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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The isolated perfused working rat heart preparation has been used to study the effects of respiratory acidosis on myocardial metabolism and contractilly. Hearts were perfused with 5 mM glucose and 10(-2) U/ml of insulin in order to enhance metabolsim of glucose relative to that of fatty acids. After perfusion with Krebs bicarbonate medium at pH 6.6, hearts rapidly ceased performing external work and peak left ventricular pressure fell by 75% after 5 minutes. Oxygen consumption, rate of ATP generation and overall glycolytic flux also declined rapidly. After about 2 minutes of perfusion, the fall of glycolytic flux showed a partial reversal, which was largely accounted for by increased lactate production, so that glucose oxidation decreased further. The reversal of glycoltic flux could be accounted for by partial release of H+ inhibition of phospho-fructokinase by increased tissue levels of adenosine 5'-diphosphate (ADP), adenosine monophosphate (AMP) and P1 and decreased levels of adenosine triphosphate (ATP) and creatine phosphate. The increased proportion of glucose uptake converted to lactate together with an increase of the tissue lactate/pyruvate ratio could be accounted for by inhibition of the malate-aspartate cycle combined with tissue hypoxia. Lactate accumulated in the tissue as a result of a decreased permeability of the plasma membrane to lactate. Decreased oxygen delivery to the myocardium was caused by secondary constriction of the coronary vessels. In further experiments, the coronary flow was regulated by an external pump which delivered fluid at a controlled rate into the aortic cannula above the coronary arteries, and the degree of tissue hypoxia was monitored by measuring changes of pyridine nucleotide reduction state by surface fluorescence techniques. The effects of acidosis uncomplicated by possible hypoxia were compared directly with those produced by ischemic hypoxia. The effects of acidosis under these conditions were similar to those described above, and to those produced by ischemia. From these and other data it is concluded that the effects of ischemia are caused by a lowering of the intracellular pH, which decreases the rate of energy production relative to the rate of energy demand. However, it is suggested that the primary cause of the decreased peak systolic pressure with either acidosis or ischemia is not a result of a defect of energy metabolism, but is due to alteration of the calcium cycle of the heart. Possible causes of irreversible heart failure after prolonged ischemia are discussed.
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PMID:Contribution of tissue acidosis to ischemic injury in the perfused rat heart. 0 93

A systematic search for cases of lactic acidosis among diabetics on biguanides revealed ten during an eight-month period, while in the preceding ten years not a single case had been definitely diagnosed. This represents a prevelance of 1 in 2000 patients admitted to hospital. All ten were over 60 years old and had previously been treated for heart failure. Most of them had suffered from renal insufficiency for some time. There was no case of biguanide overdosage. Criteria for the diagnosis of lactic acidosis are lactic concentration in blood averaging 18.4 mmol/l and a low pH, averaging 6.9. Serum-biguanide concentration (measured by radioimmuno-assay) was markedly increased. Most of the patients were in circulatory shock on admission or soon after and all of them had a history of gastro-intestinal complaints. Despite intensive treatment with insulin and glucose and careful correction of the acidosis with bicarbonate four of the ten patients died.
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PMID:[Lactic acidosis in diabetics on biguanides (author's transl)]. 1 84

Changes in myocardial water content, left ventricular diastolic stiffness, cardiac performance, coronary blood flow, myocardial contractile force, rate of change of myocardial force, and peak acceleration of the aortic volume flow were examined in twenty-five dogs during glucose-induced hyperosmolality before and after pancreatectomy, the latter with and without insulin treatment. Glucose-induced hyperosmolality accounted for myocardial dehydration, increased diastolic stiffness and consequent decrease of left ventricular performance only in the absence of insulin, while coronary blood flow, myocardial contractile force, rate of change of myocardial force and peak acceleration of the aortic volume flow increased independently from the presence or absence of insulin during the glucose-induced hyperosmolality. These findings suggest that the frequent development of heart failure in hyperosmolar diabetic coma could partly be explained by myocardial dehydration and by the consequent decrease in left ventricular compliance and performance.
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PMID:Effect of hyperglycaemia-induced hyperosmolality on heart function in the dog. 11 46

Idiopathic hemochromatosis (iH) is typically a disease of older males. The case presented here describes a 26-yr-old woman with problems presenting heart failure, insulin-dependent diabetes, hepatomegaly, and secondary amenorrhea. The diagnosis was established by serum iron and transferrin saturation measurements, liver biopsy, and bone marrow examination for iron. Twenty grams of iron were removed by phlebotomy over 30 mo, and the patient's symptoms improved. A review of the literature pertinent to people with symptomatic onset of IH before age 30 yr revealed 52 young people in addition to this case. In contrast to IH patients older than 30, there was an almost equal ratio between the sexes, a greater frequency of cardiomyopathy and hypogonadism, and a lower frequency of diabetes mellitus and hepatic involvement. An autosomal recessive mode of inheritance appears to be most likely in this young group.
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PMID:Idiopathic hemochromatosis in a young female. A case study and review of the syndrome in young people. 75 39

Past studies reported by this laboratory have documented myocardial dysfunction and progressively developing hypoglycemia in canine endotoxin shock. The purpose of the present study was to determine the effects of glucose concentrations and insulin infusions on myocardial performance following endotoxin administration. Experiments were carried out on isolated, working canine left ventricular heart preparations exchanging blood with intact dogs. Myocardial function was evaluated following endotoxin and correlated with concentrations of glucose and effects of insulin infusion. Cardiac dysfunction occurred within 2-4 hr postendotoxin and the degree of malfunction was not related to arterial blood glucose concentrations. Maintaining blood glucose at control, preshock, levels by infusion of 50% glucose did not prevent myocardial dysfunction as evidenced by elevations of left ventricular end diastolic pressure, and depressed power. Infusions of insulin reversed cardiac failure and maintained normal performance in spite of wide ranges in glucose concentration (5-120 mg%). Findings suggest that myocardial dysfunction is not precipitated or enhanced by the hypoglycemia of endotoxin shock. The beneficial actions of infused insulin on cardiac performance appear to be elicited on the basis of mechanisms other than myocardial glucose transport.
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PMID:Effects of glucose or insulin on myocardial performance in endotoxin shock. 96 82

