Whole‐cell currents were recorded in single, spontaneously active cells dissociated from porcine sino‐atrial node, and the conductance and gating properties of the delayed rectifier K+ current (IK) were investigated. The isolated cells exhibited spontaneous action potentials at a rate of 80.5 ± 5.4 min−1 (mean ± s.e.m., n= 11). Under Ca2+ current block, depolarization from ‐40 mV to various potentials activated a time‐dependent outward current (IK). The activation curve of IK showed a half‐activation potential (V½) of 20.5 ± 2.1 mV and a slope factor (S) of 16.4 ± 1.2 mV (n= 8). As the duration of the depolarizing pulse to either +10 or +60 mV was prolonged, the amplitude of the tail current increased in proportion to that of the activated outward current during depolarization. E4031 (2‐5 μM), a selective blocker for the rapidly activating component of IK (IK,r), hardly affected IK, but chromanol 293B, a selective blocker for the slowly activating component (IK,s), inhibited IK with an IC50 of 8.79 μM. The reversal potential of IK was ‐75.2 ± 2.3 mV with 5.4 mM external and 150 mM internal K+. The time courses of activation and deactivation of IK were fitted by the sum of two exponential functions at various potentials. The relationship between the time constants and membrane potential showed a bell‐shaped curve with a peak at around ‐10 mV for both fast and slow components. The results indicate that in porcine sino‐atrial node cells IK is largely derived from IK,s and that IK,s plays a functional role in the slow diastolic depolarization. IK,s may, in part, account for the relatively slower heart rate of pigs than that of rabbit in which IK,r is a functionally dominant component of IK.

The present data demonstrate an inverse correlation between serum IL-18 level and the P/F ratio, suggesting the possible involvement of IL-18 in the pathogenesis of respiratory failure in patients with ALI/ARDS. Early-stage serum IL-18, IL-12, and TNF-α levels appear to reflect the >60-day prognosis in patients with ALI/ARDS.

We present a 19-year-old man who excreted green urine after propofol infusion. The patient was admitted to our hospital for injuries sustained in a traffic accident and underwent surgery. After starting continuous infusion of propofol for postoperative sedation, his urine became dark green. Serum total bilirubin and urine bilirubin were both elevated. We believe that the green discoloration of the urine was caused by propofol infusion and was related to impaired enterohepatic circulation and extrahepatic glucuronidation in the kidneys.

The prognosis and severity of infection may be assessed more accurately by measuring the presepsin levels until day 7. Presepsin is a useful diagnostic tool for DIC with infection.