Study On The Relationship Between Plasma AVP Concentration And Myocardial Collagen Synthesis & Heart Function During Pneumococcal Pneumonia In Experimental Aging Rats

Pneumonia is a common and life-threatening disease for the elderly. Numerous investigations have shown that pneumonia usually cause extrapulmonary organ dysfunction in the elderly ,among which heart failure is the most often one. Pathological evidence has shown that pneumonia could lead to myocyte swelling. However, little is known about pneumonia's effect on cardiac collagen network. Recent reports have shown that heart failure is associated with increased deposition of extracellular collagen due to increased synthesis. The disturbance of myocardial collagen metabolism might be an important pathological stage in the occurrence and development of heart failure. So, cardiac collagen network is an essential aspect to explore the pathogenesis of heart failure derived from pneumonia in the elderly. The heart of the elderly is different from that of the youth in the structure, function and reaction to some certain stimuli because of itsdegeneration. Myocardial remodeling owing to the aging emerged in the heart of every elderly. It is unclear whether pneumonia could trigger the cardiac collagen remodeling(even, the heart failure) in the elderly during the process of myocardial remodeling owing to the aging.Recent reports have shown that AVP, a neuropeptide which is secreted by the hypothalamus, could exert great influences on cardiovascular system. Not only does AVP serve physiological events of cardiovascular system at its normal level but also be involved in the regulation of cardiovascular remodeling during some pathological processes. AVP promotes the proliferation of rat cardiac fibroblasts(CFs) in a concentration-dependent manner, and also increases their collagen synthesis and secretion into extracellular space to contribute to the formation of myocardial fibrosis. It is reported that the inappropriate increase of plasma AVP levels is responsible for secondary hyponatremia in patients with pneumonia. All that indicates that pneumonia might promote the AVP secretion. It is still required to clarify whether the increased AVP is involved in the myocardial collagen synthesis of the elderly with pneumonia. The current study aimed to develop an experimental aging rat model with pneumonia, observe changes in plasma AVP concentration and myocardial collagen content during pneumonia, investigate the relationship between the elevated plasma AVP concentration and myocardial collagen synthesis during pneumonia, explore the pathogenesis of cardiac collagen remodeling in the elderly with pneumonia, provide new experimental and theoretical evidences and treatment methods for heart failure owing to pneumonia in the elderly.Experimental contents:In the current study, the pneumonia models were established from the experimental aging rats with intrabronchial instillation of the streptococcus pneumoniae. Animals were randomly divided into 4 groups : control group, pneumonia group, pneumonia+AVP V1 antagonist group(simply as antagonist group) and pneumonia+ antibiotic group(simply as antibiotic group). Left ventricular function was determined by arterial cannulatio. The level of plasma AVP was determined by using radioimmunoassay technique. The parameters of myocardial fibrosis such as collagen I and III mRNA,interstitial collagen volume fraction(ICVF) and perivascular collagen area(PVCA) were determined by pathological examination with computed processing. Rat heart was taken out to evaluate collagen content and inducible nitric oxide synthase-nitric oxide(iNOS-NO) system activity by using spectrophotometry technique. This study was to observe the following parameters in experimental aging rats with pneumonia and the effects of AVP V1 antagonist on them. (1) the relationship between plasma AVP concentration and myocardial collagen content; (2) the distribution of myocardial collagen; (3) the configuration of collagen in myocardium; (4) left ventricular hypertrophic parameters; (5) left ventricular function; (6) the expression of collagen I IIImRNA in myocardium; (7) the expression of nuclear transcription factor activator...