Researches On The Dynamic Process And The Mechanism Of The Ultrastructure And Calcium Concentration In The Off-body Kidney

Dynamic bioinformatics is the main field for the researchers major in Biology. Nowadays quite a many groups pay more attention to the injury caused by the calcium overload during the perfusion of the off-body organs, overlooking the tremendous effect Cell edema may have on them.Based on the theory and the results achieved by our group before, the experimenter perfused the off-body kidney with the pulse-modulated hypothermic machinary continuous perfusion developed by the group. Then the experimenter examined the ultrastructure & function of the off-body kidney, especially the injury induced by the calcium overload to the ischemic reperfused kidney, by electron microscope and Laser Scanning Confocal Microscope (LSCM) integrated with the testing methods like microphotographics, Enzyme activeties examination and calcium fluorescence techniques.The paper would like emphatically indicated that after off-body kidney existing in the artificial life maintain system by 120- hour continous perfusion, it still had good activities measured with ATP. But the cells of tissue had come to appear wounded as a result of electrion microscopic examination. That was cell-to-cell junction emerged injury changes caused by cell edema while calcium overload was not the dominant element. However, both cell-wounded time and degree could be delayed and mitigated by changing the perfusate prescription to protect. In contrary to the glomerular and other renal tissues, the proximal tubular are more easily injuried during the perfusion. The pulse modulated hypothermic machinary continuous perfusion could protect the proximal tubular more effectively than the simple cold prefusion. So the conclusion could be drew that the former has superiority in surviving of the off-body kidney.Photos taken by electron microscope displayed that calcium overload may have close relation with the ischemia-reperfusion injury. More results got through LSCM and X-ray Microanalysis of Microsections all showed that the rise of the calcium concentration during the cold adaption period came from calcium pools inside the cell mainly. These calcium pools mostly distributed in endoplasmic reticulum. Then the paper used calcium channel inhibitors and LSCM to study the calcium source. The following results displayed that the calcium pools in the endoplasmic reticulum induced by the Ryanodine receptor system may be the source. Fartherly, the calcium intensity showed a gradual fade out between the 10th and 15th minute during thesurviving. The factors such as the rise of the modulation resistance, the deduce of the calcium release and the fluorescence quenching all could owe to this result. Ca2+ concentration and its variation could not be detected only by LSCM at this period. This fact indicated us that cell wounded was caused by multiple factors and it could be mitigated if calcium overload was controlled.How to prolong the surviving time and its ischemia-reperfusion injury to the off-body kidney are the hotspot for many researchers studying biomedicine. This paper got some useful developments in this area, supporting a few referenced datas for the study of modulatory mechanisms of the off-body kidney.