Background. Hemodynamic responses to laryngoscopy and endotracheal intubation are transient in most patients. However, in some patients with a history of heart disease, systemic hypertension, or cerebrovascular disease, these may lead to dangerous complications. This study is aimed at determining the effectiveness of intravenous nitroglycerin bolus doses in reducing hemodynamic responses to laryngoscopy and endotracheal intubation. Material and Method. In this double-blind randomized controlled trial, 78 patients aged 18 to 65 years were randomly divided into three groups: 1 μg/kg dose of nitroglycerin (first group), 2 μg/kg dose of nitroglycerin (second group), and normal saline or placebo (third group). 26 samples were allocated for each group. Patients’ hemodynamic responses to laryngoscopy and endotracheal intubation were measured at different times. Data were analyzed using SPSS V 16. Results. Patients in the three study groups were similar in terms of age, sex, and weight. There was no significant difference between the mean saturation of peripheral oxygen (SPO2) and the mean heart rate between the three groups before endotracheal intubation and 1 to 10 minutes after intubation ( P > 0.05 ). The difference of mean arterial blood pressure between study groups was only significant in the first and fifth minutes after intubation. Mean systolic and diastolic blood pressure in the first, third, and fifth minutes after intubation was significantly lower in the intervention groups than the control group ( P < 0.05 ). However, no significant difference was observed between the intervention groups. The frequency of systolic blood pressure decrease was significantly different in the first and fifth minutes after intubation in the three study groups ( P < 0.05 ). Conclusion. Bolus doses of 1 and 2 μg/kg nitroglycerin in noncardiac elective surgery prevents the increase of mean systolic, diastolic, and arterial blood pressure but has no significant effect on heart rate after intubation.

The levels of IL-22 and IL-25 in patients with severe asthma are no higher than those of non-asthmatic individuals. Any major role for IL-22 and IL-25 in severe asthma is likely to be localised to the lungs and bronchial tissues.