Endogenous vasopressin increases acute endotoxin shock-provoked gastrointestinal mucosal injury in the rat

Administration of a low dose of endotoxin (from Escherichia coli, 3 mg kg(-1), i.v.), which does not affect vascular permeability or blood pressure over 1 h, leads to the release of endogenous vasopressin and damage to the mucosal microvasculature. Thus, endogenous vasopressin could be involved in septic shock. In the present study, we investigated the role of endogenous vasopressin in gastrointestinal mucosal injury induced by acute endotoxin shock, which was generated in rats by administering a high dose of E. coli endotoxin (50 mg kg(-1), i.v.). Tissues were removed 15 min after endotoxin. The vasopressin V1 receptor antagonist, d[CH2]5Tyr[Me]arginine-vasopressin (0.2-1 microg kg(-1), i.v.), was injected 10 min before endotoxin. Monastral blue (30 mg kg(-1), i.v.), which stains damaged vasculature, was injected 10 min before autopsy. Endotoxin reduced systemic arterial blood pressure (from 115+/-5 to 42+/-4 mmHg), generated macroscopic and microvascular injury, and elevated plasma vasopressin levels (from 3.4+/-0.2 to 178+/-16 pg ml(-1)). The vasopressin V1 receptor antagonist reduced this macroscopic injury, and in the vasopressin-deficient Brattleboro rat a similar reduction of gastrointestinal mucosal damage was found. Substantial decreases in endotoxin-induced microvascular damage were observed in each tissue, e.g., the gastric Monastral blue staining was reduced by 47+/-3% and 96+/-3% (P < 0.01) after vasopressin V1 receptor antagonist treatment and in Brattleboro rats, respectively. Vasopressin, acting through its V1 receptors, thus appears to be involved in acute endotoxin shock-provoked gastrointestinal injury.     

Alternative medicine. Is it all in your mind?

Therapeutic interventions may trigger nonspecific mechanisms whose effects are not attributable to the specific properties of a given treatment. Recent investigations on the placebo effect as well as other mind-body interactions are helping us to understand some of the underlying mechanisms, as well as beginning to provide us with potentially effective adjuvant treatment strategies for a variety of human diseases.     

The rat epididymal fat pad as an implantation site for the study of microcapsule biocompatibility: validation of the method

The study of microcapsule biocompatibility is hindered by their uneven distribution and low recovery when implanted into the peritoneum. We evaluated the use of the rat epididymal fat pad as a microcapsule implantation site for biocompatibility studies. The recovery rate of microcapsules containing 85Sr-labeled microspheres was 99.6 +/- 0.75%. Microcapsules made from the same batch of nonpurified alginate, were injected into both fat pads of male Lewis rats (n = 18) and retrieved 14 days later. A semiquantitative fibrosis score scaled from 0 to 3.0 showed that the pericapsular reaction was uniform throughout a fat pad, and that the results of the two fat pads were equivalent because the null hypothesis of inequivalence was rejected (P < .001). Thus, this method can be used to compare the biocompatibility of microcapsule of differing compositions.     

Postinjury multiple organ failure: a bimodal phenomenon

To better define the epidemiology of postinjury multiple organ failure (MOF), we prospectively evaluated 457 high-risk trauma patients who survived more than 48 hours. Overall, 70 (15%) developed MOF. In 27 (39%) patients, the occurrence was early, while in 43 (61%) patients the presentation was delayed. At presentation, early MOF had more cardiac dysfunction, while late MOF had greater hepatic failure. Indices of shock were more critical risk factors for early MOF, while advanced age was more important for late MOF. While early and late MOF had a similar high incidence of major infections, these appeared to be more important in precipitating late MOF. Finally, while mortality is similar, early MOF patients appear to succumb faster. In conclusion, postinjury MOF remains a significant challenge and appears to present in at least two patterns (i.e., early versus late). Better understanding of the relative roles of the dysfunctional inflammation and infections in early MOF versus late MOF may facilitate the development of new strategies for the prevention and treatment of morbid syndrome.     

Renal toxicity. Tobramycin and gentamicin

To see if urinary 2-methyl-4-chlorophenoxyacetic acid (MCPA) excretion could be used to estimate MCPA exposure, four healthy males ingested 5 mg MCPA. The MCPA in the urine was extracted and anlyzed by high pressure liquid chromatography. About 50% of the ingested dose was detected in the urine within 48 h. On the fifth day after intake the MCPA concentration in the urine was below the level of detection, 0.2 microgram/ml. The MCPA did not increase those serum enzymes indicating liver cell damage (S-alanine-aminotransferase, S-alkaline-phosphate). Some creatine kinase (CK) and S-aspartate-aminotransferase (ASAT) values were pathological, but, as all CK values were normal in two persons and all ASAT values were normal in three persons, it not likely that MCPA had a toxic effect on muscle cells. MCPA in urine seems to be a useful indicator of MCPA intake in humans. All the urine passed within 48 h of MCPA exposure must be collected.     

A multiaperture collimator for use at 511 keV

The addition of autologous serum to mixtures containing human red cells, from pregnant and nonpregnant females, and sheep cells resulted in the formation of mixed aggregates containing both human and sheep red cells. In contrast, no aggregate formation occurred when autologous cord serum was added to mixtures containing cord red cells and sheep red cells. Heat inactivation of the adult serum or the presence of 0.15 M EDTA prevented the formation of mixed aggregates. These observations indicated that the mixed aggregates occurred through the complement-dependent red cell immune adherence (RCIA) phenomenon. The addition of untreated cord serum to mixtures containing inactivated adult serum restored the formation of mixed aggregates, indicating that the cord serum contained sufficient complement for RCIA. Natural antibody against sheep red cells was present in adult sera but was absent in cord sera. Using the RCIA receptor assay, the RCIA receptor activity of cord red cells was found to exceed significantly that of the adult pregnant cells (p less than 0.0025). It is postulated that this may represent an aspect of immune adaptation between mother and fetus.