiolabeled microsphere method decreased in endocardium from 0.12 +/- 0.05 at 5 min of ischemia to 0.09 +/- 0.04 ml X min-1 X g-1 at 60 min of ischemia and in epicardium from 0.27 +/- 0.17 to 0.21 +/- 0.16 ml X min-1 X g-1, both P less than 0.05. In granulocyte-depleted blood-perfused hearts, flow increased over the same period from 0.18 +/- 0.15 to 0.29 +/- 0.18 ml X min-1 X g-1 in endocardium (P less than 0.05) and did not change significantly in epicardium (0.36 +/- 0.22 to 0.41 +/- 0.24 ml X min-1 X g-1). The LEU-depleted blood perfusate contained less than 33 granulocytes/microliter, whereas control perfusate contained 4,265/microliter. Reperfusion at normal pressures with carbon suspension allowed for histologic evaluation of the no-reflow phenomenon. With whole blood perfusion the no-reflow phenomenon in the endocardium was present with 27% of capillaries occluded, compared with nearly complete reperfusion in LEU-depleted animals (1% of capillaries occluded, P less than 0.05). Furthermore, LEU depletion prevented the increases in tissue water content seen in control hearts and decreased the incidence of ventricular arrhythmias. These studies demonstrate the significant participation of granulocytes in the unfavorable responses of flow, edema formation, and arrhythmias to the 1st h of myocardial ischemia and further document their role in the no-reflow phenomenon.
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PMID:Role of leukocytes in response to acute myocardial ischemia and reflow in dogs. 374 Feb 86

Seven healthy subjects immersed a hand in random order in either warm water or in cold water at 5 degrees C for 2 min, after taking orally a single dose of 120 mg of propranolol or a placebo in a double blind fashion. The cold stress resulted in a significant increase in blood pressure and the rate pressure product without a change in heart rate. Beta-adrenoceptor blockade did not affect the pressor response the cold. The changes induced by the cold stress in the cardiovascular variables in the placebo and propranolol experiments were not statistically different. The highest rate pressure product during the cold pressor test was about 109 units. This was well below the pain threshold value of about 200 found during exercise in patients with ischaemic heart disease. In the recovery phase, the cardiovascular variables reverted to pre-immersion values within 1 min inspite of continued low hand skin temperature.
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PMID:Beta-adrenoceptor blockade and cardiovascular response to the cold pressor test. 381 24

This paper describes how Poisson regression techniques can be used to examine the relationship between mortality and possible explanatory variables over a series of areas in cases where the number of deaths involved is relatively low. As an example an analysis is carried out on deaths from ischaemic heart disease among young adults in the county boroughs of England and Wales during 1969-1973. The results of the study indicate that the number of deaths was higher for males than females and was positively related to age, the size of the 'at risk' population and crowding, but negatively associated with water hardness and the size of the New Commonwealth population. A comparison of the Poisson and log-normal regression models clearly shows that the latter provides an inferior goodness of fit and unreliable results. It is therefore concluded that when the number of deaths is small there are both theoretical and practical advantages in using Poisson regression to analyse mortality data.
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PMID:Analysing geographic variations in mortality using Poisson regression: the example of ischaemic heart disease in England and Wales 1969-1973. 382 77

Positron emission tomography (PET) is a new technique for noninvasively assessing myocardial metabolism and perfusion. It has provided new insight into the dynamics of myocardial fatty acid and glucose metabolism in normal subjects, patients with ischemic heart disease and those with cardiomyopathies, documenting regionally depressed fatty acid metabolism during myocardial ischemia and infarction and spatial heterogeneity of fatty acid metabolism in patients with cardiomyopathy. Regional myocardial perfusion has been studied with PET using water, ammonia and rubidium labeled with positron emitters, permitting the noninvasive detection of hypoperfused zones at rest and during vasodilator stress. With these techniques the relationship between perfusion and the metabolism of a variety of substrates has been studied. The great strides that have been made in developing faster high-resolution instruments and producing new labeled intermediates indicate the promise of this technique for facilitating an increase in the understanding of regional metabolism and blood flow under normal and pathophysiologic conditions.
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PMID:Cardiac positron emission tomography. 387 48


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