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To examine the role of myocardial interleukin-6 (IL-6) in myocardial inflammation and dysfunction after burn complicated by sepsis, we performed 40% total body surface area contact burn followed by late (7 days) Streptococcus pneumoniae pneumonia sepsis in wild-type (WT) mice, IL-6 knockout (IL-6 KO) mice, and transgenic mice overexpressing IL-6 in the myocardium (TG). Twenty-four hours after sepsis was induced, isolated cardiomyocytes were harvested and cultured in vitro, and supernatant concentrations of IL-6 and tumor necrosis factor (TNF)-[alpha] were measured. Cardiomyocyte intracellular calcium ([[[Ca.sup.2+]].sub.i]) and sodium ([[[Na.sup.+].sub.i]) concentrations were also determined. Separate mice in each group underwent in vivo global hemodynamic and cardiac function assessment by cannulation of the carotid artery and insertion of a left ventricular pressure volume conductance catheter. Hearts from these mice were collected for histopathological assessment of inflammatory response, fibrosis, and apoptosis. In the WT group, there was an increase in cardiomyocyte TNF-[alpha], [[[Ca.sup.2+]].sub.i], and [[[Na.sup.+].sub.i] after burn plus sepsis, along with cardiac contractile dysfunction, inflammation, and apoptosis. These changes were attenuated in the IL-6 KO group but accentuated in the TG group. We conclude myocardial IL-6 mediates cardiac inflammation and contractile dysfunction after burn plus sepsis. tumor necrosis factor-[alpha]; [alpha]-myosin heavy chain; cardiac contractile function; fibrosis; apoptosis doi:10.1152/ajpheart.01150.2006.

The present study was designed to assess hemodynamics and myocardial function at 18 h after injury caused by cecal ligation and puncture (CLP) in CD8-knockout mice treated with anti-asialoGM1 (CD8KO/[alpha]AsGM1 mice). Arterial pressure was measured by carotid artery cannulation, and left ventricular pressure-volume measurements were obtained by use of a 1.4-Fr conductance catheter. Blood acid-base balance and indexes of hepatic, renal, and pulmonary injury were also measured. CD8KO/[alpha]AsGM1 mice exhibited higher mean arterial pressure and increased systemic vascular resistance compared with wild-type mice. Cardiac output was significantly decreased in wild-type, but not CD8KO/[alpha]AsGM1, mice compared with sham controls. Myocardial function was better preserved in CD8KO/[alpha]AsGM1 mice as indicated by less impairment of left ventricular pressure development over time, time varying maximum elastance, end-systolic pressure-volume relationship, and preload recruitable stroke work. The impairment in myocardial function was associated with induction of proinflammatory cytokine mRNAs in the hearts of wild-type mice. The hemodynamic derangements in wild-type mice were coupled with significant metabolic acidosis and elevated serum creatinine levels. Overall, this study shows that cardiovascular collapse and shock characterized by hypotension, myocardial depression, low systemic vascular resistance, and metabolic acidosis occurs after CLP in wild-type mice but is attenuated in CD8KO/[alpha]AsGM1 mice. These observations likely explain, in part, the previously observed survival advantage of CD8KO/ [alpha]AsGM1 mice following CLP. blood pressure; vascular resistance; cardiac output; left ventricular function; perfusion

We previously showed that [beta]2-microglobulin knockout mice treated with anti-asialoGM1 (132M/[alpha]AsGM1 mice) exhibit less hypothermia, reduced production of proinflammatory cytokines, less metabolic acidosis, and improved survival after cecal ligation and puncture (CLP) compared with wild-type mice. The present study was designed to assess hemodynamics and left ventricular contractility at 18 h after CLP. Arterial pressure was measured by carotid artery cannulation, and left ventricular pressure-volume loops were obtained by insertion of a 1.4-F conductance catheter into the left ventricle. Heart rate, stroke volume, and cardiac output were not significantly different between wild-type and [beta]2M/[alpha]AsGM1 mice after CLP. However, [beta]2M/[alpha]AsGM1 mice exhibited improved mean arterial pressure and systemic vascular resistance compared with wild-type mice. Myocardial function was also better preserved in 132M/[alpha]AsGM1 mice as indicated by improved left ventricular pressure development over time, time-varying maximum elastance, end-systolic pressure-volume relationship, and preload recruitable stroke work. Overall, this study shows that cardiovascular collapse characterized by hypotension, myocardial depression, and low systemic vascular resistance occurs after CLP in wild-type mice. However, [beta]2M/[alpha]AsGM1 mice exhibit improved hemodynamics and cardiac contractile function after CLP that may account, in part, for our previously observed survival benefit. cecal ligation and puncture; blood pressure; vascular resistance; cardiac output; pressure-volume relationships

Thrombocytopenia in pregnancy could potentially lead to epidural hematoma and associated morbidity when neuraxial anesthesia is performed. We present a case of a 24-year-old parturient, who was otherwise healthy and without prior thrombocytopenia, who underwent epidural placement in the setting of undiagnosed severe thrombocytopenia. Her workup remained inconclusive, and the presumptive diagnosis of severe preeclampsia was made. She was given a platelet transfusion and underwent an uncomplicated spontaneous vaginal delivery. After recovery of her platelet count, the epidural catheter was safely removed approximately 60 hours after placement without any signs or symptoms of an epidural hematoma. [ABSTRACT FROM AUTHOR]