ABSTRACT
To stop or reverse progression of congestive heart failure is so far an unreached therapeutic goal. Several prospective studies have now clearly shown that treatment with angiotensin-converting enzyme (ACE) inhibitors resulted in a clear reduction of cardiovascular and total mortality in patients with congestive heart failure. As a consequence, ACE-inhibitors are now standard therapy for congestive heart failure in addition to diuretics and glycosides. Of pathophysiologic importance is that ACE-inhibitors are potent vasodilators and counteract the neuroendocrine stimulation of the sympathetic nervous system and the renin-angiotensin-aldosterone system which both contribute to the detrimental outcome in congestive heart failure. New results of the prevention trial of the SOLVD-Study showed that in patients with reduced ejection fraction the development of congestive heart failure could be attenuated or even stopped. The questions remain of what is the optimal dose, when should treatment with ACE-inhibitors be started, and how long should it be maintained. Thus, in patients with reduced ejection fraction after myocardial infarction ACE-inhibitors are today a cornerstone for preventing progressive congestive heart failure and improving cardiovascular prognosis. Whether beta-blockers offer additional benefit in subgroups of patients with congestive heart failure remains to be determined in future trials.
Subject(s)
Angiotensin-Converting Enzyme Inhibitors/therapeutic use , Heart Failure/drug therapy , Hemodynamics/drug effects , Aged , Angiotensin-Converting Enzyme Inhibitors/adverse effects , Aortic Valve Stenosis/drug therapy , Aortic Valve Stenosis/mortality , Aortic Valve Stenosis/physiopathology , Cardiomyopathy, Hypertrophic/drug therapy , Cardiomyopathy, Hypertrophic/mortality , Cardiomyopathy, Hypertrophic/physiopathology , Echocardiography, Doppler/drug effects , Female , Heart Failure/mortality , Heart Failure/physiopathology , Hemodynamics/physiology , Humans , Male , Middle Aged , Renin-Angiotensin System/drug effects , Renin-Angiotensin System/physiology , Survival RateABSTRACT
To examine the combined hepatotoxic and nephrotoxic effects of cadmium and ethanol, rats maintained on an ethanol containing liquid diet (5% w/w) were given cadmium either acutely (3 x 1 mg/kg IP) or subacutely (about 14 mg/kg/day PO for 6 weeks). Parameters tested were cadmium, zinc and copper contents of blood and various organs, metallothionein (MT) contents, polysome profile of liver and kidneys, serum SDH and GPT levels and creatinine clearance. Ethanol reduced the hepatic MT contents without altering the polysome profile and the zinc and copper contents. Cadmium on the other hand raised the MT contents in liver and kidneys. This effect of cadmium predominated in the combined treatment. Morphological examination and functional tests (SDH, GPT, creatinine clearance) indicate that cadmium does not enhance the toxic effects of ethanol, and vice versa.
