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Pancreatic phospholipase A2 in proximal tubules of rat kidney in experimental acute pancreatitis and after intravenous injection of the enzyme.

Kinetics and distribution of i.v. human pancreatic phospholipase A2 (h-PLA2) were determined in intact and nephrectomized rats, and tissue localization of rat pancreatic PLA2 (r-PLA2) was studied by immunohistochemistry in experimental acute pancreatitis. The concentration of h-PLA2 and the catalytic activity of phospholipase A2 in plasma decreased exponentially in intact and nephrectomized animals after the injection. The initial 15-min half-life was considerably longer in nephrectomized animals, and higher h-PLA2 concentrations and PLA2 catalytic activities were found in plasma. h-PLA2 was localized in endocytotic vesicles and apical cytoplasmic vacuoles in proximal tubule cells of the kidney. The intensity of the immunoreaction decreased considerably between 15 and 50 min in these cells. No signs of tubular damage were seen by light microscopy. Neither immunoreactive h-PLA2 nor PLA2 catalytic activity was found in urine. r-PLA2 was observed in proximal tubule cells 15 min after an injection of sodium taurocholate (necrotizing pancreatitis group) or saline (edematous pancreatitis group) into the pancreatic duct. Signs of tubular damage were present in necrotizing pancreatitis, but tubular morphology was normal in the animals with edematous pancreatitis. We conclude that the proximal tubule cells of the kidney participate in the metabolism of circulating pancreatic PLA2, and considerably higher PLA2 levels persist in plasma in nephrectomized animals. Endogenous pancreatic PLA2 is detected in kidneys in acute pancreatitis.

Acute Disease↗

Air embolism after intravenous injection of contrast material.

Venous air embolism, though considered rare, occurs more frequently than it is recognized. We report the case of a 54-year-old man who was incidentally found to have air in the left brachiocephalic vein and right ventricle after contrast-enhanced computed tomography (CT). Air embolism has been noted to occur after contrast-enhanced CT examination in up to 23% of patients. Because these emboli are small to moderate size and are usually venous, the patients are usually asymptomatic. We review the pathophysiology of air embolization and the recommended treatment.

Contrast Media↗

Intravenous injection of methylprednisolone reduces the incidence of postextubation stridor in intensive care unit patients.

OBJECTIVE: To determine whether treatment with corticosteroids decreases the incidence of postextubation airway obstruction in an adult intensive care unit. DESIGN: Clinical experiment. SETTING: Adult medical and surgical intensive care unit of a teaching hospital. PATIENTS: One hundred twenty-eight patients who were intubated for >24 hrs with a cuff leak volume <24% of tidal volume and met weaning criteria. INTERVENTIONS: : Patients were randomized into a placebo group (control, n = 43) receiving four injections of normal saline every 6 hrs, a 4INJ group (n = 42) receiving four injections of methylprednisolone sodium succinate, or a 1INJ group (n = 42) receiving one injection of the corticosteroid followed by three injections of normal saline. Cuff volume was assessed 1 hr after each injection, and extubation was performed 1 hr after the last injection. Postextubation stridor was confirmed by examination using bronchoscopy or laryngoscopy. MEASUREMENTS AND MAIN RESULTS: The incidences of postextubation stridor were lower both in the 1INJ and the 4INJ groups than in the control group (11.6% and 7.1% vs. 30.2%, both p < .05), whereas there was no difference between the two treated groups (p = .46). The cuff leak volume increased after the second and fourth injection in the 4INJ group and after a second injection in the 1INJ group compared with the control group (both p < .05). CONCLUSIONS: A reduced cuff leak volume is a reliable indicator to identify patients at high risk to develop stridor. Treatment with a single or multiple injections of methylprednisolone can effectively reduce the occurrence of postextubation stridor.

Aged↗

Intravenously injected, TNP-derivatized, Langerhans cell-enriched epidermal cells induce contact hypersensitivity in Syrian hamsters.

The ability of haptenated subpopulations of epidermal cells (EC) to induce contact hypersensitivity (CH) in Syrian hamsters was investigated. Crude haptenated EC and haptenated EC enriched for Langerhans cells (LC) inoculated i.v. into hamsters induced CH that was equivalent in intensity to that induced by epicutaneous application of hapten. By contrast, haptenated EC, relatively depleted of LC, failed to induce CH hypersensitivity responses. Upon subsequent reimmunization of all animals with epicutaneously applied hapten, hamsters that had first received haptenated EC depleted of LC failed to respond in CH assays, indicating that these animals had been rendered unresponsive. These data suggest that haptenated LC are capable of inducing CH regardless of the route of inoculation, whereas haptenated EC, when depleted of LC, deliver a down-regulating signal via the i.v. route.

Animals↗