Intrapericardial caval injury due to blunt trauma.

BACKGROUND: Report of diagnosis and treatment of intrapericardial vena caval injury caused by blunt thoracic trauma, an unusual cause of cardiac tamponade. METHODS: A 43-year-old male motor vehicle accident victim suffered a lacerated intrapericardial inferior vena cava leading to cardiac tamponade. Positive clinical findings were hypotension and tachycardia without indication of external chest trauma. RESULTS: Abdominal computed tomography was negative, but ultrasound demonstrated cardiac tamponade and fluid in the abdomen. Pericardiocentesis was performed, and nonclotted blood was aspirated. Laparotomy showed intra-abdominal blood and splenic capsule avulsion. Sternotomy revealed a laceration of the inferior vena cava, which was repaired. CONCLUSIONS: Signs of cardiac tamponade and a history of blunt thoracic trauma caused by deceleration injury suggests intrapericardial inferior vena cava injury. Median sternotomy is the optimal choice for caval repair.

Role of calcium and calmodulin in the regulation of the rabbit ileal brush-border membrane Na+/H+ antiporter.

In rabbit ileum, Ca2+/calmodulin (CaM) appears to be involved in physiologically inhibiting the linked NaCl absorptive process, since inhibitors of Ca2+/CaM stimulate linked Na+ and Cl- absorption. The role of Ca2+/CaM-dependent phosphorylation in regulation of the brush-border Na+/H+ antiporter, which is believed to be part of the neutral linked NaCl absorptive process, was studied using purified brush-border membrane vesicles, which contain both the Na+/H+ antiporter and Ca2+/CaM-dependent protein kinase(s) and its phosphorprotein substrates. Rabbit ileal villus cell brush-border membrane vesicles were prepared by Mg precipitation and depleted of ATP. Using a freezethaw technique, the ATP-depleted vesicles were loaded with Ca2+, CaM, ATP and an ATP-regenerating system consisting of creatine kinase and creatine phosphate. The combination of Ca2+/CaM and ATP inhibited Na+/H+ exchange by 45 +/- 13%. This effect was specific since Ca2+/CaM and ATP did not alter diffusive Na+ uptake, Na+-dependent glucose entry, or Na+ or glucose equilibrium volumes. The inhibition of the Na+/H+ exchanger by Ca2+/CaM/ATP was due to an effect on the Vmax and not on the Km for Na+. In the presence of CaM and ATP, Ca2+ caused a concentration-dependent inhibition of Na+ uptake, with an effect 50% of maximum occurring at 120 nM. This Ca2+ concentration dependence was similar to the Ca2+ concentration dependence of Ca2+/CaM-dependent phosphorylation of specific proteins in the vesicles. The Ca2+/CaM/ATP-inhibition of Na+/H+ exchange was reversed by W13, a Ca2+/CaM antagonist, but not by a hydrophobic control, W12, or by H-7, a protein kinase C antagonist. We conclude that Ca2+, acting through CaM, regulates ileal brush-border Na+/H+ exchange, and that this may be involved in the regulation of neutral linked NaCl absorption.

Modulation of human peripheral blood eosinophil function by tumor necrosis factor-alpha.

Eosinophils are important effectors in helminthic parasitic infection. Tumor necrosis factor (TNF-alpha) has been implicated as a mediator in the host response to parasitic infection and enhances eosinophil-mediated helminthotoxicity. We have examined the direct effects of recombinant human (rh) TNF on eosinophil functions of degranulation and oxidative metabolism. This report describes the minimal effects of rhTNF-alpha on eosinophil superoxide anion generation and enzyme secretion, which do not satisfactorily explain the observed increases in helminthotoxicity. In contrast to other cell types, eosinophils are unique in their differential responses to interleukin-1 beta and TNF.