1-3-dimethylthiourea and Shock--Septic

The effects of endotoxemia on the cardiac function and contractility, oxygen radical production by polymorphonuclear leukocytes (PMNL-CL), cardiac antioxidant reserve (LV-CL), antioxidant enzymes (superoxide dismutase [SOD], catalase, glutathione peroxidase [GSH-P(X)]) and malondialdehyde (MDA); and plasma creatine kinase (CK) and lactate in the absence or presence of dimethylthiourea (DMTU), an antioxidant, in anesthetized dogs were studied. Dogs were assigned to three groups: group 1, control; group II, endotoxin (ET) (5 mg/kg body wt intravenously), and group III, ET + DMTU (500 mg/kg intravenously). ET produced decreases in the cardiac function and contractility, antioxidant reserve, antioxidant enzymes; and increases in PMNL-CL, cardiac MDA, plasma CK, and lactate. Pretreatment with DMTU attenuated the ET-induced cardiac dysfunction and changes in the cardiac MDA, antioxidant reserve, and antioxidant enzymes, PMNL-CL, and plasma CK and lactate levels. These results suggest that reactive oxygen species may be involved in the deterioration of cardiac function and contractility, and cellular injury during endotoxic shock and that antioxidants may be of value in the treatment of endotoxic shock.

Topics: Animals; Blood Pressure; Dogs; Female; Free Radical Scavengers; Heart Rate; Male; Myocardial Contraction; Reactive Oxygen Species; Shock, Septic; Superoxide Dismutase; Thiourea; Vascular Resistance; Ventricular Function, Left

A rat model of endotoxic shock was used to evaluate the effects of dimethylthiourea, a putative hydroxyl radical scavenger, in the alterations of lung phosphatidylcholine biosynthesis found during endotoxemia. Treatment of rats with dimethylthiourea, just before lipopolysaccharide injection, resulted in a decreased lipid peroxidation and an increase in phosphatidylcholine biosynthesis, although it did not prevent the body weight loss or the increase in lung weight and lung protein content associated with the lung injury induced by lipopolysaccharide. Our results suggest that phosphatidylcholine biosynthesis is impaired by processes in which hydroxyl radicals are implicated, although other oxygen free radical species, not removed by dimethylthiourea, can be also involved in lipopolysaccharide mediated lung injury.

Topics: Animals; Body Weight; Hydroxyl Radical; Lipid Peroxidation; Lipopolysaccharides; Lung; Male; Organ Size; Phosphatidylcholines; Rats; Rats, Wistar; Shock, Septic; Superoxide Dismutase; Thiourea