Given an abstract of a paper, generate a title for this paper such that conveys the key focus of the paper.

[Q]: Abstract: Pulmonary edema due to upper airway obstruction can be observed in a variety of clinical situations. The predominant mechanism is increased negative intrathoracic pressure, although hypoxia and cardiac and neurologic factors may contribute. Laryngospasm associated with intubation and general anesthesia is a common cause of pulmonary edema in children. However, only seven cases of pulmonary edema presumably due to laryngospasm have been reported in adolescents and adults. Five of the seven had other risk factors for upper airway obstruction, and in four, the diagnosis of "laryngospasm" could be explained by other factors. Patients with underlying risk factors for upper airway obstruction, such as a forme fruste of sleep apnea or nasopharyngeal abnormalities, appear to be at increased risk for the development of pulmonary edema in the setting of intubation and anesthesia. This form of pulmonary edema usually resolves rapidly without the need for aggressive therapy or invasive monitoring.
[A]: Post-extubation pulmonary edema following anesthesia induced by upper airway obstruction. Are certain patients at increased risk?

[Q]: Abstract: The effects of chronic denervation on sodium (Na) channels in rabbit muscle membrane were determined using intracellular microelectrodes and Vaseline gap voltage clamp techniques. The Hodgkin-Huxley model was used to describe the kinetic and steady-state parameters of channel activation and fast inactivation. Chronic (7-10 days) denervation was found to cause a decreased resting potential, lowered action potential peak, and fibrillation potentials in rabbit extensor digitorum longus (EDL) muscles. Under voltage clamp conditions, no differences were observed between denervated and normal fibers in the voltage dependence of the steady-state Na channel activation and fast inactivation curves, or in the time course of development of fast inactivation. However, in denervated fibers, the time course of recovery from fast inactivation was approximately half that measured in normal fibers. Also, whereas depolarizing holding potentials induced a long-term inactivation to varying degrees in normal EDL fibers, denervated EDL fibers and normal soleus fibers were uniformly resistant to prolonged depolarization. These results suggest that the denervation-induced development of spontaneous activity may be due in part to changes in the mechanisms that control the refractoriness of Na channels.
[A]: Sodium channel kinetics in normal and denervated rabbit muscle membrane.

[Q]: Abstract: The possible role of prostaglandins in mediating large coronary artery vasodilation by nitrates was investigated by quantitative magnification coronary angiography. The effects of aspirin (1 g systemically and 100 mg intracoronary) in preventing large coronary artery vasodilation induced by intracoronary isosorbide dinitrate was investigated in 16 patients. Of these, 5 received 0.3 mg (Group 1A) and 11 received 3 mg (Group 1B) intracoronary isosorbide dinitrate, before and 15 minutes after aspirin. Relative to control, 0.3 mg isosorbide dinitrate induced a 19 +/- 9% (mean +/- SD) (p less than 0.01) and 19.5 +/- 11% (p less than 0.01) increase in coronary diameter before and after aspirin, respectively (p = NS). Changes after 3 mg isosorbide were 23 +/- 12% (p less than 0.01) and 26.5 +/- 14% (p less than 0.01), respectively, before and after aspirin (p = NS). In 10 additional patients (Group 2), the effect of the same dose of aspirin on rest coronary artery tone was assessed: changes relative to control were 0.9 +/- 5.5% (p = NS) minutes after aspirin. The intracoronary administration of 3 mg isosorbide dinitrate produced a 24.7 +/- 11% increase in coronary diameter (p = NS versus pre- and postaspirin isosorbide in Group 1B). Urinary 6-ketoprostaglandin-F1 alpha values in urine samples collected in the 8 hours before and the 8 hours after the study in five patients in Group 1B and five patients of Group 2, revealed a 36 +/- 14% (mean +/- SD) reduction in excretion of prostacyclin (p less than 0.01). These data rule out a role for prostaglandins both in mediating dilation of large coronary arteries by nitrates and in affecting their vascular tone at rest.
[A]:
Coronary vasodilation by nitrates is not mediated by the prostaglandin system: a quantitative cineangiographic study.