On the pathogenesis of platelet dysfunction of undialyzed and hemodialysed chronic renal failure [CFR] patients

Patients with chronic renal failure CRF suffer form abnormalities of primary hemostasis due to platelet dysfunction. Dialysis improves platelet abnormalities but does not eliminate the risk of hemorrhage. Hemodialysis can even contribute to the bleeding through the continuous platelet activation induced by the interaction between blood and artificial surfaces. The aim is to study the changes in the biostructure of platelets in ESRD and the effect of HD on it, and to find its relation to its function. The platelet biostructure [total protein, total lipids, total carbohydrates, total phospholipids [PL], total cholesterol] and enzymatic activities [Na[+]-K[+]-ATPase, monoamine oxidase, [MAO] often healthy control, 15 undialyied CRF patients, and 15 hemodialyzed CRF patients [before and after dialysis] were studied. The results revealed an increase of total lipids, total PL concentrations and decrease in the activities of Na[+]-K[+]-ATPase, MAO of platelets of CRF compared to their healthy controls. After dialysis results as compared to those before dialysis revealed decreased concentration of total PL of the platelets and increased activity of Na[+]-K[+]-ATPase. Whereas if the results after dialysis were compared to those of healthy controls total lipids, PL, total cholesterol concentration and Na[+]-K[+]-ATPase showed significant increased values whereas MAO activity decreased significantly. Correlation studies showed insignificant correlation for all the parameters studied before or after dialysis as compared with the age of patients or duration of dialysis-in years. It may be concluded that the biochemical aberrations that were revealed form the present study concerning End Stage Renal Disease [ESRD] patients [dialyzed and undialyzed] may be looked upon as a causative factor in the well known physiological impairment of platelet function in uremia which appears not to be totally corrected by hemodialysis

Functional significance of lipid changes under the effect of inhalational anesthetics

Small concentrations of inhaled anesthetics can induce type II pneumocytes dysfunction and affect surfactant production and exacerbate oxidant mediated lung injury. The aim of the present work was to study the interrelationship between alveolar surfactant lipid composition and that of the lung tissue aiming to understand the sequence of events in the pathogenesis and pathophysiology of acute lung injury [ALI] after inhalation anesthesia. 60 albino rats were used in this study. Lipids were extracted from the lung tissue and alveolar surfactant obtained by bronchoalveolar lavage from rats which were subjected to 1-2% halothane or nitrous oxide anesthetics. The following parameters were determined on the extracted lipids: total lipids [TL], triglycerides [TG], total cholesterol [T-ch], total free fatty acids [FFA], total phospholipids [TPL], phospholipids fractions, lecithin [phosphatidyl cholin Pc], lysolecithin, cephalin [phosphatidyl ethanol amine PI] and sphingomyelin. I- Effect of halothane In the surfactant: Halothane decreased all parameters studied with the exception of FFA and sphingomyelin which was increased compared to controls. Cephalin did not change. However, in the lung FFA, lecithin and lysolecithin increased while all other parameters decreased. II- Effect of nitrous oxide [N[2]O]: In the surfactant: All parameters also decreased except lysolecithin, cephalin and sphingomyelin, which were increased. However, FFA did not change significantly from controls. In the lung: Lecithin, lysolecithin and FFA increased whereas the other parameters decreased. Halothane and N[2]O differ as regards their effect on the lipid profile of the surfactant or lung tissue. The functional significance of the alteration was discussed