SUMMARY1. We studied the effects of low temperature on the action potentials and membrane currents of guinea-pig ventricular myocytes, using a tight-seal whole-cell clamp technique.2. The action potential duration at 95 % repolarization was prolonged from 146+ 33 ms (mean+ S.D., n = 6) at 33-34°C (control temperature) to 314+ 83 ms at 24-25°C (low temperature).3. In whole-cell clamp experiments, low temperature decreased the calcium current (ICa), the delayed rectifier potassium current (IK)' and the inwardly rectifying potassium current (IK.) with 'apparent' Qlo (temperature coefficient) values of 2-3 + 06 for ICa' 4-4 + 1-2 for 'K tail current and 1-5 + 03 for IK. (n = 7).4. The effect of low temperature onIK was further studied in the presence of 06 ,(M nicardipine to block ICa. The decay phase of the IK tail consisted of two exponential components. The fast but not the slow component was highly sensitive to the temperature change with an apparent Q1o of 4-5.5. We found that a component of time-independent current is also sensitive to the temperature. The current had a linear I-V relationship and remained almost unchanged after inhibition of Na+-K+ pump in K+-free external solution.6. Using our mathematical model of the ventricular action potential (a modification from the DiFrancesco-Noble model), we simulated the action potential at low temperature by modifying some of the membrane currents, namely IK' IK1, ICa and a component of background current. It was shown that simultaneous changes in these currents could reproduce approximately 75 % of the action prolongation induced by low temperature.

A tetrodotoxin (TTX)-sensitive Na+ current (iNa) was investigated in single pacemaker cells after 1-4 days in culture. Ruptured-patch and perforated-patch whole cell recording techniques were used to record iNa and spontaneous electrical activity, respectively. For seven cells exposed to 20 mM Na+ (22-24 degrees C) and held at -98 mV (25% of the channels inactivated), the uncorrected maximum iNa was -39 +/- 10 pA/pF at -29.1 +/- 2.4 (SE) mV, maximum conductance was 0.9 +/- 0.2 nS/pF (1.6 +/- 0.2 mS/cm2). Half-activation and inactivation potentials were -41.4 +/- 2.0 and -90.6 +/- 2.5 mV, and the corresponding slope factors were 6.0 +/- 0.4 and 6.4 +/- 0.6 mV. Inactivation and recovery from inactivation were best fit by sums of two exponentials. During action potential clamp, a TTX-sensitive compensation current accounted for 55% of the upstroke velocity. The results suggest that iNa contributes significantly to the action potential in some nodal pacemaker cells, and the characteristics of iNa are similar to those of atrial and ventricular myocytes.

This study presents two adult patients who experienced pleural effusion during hospitalization for stroke rehabilitation therapy after ventriculoperitoneal shunt placement for normal pressure hydrocephalus associated with aneurysmal subarachnoid haemorrhage. The pleural effusion appeared without migration of the catheter into the thoracic cavity. Because of respiratory insufficiency, which prevented progress in their rehabilitation programme, thoracentesis was repeated for recurrent pleural effusions, the composition of which differed significantly from that of cerebrospinal fluid. Both cases had past histories of laparostomies; therefore, the distal end of the catheter was placed in the right anterior subphrenic recess. One was able to resolve the pleural effusion and rehabilitate the patients by replacing the ventriculoperitoneal shunt with a vetriculoatrial shunt. In the literature, there have been only 23 reports of pleural effusion associated with a ventriculoperitoneal shunt. Among those reports, four involved pleural effusion without migration of the distal catheter; however, all of those cases were in children. Thus, this study reports the first adult cases of pleural effusion without migration of the catheter into the pleural cavity and discusses a putative mechanism.

No abstract