SUMMARY Dihydropyridine (DHP) Ca2+ channel blockers decrease L-type Ca 2+ channel current (I CaL ) by enhancing steady-state inactivation, whereas β-adrenergic stimulation increases I CaL with small changes in the kinetics. We studied the effects of DHP Ca 2+ channel blockers on cardiac I CaL augmented by β-adrenergic stimulation. We recorded I CaL as Ba 2+ currents (I Ba ) from guinea pig ventricular myocytes using the whole-cell patch clamp technique, and compared the effects of nitrendipine (NIT) in the absence and presence of isoproterenol (1 µM, ISO) or forskolin (10 µM, FSK). Maximal I Ba elicited from a holding potential of -80 mV were diminished to 69.4±13.5% (mean and SE, n=5) of control by NIT (100 nM) and the diminished I Ba were increased to 180.3±23.2% of control by ISO in the presence of NIT, which was similar to the enhancement seen in the absence of NIT. NIT shifted the V 1/2 of the I Ba inactivation curve from -34.6±1.9 mV (n=5) to -48.7±1.2 mV, enhancing I Ba decay with shortening T 1/2 at -10 mV from 164.6±24.2 ms (n=7) to 105.4±15.2 ms. ISO elicited a small additional shift in the V 1/2 of I Ba inactivation in the same direction. ISO and FSK each slowed I Ba decay in the absence of NIT, but not in its presence. Thus, β-adrenergic agonists increase and DHP Ca 2+ channel blockers decrease the amplitude of cardiac I CaL independently and the kinetics of I CaL is determined mainly by the latter when these drugs coexist. ( 1,2) They act by depressing L-type Ca 2+ channel currents (I CaL ), which play key roles in excitation-contraction coupling in cardiac and vascular smooth muscle cells (VSM), thereby exhibiting negative inotropic and vasodilatory actions. DHP Ca 2+ channel blockers inhibit I CaL in VSM more readily than in cardiac muscle as a consequence of differences in the resting membrane potentials, which are more

A 44-year-old man underwent radical thymectomy for malignant thymoma 5 years ago. He subsequently underwent right extrapleural pneumonectomy because a right pleural metastatic lesion had developed. The operation was completed uneventfully. Immediately after arrival at the intensive care unit, the patient appeared restless and in pain. His heart rate increased to 140 bpm and then abruptly decreased to 20-30 bpm concomitant with profound systolic hypotension of 30-40 mmHg. Chest X-ray showed that the heart was shifted into the right thorax. Emergent re-thoracotomy was performed and the heart was found to be malrotated and herniated from an upper defect of the pericardial patch in the right thoracic cavity. The heart was returned to the pericardium and the defect was covered with a pericardial patch. The blood pressure and heart rate became stable. He was transferred to the surgical ward from the intensive care unit on the first postoperative day. The rest of the course was uneventful and the patient was discharged on the seventh postoperative day. The incidence of cardiac herniation after extrapleural pneumonectomy following chemotherapy for malignant pleural mesothelioma has been reported to be around 3%. The risk of cardiac herniation should always be considered, especially after extrapleural pneumonectomy.

Background A patient with undiagnosed tracheomalacia undergoing surgery experienced accidental expiratory central airway collapse after tracheal intubation. Here, we aimed to diagnose tracheomalacia from the preoperative data. Case Presentation A 73‐year‐old man, scheduled for abdominal surgery, had a clinical history of chronic obstructive pulmonary disease. Preoperative chest computed tomography revealed a lateral narrowing of the tracheal shape. After tracheal intubation, we could not manually ventilate the inflated lung. Emergent bronchoscopy findings, including severe expiratory tracheal collapse, indicated a diagnosis of tracheomalacia. We could fully ventilate the patient by moving the endotracheal tube near the tracheal carina and finally changing it to a double‐lumen tube. Airway collapse did not occur under spontaneous breathing. Conclusion Accidental expiratory central airway collapse could occur in patients with undiagnosed tracheomalacia during surgery. A diagnosis of tracheomalacia should be presumed from a deformed trachea on preoperative imaging and history of chronic obstructive pulmonary disease.

Case: A 20-year-old woman developed acute psychotic symptoms and altered level of consciousness. She presented with neck stiffness, tremulous arms, facial dyskinesia, and distension of the lower abdomen. Pelvic magnetic resonance imaging showed bilateral ovarian teratomas. Anti-N-methyl-D-aspartate receptor antibodies were detected in her cerebrospinal fluid.Outcome: Resection of the tumors and immunotherapy were carried out. She gradually recovered and was discharged with few neurological deficits on the 105th day of hospitalization. Conclusion:Our survey of 63 previous reports describing 92 cases revealed that 21.7% of the patients were sent to emergency departments and 59.8% of the patients were managed in intensive care units. Emergency physicians and intensivists should be aware of this disorder, as they may encounter undiagnosed disorders in patients with epileptic attacks, acute psychotic signs, dyskinesia, or hypoventilation in the course of the illness.

morphology was examined on lateral cervical radiographs that show the thickness of the retropharyngeal wall and the morphological state of the airway around the root of the tongue before and after anesthesia for the two groups of patients. Materials and methodsThe study was carried out in Mitsui Memorial Hospital. The study was approved by the ethics committee of the hospital. Sixteen patients rated as ASA 1 or 2 scheduled for gynecologic or breast surgery received a detailed explanation of the study and subsequently gave their consent. They were allocated randomly to the two groups. For the cuff-adjusted group, the internal cuff pressure was adjusted every 30 min so that an air leak developed when the airway pressure exceeded 15 cm H 2 O with manual ventilation. For the cuff-unadjusted group, the cuff pressure was adjusted only once, at the time of LMA placement, so that a leak occurred at an airway pressure of 20 cm H 2 O.The subjects received intramuscular injection of 0.5 mg of atropine and 50 mg of hydroxyzine 30 min before they were admitted to the operating room. Following epidural catheterization, anesthesia was induced with 5 mg·kg Ϫ1 of thiopental, followed by muscle relaxation with 1 mg·kg Ϫ1 of succinylcholine. A no. 3 LMA with a cuff that had been deflated was manually inserted. Mepivacaine was administered through an epidural catheter, and anesthesia was maintained with 2 ᐉ·min Ϫ1 of oxygen, 4 ᐉ·min Ϫ1 of nitrous oxide, and 0.5% to 2.0% of sevoflurane under spontaneous ventilation assisted manually. At the end of surgery, when it was confirmed that the patient had regained consciousness, the LMA was removed. Lateral cervical radiographs were taken before anesthesia and about 60 min after LMA removal without the pillow. Retropharyngeal wall thickness was measured at the thinnest portion at