Participation of angiotensin converting enzyme, prostaglandins and nitric oxide and possibility of their interaction in glycerol induced acute renal failure [A high microscopic, semi quantitative study]

This study was performed using adult male albino rats and acute tubular necrosis was induced by glycerol injection into the hind limbs. Inhibitors for angiotensin converting enzyme [ACE], prostaglandins [PG] and nitric oxide [NO] synthase were injected intraperitonealy before and after glycerol injection to study their roles in acute renal failure and the possibility of their interaction in the kidney in a similar pattern to that takes place in the heart. Tubular damage occurring was semi-quantified in kidneys of different groups. ACE inhibitor [perindopril] was found to reduce the glycerol-induced acute tubular necrosis establishing the injurious role of angiotensin converting enzyme in the pathogenesis of this condition. Injection of either PG synthesis inhibitor [voltaren] or NO synthase inhibitor [L-NAME] has caused increase of the glycerol-induced acute tubular necrosis indicating that both prostaglandins and NO has renoprotective effects. Injection of either PG synthesis inhibitor [voltaren] or the NO synthase inhibitor [L-N AME] together with the ACE inhibitor impairs its renoprotective effect denoting that prostaglandins and NO may mediate this renoprotection

Ultrastructural changes in pancreatic acini at different intervals after induction of acute haemorrhagic pancreatitis with diazinon

Thirty healthy adult male guinea pigs were utilized in this study. They were divided into six equal groups. The first was used as a control group. Acute pancreatitis was induced in the remaining 5 groups by a sublethal dose of the organophosphate insecticide Diazinon [DZ]. Animals of the 2[nd], 3[rd], 4[th], 5[th]. and 6[th] groups were sacrificed 0.5, 1, 2.6 and 12 hours respectively after DZ ingestion. Pancreatic acinar alterations occurring after DZ intake can be arranged as follow: 1] excessive stimulation of the pancreas appears after 0.5 hour, 2] initiation of intracellular autolytic changes and interstitial tissue degeneration after 1 hour, 3] appearance of peripheral vacuolation may be created by extracellular enzymes after 2 hours, 4] augmentation of peripheral vacuolation and occurrence of cellular necrosis after 6 hours, 5] disappearance of peripheral vacuolation with reduction in the size of the acini after 12 hours. The interstitial tissues showed increasing width and degeneration. Conclusively, the contribution of intracellular activation of zymogen in the pathogenesis of DZ induced acute pancreatitis beside the other mechanism of increased intraductal hydrostatic pressure resulting from hypersecretion became evident Also, correlation between the ultrastructural changes in pancreatic acini and the time passing after DZ poisoning became manifest. This finding may pay the attention of medicolegal experts to put in their consideration the ultrastructure study of pancreas while investigating the obscure deaths