Postoperative respiratory failure secondary to Pneumocystis carinii pneumonia.

Pneumocystis carinii pneumonia (PCP) occurs frequently in individuals infected with the HIV virus. Malignancy, immunosuppressive drugs, and congenital immune deficiency may be associated with PCP. We describe a patient with stage 1 testicular carcinoma who developed hypoxemic respiratory failure two days after retroperitoneal lymph node dissection. Pneumocystis carinii organisms were demonstrated by catheter lavage samples and confirmed on bronchoalveolar lavage. Testing for HIV antibody by ELISA and the Western blot test were negative; HIV viral culture and polymerase chain reaction were also negative. Pneumocystis carinii pneumonia is unusual in localized surgically cured malignancies without obvious immunodeficiency and, to our knowledge, has not been described as a cause of postoperative respiratory failure.

Ionic composition of small intestinal secretion induced by PGE2.

Small intestinal fluid secretion induced by oral prostaglandin E2 in fasted rats was analyzed for various ionic components. Rat intestinal fluid had elevated calcium and potassium as well as decreased sodium and chloride concentrations relative to plasma electrolytes. Either low dose prostaglandin (0.15 mg/kg) or 1 ml of intragastric mannitol (5%) induced accumulation in the small intestine of fluid that had elevated chloride and depressed calcium and sodium concentrations compared to vehicle-treated controls. Higher doses of prostaglandin (1.0 mg/kg) led to secretions with increased sodium and chloride concentrations with respect to mannitol-induced fluid. Electrolyte concentrations in fluid induced by low dose prostaglandin appear to be similar to those in fluid caused by osmotically-induced changes. Higher doses of prostaglandin E2 induce additional electrolyte alterations which may result from modified gut transport of water and ions.

Clonidine delays small intestinal transit in the rat.

Subcutaneous clonidine (0.01--1.0 mg/kg) was found to delay small intestinal transit but not gastric emptying in the unanesthetized rat, with a maximal effect seen at 0.1 mg/kg. Gastric emptying was expressed as the percentage of intragastrically administered 51Cr emptied into the small intestine after 45 min. Small intestinal transit was the percentage of the small intestinal length traveled 45 min after oral or duodenal administration of black ink. The depression of small intestinal transit by clonidine to 20 to 30% of control values was blocked by phentolamine and yohimbine, but not by prazosin or phenoxybenzamine, suggesting a presynaptic (alpha-2) agonist action of clonidine. Pretreatment of rats with 6-hydroxydopamine, propranolol, atropine, methysergide, naloxone, mepyramine or metiamide failed to alter the effects of clonidine. These results suggest that an alpha adrenergic receptor, possibly presynaptic, regulates small bowel propulsion in rat without involvement of acetylcholine, norepinephrine, endorphins, histamine or serotonin.

Prostaglandin stimulation of gastrointestinal transit in post-operative ileus rats.

The prostaglandins PGF2 alpha, PGE2 and 16,16-dimethyl PGE2, when administered intravenously, orally, subcutaneously or intraduodenally to laparotomized rats, decreased gastric emptying, small intestinal transit and colonic transit as compared to unoperated controls. All three prostaglandins increased colonic transit above that found with unoperated controls. This activity was independent of small intestinal fluid accumulation (i.e., enteropooling) since ligating the ileal-cecal junction had no effect on colonic transit. Small intestinal transit was increased, but not normalized, by PGE2 and 16,16-dimethyl PGE2. 16,16-Dimethyl PGE2 completely restored gastric emptying when given intravenously to laparotomized rats of doses greater than 5.0 microgram/kg. This effect on gastric emptying lasted approximately 4 hrs. Thus, 16,16-dimethyl PGE2, when given intravenously, normalized gastric emptying, significantly increased small intestinal transit, and made the colon hypermotile. Prostaglandins may be beneficial in the treatment of postoperative ileus and other conditions of sluggish gastrointestinal propulsion.

Enteropooling assay: a test for diarrhea produced by prostaglandins.

An assay (enteropooling assay) to test the diarrheogenic property of prostaglandins is described. Fasted rats are given a prostaglandins either orally or subcutaneously, and are killed 30 min later. The entire small intestine is removed and its contents collected into a test tube. The greater the volume of this intestinal fluid, the more diarrheogenic is the prostaglandin. The assay is simple, rapid, quantitative, and predictive of diarrhea. It can be used to grade the relative diarrhoegenic activity of prostaglandins as well as to test agents that may block this effect. The accumulation of fluid into the small intestine is called "enteropooling". It is the sum of (a) the fluid being excreted from the blood into the lumen, and (b) to a lesser extent, the portion of fluid already into the lumen but whose absorption is inhibited by the prostaglandin. The degree of enteropooling depends also on how much fluid flows from the small to the large intestine. Our results support the hypothesis that the diarrhea observed after administration of high doses of prostaglandins is due to accumulation of abundant fluid into the small intestine, and not intestinal hypermotility. This fluid is then carried into the large intestine and eventually expelled as diarrhea. Agents other than prostaglandins were tested for enteropooling activity. Laxatives such as castor oil, hypertonic solutions and bile salts caused enteropooling.