| Acute myocardial ischemia/infarction(AMI) is a clinically common emergency. AMI merges with complications make mortality significantly increased. In which pulmonary complications is one of the serious complications.Sensory nerves involve in the body conduction to a stimulus, including noxious stimuli. Sensory neuropeptides is a kind of peptides which widely present in the body tissue and participate in regulation of a variety of organs'physiologic function, its effects on the cardiovascular function has been studied. In myocardial ischemia this complex pathophysiological process, caused the nociceptive perception can be mediated by neuropeptides, which in turn by neurogenic mechanism and/or neuro-endocrine-immune mechanism, activated the "dialogue" of brain-endocrine-immune system, and evoked the organism ripple, result in multiple organ systems' pathophysiological changes. Now in acute myocardial ischemia study, the concentrations of the sensory peptide substance p increased in lung tissue was found, which prompt tips on sensory nerve may be involved in this pathological process, however at present on its mechanism of action is unclear. Sensory nerves regulate lung's pathophysiology after acute myocardial ischemia directly or not? and the mechanism of how? So we do more further research.Purpose:by studying the expression of sensory peptide OFQ and his receptor ORL1 in the lung after acute myocardial ischemia, and the effect and mechanism in pulmonary inflammation and injury, with a view to further clarify the capsaicin sensitive nerve and its neuropeptides to participate in the regulation of lung function of pathological physiology.Methods:this experiment using health SD cultured rats and denervated the capsaicin sensitive nerve different adults rat model, divided into normal rats group (N group) and denervation group (D group), each group are all be further divided in to false operation control group (Sham group as 3 hours group and sham 6 hour group) and surgery ischemia group (CAO(coronary artery occlusion) 3 hour group and CAO 6 hour group), where normal rats surgery ischemia group is divided into normal rats CAO group(NC group), NK1 receptor antagonist group(NK group) and OFQ antagonist group(UFP group). Above all, all the experimental groups are divided into 12 groups, each group including 6 rats only.This experiment from the four aspects of an inquiry:1. By Immunohistochemistry (IHC) dyeing and Western Blot(immunoblotting) observate the expression changes of OFQ and ORL1 in lung tissue after acute myocardial ischemia/infarction.2. By HE dyeing, the ratio of wet and dry(W/D) in the lung tissue and neutrophil IHC dyeing, investigate the circumstance of inflammation response in the lung tissue after AMI.3. Adopt TUNEL staining and Western Blot method observing the circumstances of apoptosis and expression changes anti-apoptotic protein Bcl2 in the lung tissue and studying alveolar surfactant SP-A changes in serum after AMI, to approach the circumstance of acute myocardial ischemia-induced lung injury.4. By early acute myocardial ischemia blood gas analysis, analyzing pulmonary function after AMI.Results:1. In early stage of acute myocardial ischemia/infarction, existing varying degrees of inflammation responses, pulmonary edema and neutrophil infiltration obvious in lung tissue, and all these phenominan are more server in 6 hours than in 3 hours after myocardial infarction;2. In early stage of acute myocardial ischemia/infarction, emerging various degrees of pulmonary injury, apoptosis in lung tissue and pulmonary surfactant concentration in serum increased, all these aggravating in 6 hours than 3 hours after myocardial infarction;3. After denervating the capsaicin sensitive nerves and administrating normal rats NK1 and ORL1 receptor antagonist, makes lung injury and inflammation graveness;4. In normal rats'lung tissue, OFQ expressed leaser after AMI than Sham group, and after giving the nociceptin(OFQ) receptor (ORL1) antagonist UFP101, lung injury worse, consider OFQ may play a protective role in lung tissue in early stage of acute myocardial ischemia/infarction.Conclusion:1. excluding cardiogenic factors, in early stage of AMI, pulmonary inflammation response and varying degrees of pulmonary injury appeared, and aggravate as time extending.2. Sensory nerve and its peptides conditioning involved in acute myocardial ischemia-induced lung injury.3. Some sensory nerve components, such as capsaicin sensitive fibers and its' neurotransmitter involved in inflammatory process and worked on a certain degree of protection in lung tissue.4. SP and OFQ, as sensory nerve neurotransmitters involved in inflammation and protection process of lung tissue, and also worked as a protective role.
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