| Backgroud The general process by which the left ventricular experiences changes in structure, shape and function after acute myocardial infarction is often referred as "left ventricular remodeling". Recently, it also involves the changes in myocardial cells and in both the quantity and quality of the extracellular matrix. A great deal of clinical and experimental studies indicate that left ventricular remodeling is the main reason of progressing left ventricular dysfunction and congestive heart failure after myocardial infarction and it is also the most important risk factor of late cardiac death. Therefore, the pathophysiologic process of left ventricular remodeling and to find better treatment have been better appreciated recently.Both experimental and clinical studies indicated that early reperfusion of infarct-related artery may salvage the endocardial tissue and restore stuned myocardium in the infarct border zone, reduce infarct size and prevent infarct expansion. It is an efficient treatment in acute phase to prevent left ventricular remodeling after myocardial infarction. But patients with a patent infarct-artery also may undergo left ventricular remodeling. Other experiments and clinical trials have studied the effects of nitrate-based vasodilating agents,antiimflammation drugs and Ca2+ channel blockers on the left ventricular remodeling, but the results were controversial. The efficacy of ACE inhibitors in reducing infarct size, attenuating left ventricular dilation after infarction was associated with improved survival. But with the different time of treatment after infarction, the effects of ACE inhibitors on left ventricular remodeling are different and when to use ACE inhibitors in AMI need to be further studied.Treatment with J3 -blockers reduces mortality among patients with myocardial infarction, but studies on the effect of ?-blockers on remodeling after myocardial infarction have been sparse and some experimental observations were in conflict with the beneficial effects of & -blockers reported in clinical studies. Various factors may have influenced the experimental studied available so far: |3 -blocker type, size of infarction and time to start treatment after myocardial infarction. In addition, detailed hemodynamic studies have not been performed to determine the long-term effect of P -blockers after myocardial infarction. Therefore, the present study aimed to develope a rabbit model with left ventricular dysfunction after myocardial infarction, abserve the effects of early and late use of ?-blocker bisoprolol on hemodynamic function and left ventricular remodeling and discuss effects of P -blocker clinical use on left ventricular remodeling after myocardial infarction.MethodsRabbit left ventricular myocardial infarction was produced by ligation of the left coronary artery. 4 weeks later, LV dysfunction and left ventricular remodeling developed. 48 rabbits weight from 1.8 to 2.5kg were used and 11 rabbits died during and after the operation. 10 of the rabbits randomized to sham-operated group (S group), 8 to myocardial infarction group (MI group), 9 to bisoprolol used within 48 hours after myocardial infarction group (early-B group) and 10 to bisoprolol used about 14 days after myocardial infarction group (late-B group). Before operation and 4 weeks after operation heart rates were determined from the electrocardiographic records. Hemodynamic measurements 4 weeks after operation were obtained under 3%pentobarbital anesthesia. A micro-tip pressure transducer catheter was inserted successfully into the right carotid artery. Left ventricular end-diastolic pressure (LVEDP) and LV pressure with first positive and negative derivates of pressure (i dp/dt max ) obtained. Plasma noraurenalme (NE) was measured by a simplified liquid chromatography and electrochemical detection method and plasma angiotensin II (Ang II ) and endothelin (ET) were measured by radioimmunoassay. Then the heart was rapidly excised and immersed in 10% buffered formalin, dehydrated in 95?ethanol and...
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