[Case of pulmonary edema and transient heart failure during difficult airway management].

Many kinds of side effects are likely to occur while managing difficult airway. This article describes a case of a man who fell into pulmonary edema and heart failure during the difficult airway management. He was to undergo arthroscopic surgery on his knee. At first, we planed spinal anesthesia but he took an antiplatelet drug (aspirin). Since we wanted to avoid the epidural hematoma, we chose general anesthesia. After induction of general anesthesia, positive pressure ventilation via face mask was possible, but laryngeal mask ventilation was impossible. Although tracheal intubation was attempted, we recognized that he had difficult airway. After some intubation trials, we decided to quit the operation and awoke the patients. Spontaneous breathing appeared soon, but the oxygenation was getting worse. We performed fiberoptic nasal intubation under spontaneous breathing. Although his blood pressure was quite high during intubation, after intubation the vasopressor was needed to maintain blood pressure. Ventilation with 100% O2 could not maintain the oxygenation well. Chest X-ray revealed the pulmonary edema. We presumed that hypertension associated with airway stimulation had caused acute pulmonary edema and heart failure resulting from diastolic dysfunction induced by increased catecholamine.

Nicorandil, an adenosine triphosphate-sensitive potassium channel opener, inhibits muscarinic acetylcholine receptor-mediated activation of extracellular signal-regulated kinases in PC12 cells.

BACKGROUND: Nicorandil, an adenosine triphosphate-sensitive potassium channel opener, is reported to have an antinociceptive effect by hyperpolarization through the K(+) channel. The activation of extracellular signal-regulated kinase (ERK), a family of mitogen-activated protein kinases, plays an important role in synaptic plasticity and noxious stimulation in the dorsal root ganglion, and spinal neurons have been reported to induce its activation. To understand the biological mechanisms of nicorandil, we examined the effects of nicorandil on muscarinic acetylcholine (ACh) receptor-mediated activation of ERK in a neuronal model cell, rat pheochromocytoma PC12 cells. METHODS: PC12 cells were stimulated with ACh in the presence or absence of nicorandil, and phosphorylation of ERK was examined by a Western blot analysis. We also examined the effects of nicorandil on the ERK activation induced by 4beta-phorbol 12-myristate 13-acetate, an activator of protein kinase C, or ionomycin, a calcium ionophore. Intracellular Ca(2+) increase was visualized in fluo-3-loaded PC12 cells using fluorescence microscopy. RESULTS: Nicorandil inhibited ACh-induced ERK activation in a concentration-dependent manner. The inhibition was abolished by glibenclamide, an adenosine triphosphate-sensitive potassium channel blocker. Nicorandil suppressed the ERK activation induced by ionomycin but not 4beta-phorbol 12-myristate 13-acetate. Pretreatment of PC12 cells with nicorandil reduced the intracellular Ca(2+) concentration stimulated by ACh. CONCLUSIONS: Nicorandil inhibits muscarinic activation of the ERK signaling pathway by reducing the intracellular Ca(2+) concentration.