Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The strategy of diuretic drug administration remains to be defined in heart failure as experimental and clinical evidence have clearly established the benefit of neurohormonal blockade. The impact of addition of diuretic treatment to angiotensin-converting enzyme inhibition on survival remains to be demonstrated. The objectives of the study were to evaluate cardiovascular and renal effects of addition of diuretic treatment to captopril (2 g/L, in drinking water), on survival, on the experimental model of heart failure. Rats were followed for 10 months after coronary ligation. Echocardiographic, hemodynamic, morphometry and renal function investigations were then performed on surviving rats. Survival (from 34 to 61%), diuresis and natriuresis were significantly improved compared to control group only in animals treated with a combination of captopril + furosemide. In treated group: cardiac dimensions were reduced with left ventricular fractional shortening significantly increased in combination group (from 22.4 to 28%); captopril + furosemide animals had highest heart rate and lowest systolic and diastolic blood pressures; body and heart weight were reduced, but kidney weight was significantly increased with furosemide (1.7 g in control vs. 2 g in capto + furo); plasma renin activity and angiotensin 1 were greatly increased, and moderately stimulated in control. In conclusion, this combination of drugs significantly improved cardiac remodeling and survival of animals, increased diuresis and natriuresis despite stimulation of plasma renin activity and kidney hypertrophy.
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PMID:Captopril-furosemide survival study in experimental heart failure. 1601 33

Diabetic cardiomyopathy is a major contributor to the increasing burden of heart failure globally. Effective therapies remain elusive, in part due to the incomplete understanding of the mechanisms underlying diabetes-induced myocardial injury. The objective of this study was to assess the direct impact of insulin replacement on left ventricle structure and function in a rat model of diabetes. Male Sprague-Dawley rats were administered streptozotocin (55 mg/kg i.v.) or citrate vehicle and were followed for 8 weeks. A subset of diabetic rats were allocated to insulin replacement (6 IU/day insulin s.c.) for the final 4 weeks of the 8-week time period. Diabetes induced the characteristic systemic complications of diabetes (hyperglycaemia, polyuria, kidney hypertrophy) and was accompanied by marked left ventricle remodelling (cardiomyocyte hypertrophy, left ventricle collagen content) and diastolic dysfunction (transmitral E/A, left ventricle-dP/dt). Importantly, these systemic and cardiac impairments were ameliorated markedly following insulin replacement, and moreover, markers of the diabetic cardiomyopathy phenotype were significantly correlated with the extent of hyperglycaemia. In summary, these data suggest that poor glucose control directly contributes towards the underlying features of experimental diabetic cardiomyopathy, at least in the early stages, and that adequate replacement ameliorates this.
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PMID:Insulin replacement limits progression of diabetic cardiomyopathy in the low-dose streptozotocin-induced diabetic rat. 2856 41