Chronic diabetes mellitus can alter left ventricular function independent of vascular effects. On the basis of available morphologic data in human and canine diabetics, alterations of myocardial interstitium may be the basis for this preclinical abnormality. The abnormal function is independent of apparent duration and treatment by diet, insulin, or hypoglycemic agents. It occurs in both sexes and is independent of age. Whether the observed functional abnormality progresses to clinical heart failure may depend on intensification of the underlying pathophysiology of the myocardium or superimposition of complications such as hypertension, obesity, and obstructive disease of the coronary vessels.
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PMID:Diabetes mellitus and left ventricular function. 97 64

Two hundred and twelve patients with acute myocardial infarction were treated for 14 days with daily doses of potassium (3 gm orally), glucose (280 gm orally) and regular insulin (16 units subcutaneously), all given in 4 fractional doses. The incidences of arrhythmias, heart failure and systolic blood pressure below 70 mm Hg, as well as the mortality rate, were compared with those for another group of 600 myocardial infarction patients who were not given this treatment. Though there was some reduction in the incidence of cardiac arrhythmias, it was not statistically significant. However, there was a strikingly significant decrease in the incidences of heart failure and blood pressure below 70 mm, as well as in the early mortality rate. Our findings should encourage the continued use of potassium, glucose and insulin therapy in acute myocardial infarction.
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PMID:Potassium, glucose and insulin administration in acute myocardial infarction: a five-year study. 99 44

The plasma level of the immunoreactive insulin and the blood level of sugar on an empty stomach and following carbohydrate provocation were determined in 31 patients with congestiva heart failure due to ischaemic heart disease. In 26 of them the plasma levels of adrenalin and noradrenalin were also studied. After 30-35 days of active therapy 15 patients were reexamined. The immunoreactive insulin plasma level was determined by the Hales and Randle technique, that of catecholamines-flowmetrically by the trioxyindol method after Vendsalu modified by E. Sh. Matlina. Carbohydrate metabolism disorders that manifested themselve in fasting hyperglycemia and in changing tolerance of glucose were noted in 13 of the 31 patients, examined. In the majority of patients with congestive heart failure insulin secretion was reduced both after fasting and after glucose administration. The improvement of the patients state in response to the employed therapy was accompanied by an increasing insulin secretion. One of the causes of the inhibition of insulin secretion in patients with congestive heart failure consisted in hypercatecholaminemia that was noted in most of the examined cases. The obtained data prove the necessity of a careful control of carbohydrate metabolism in patients with congestive heart failure and of a more active employment of insulin for their treatment.
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PMID:[Levels of immunoreactive insulin and catecholamines in the blood plasma of patients with congestive heart failure]. 115 39

The past decade has seen a shift in the strategy for hypertension treatment from stepped therapy--a highly structured monolithic series of steps--to recommendations for a more individualized selection of treatment. Severe hypertension is a clear indicator to bypass traditional steps. Demographic factors, such as age, gender, and race, are often cited, but have proved to be less helpful. Concomitant medical conditions and problems are very common and are more often the crucial determinants in the selection of antihypertensive therapy. Coronary artery disease, diabetes mellitus, heart failure, azotemia, asthma, and chronic obstructive pulmonary artery disease, anxiety, and depression are all common, and each has implications for the selection of antihypertensive therapy. Blood pressure reduction is a surrogate for reduction of cardiovascular risk, and therefore, consideration of concomitant medical problems has extended to left ventricular hypertrophy, obesity, mild hyperlipidemia, and insulin resistance, as additional risk factors in hypertension. Consideration of all these factors makes it possible to individualize antihypertensive therapy in most patients today.
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PMID:Treatment of hypertension: the place of angiotensin-converting enzyme inhibitors in the nineties. 128 28

Angiotensin-converting enzyme (ACE) inhibitors are established in the treatment of hypertension and heart failure; both conditions are complicated by resistance to insulin-mediated glucose disposal. The defect in essential hypertension is both tissue and pathway specific, i.e., confined to nonoxidative (glycogen synthetic) routes of intracellular glucose utilization in skeletal muscle, whereas heart failure and non-insulin-dependent diabetes mellitus (NIDDM) are associated with more widespread abnormalities of carbohydrate and lipid metabolism. Thus, the mechanisms of the insulin resistance in hypertension, NIDDM, and heart failure are fundamentally different, so metabolic responses to drug therapy may not be the same in all insulin-resistant states. There have been conflicting reports about the effects of ACE inhibitors on insulin sensitivity and glycemic control. A number of studies, both with captopril and with enalapril, have shown small increases in insulin sensitivity, and there is evidence that this is due to enhanced glucose uptake into skeletal muscle. The interpretation of these studies, however, is often compromised by poor trial design, lack of full placebo data, various indirect measurements of insulin sensitivity, and heterogeneous patient populations in whom the biochemical mechanisms of insulin resistance (and drug responses) may not be the same. Overall, there probably is a modest class effect of ACE inhibitors that enhances insulin-mediated glucose disposal; the mechanism of this effect is likely to be a combination of increased muscle blood flow, local renin-angiotensin system blockade, and elevated kinin levels.
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PMID:Angiotensin-converting enzyme inhibitors and insulin sensitivity: metabolic effects in hypertension, diabetes, and heart failure. 128 42


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