The present work was carried out in order to determine whether a decrease in cardiac Na+‐Ca2+ exchanger (NCX) activity observed in diabetes is caused by a reduction in NCX protein and mRNA levels and to elucidate the significance of this decrease in alterations in [Ca2+]i homeostasis in diabetic cardiomyocytes. The NCX current was significantly reduced in ventricular myocytes freshly isolated from streptozotocin‐induced diabetic rat hearts, and its current density was about 55 % of age‐matched controls. Diabetes resulted in a 30 % decrease in cardiac protein and mRNA levels of NCX1, a NCX isoform which is expressed at high levels in the heart. The reduced NCX current and the decreased protein and mRNA levels of NCX1 in diabetes were prevented by insulin therapy. Although both diastolic and peak systolic [Ca2+]i were not different between the two groups of myocytes, increasing external Ca2+ concentration to high levels greatly elevated diastolic [Ca2+]i in diabetic myocytes. Inhibition of NCX by reduction in extracellular Na+ by 50 % could produce a marked rise in diastolic [Ca2+]i in control myocytes in response to high Ca2+, as seen in diabetic myocytes. However, cyclopiazonic acid, an inhibitor of sarcoplasmic reticulum Ca2+ pump ATPase, did not modify the high Ca2+‐induced changes in diastolic [Ca2+]i in either control or diabetic myocytes. Only in papillary muscles from diabetic rats did the addition of high Ca2+ cause a marked rise in resting tension signifying a partial contracture that was possibly due to an increase in diastolic [Ca2+]i. In conclusion, the diminished NCX function in diabetic myocytes shown in this study results in part from the decreased levels of cardiac NCX protein and mRNA. We suggest that this impaired NCX function may play an important role in alterations in Ca2+ handling when [Ca2+]i rises to pathological levels.

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We systematically elucidated the time course of coagulation and fibrinolysis after isolated head injury. We further demonstrated that changes in coagulofibrinolytic and antifibrinolytic systems in patients with isolated head injury are not different from those in patients without head injury.

We systematically elucidated coagulation disorders in newly defined sepsis. The extrinsic coagulation pathway is activated in patients with severe sepsis and septic shock. In these patients, enhanced thrombin generation and activation, and fibrin formation were demonstrated when compared with the control subjects. Furthermore, the thrombin generated appears not to be fully neutralized by antithrombin III.

P Pu ur rp po os se e: : In order to examine the efficacy of tracheal lidocaine (TL) for attenuation of the cardiovascular responses to endotracheal intubation (EI), we compared the cardiovascular responses to TL alone and EI with TL, with those to EI without TL.M Me et th ho od ds s: : Seventy-five patients (ASA I-II) were studied. Anesthesia was induced with fentanyl 2 µg·kg 1 iv, thiamylal 5 mg·kg 1 iv and sevoflurane 1.0% in oxygen. Vecuronium 0.12 mg·kg 1 was used to facilitate EI. In Group A (n=25), three minutes after induction, EI was performed. In Group B (n=25), three minutes after induction, the patients received TL (4% lidocaine, 4 mL). This was followed by immediate EI. In Group C (n=25), EI was performed two minutes after TL. Heart rate, arterial blood pressure and rate-pressure product (RPP) were measured from one minute before induction until five minutes after EI.R Re es su ul lt ts s: : The changes of RPP caused by TL alone in Group C (TL; +34.6 ± 29.0%, mean ± SD) were significantly (P <0

Disseminated intravascular coagulation and sustained SIRS are strong determinants for posttrauma MODS. This retrospective analysis supports the possibility that platelet counts can be used as a simple laboratory test for predicting MODS. This hypothesis requires proof using a prospective clinical survey.

We systematically elucidated the relationship between tissue factor and TFPI in patients with sepsis, severe sepsis, and septic shock. Activation of tissue factor-dependent coagulation pathway not adequately balanced by TFPI has important roles in sustaining DIC and systemic inflammatory response syndrome, and it contributes to multiple organ dysfunction syndrome and death. High concentrations of neutrophil elastase released from activated neutrophils may explain, in part, the imbalance of tissue factor and TFPI in sepsis.

As evidence of inflammatory responses in whole-body ischemia and reperfusion, our study demonstrates neutrophil-endothelium interaction with signs of endothelial injury in patients with out-of-hospital cardiac arrest. These inflammatory changes may have an important role in post-resuscitation syndrome after human cardiac arrest.