1Associate Professor of Physiology, Institute of Medical Sciences, BHU, Varanasi
2Assistant Professor of, Physiology, RAK Medical & Health Sciences University, UAE
3Research Associate, CCMB, Hyderabad
4Professor of, Physiology, Institute of Medical Science, BHU, Varanasi
*Corresponding author: Dr. S B Deshpande, Department of Physiology, Institute of Medical Science Banaras Hindu University, Varanasi-221005, India, Tel. No: 91-542-6703274, FAX: 91-542-2367568 E- mail address: desh48@yahoo.com
Online published on 2 August, 2016.
Acute respiratory distress syndrome (ARDS) is a fatal disease associated with hypoxemia and lung injury. Recently it was shown that indomethacin exacerbated oleic acid (OA)-induced ARDS. Neurally mediated mechanisms were speculated in the exacerbation. Vagus supply the pulmonary tissue and possess protective actions directly (via efferent) or indirectly (via reflexes).
Present study was undertaken to elucidate the involvement of vagus in indomethacin-induced exacerbation of ARDS.
Respiratory excursions, ECG (for heart rate; HR) and blood pressure were recorded. PaO2/FiO2 ratio and pulmonary water content were also determined.
OA produced immediate tachypnea followed by progressive bradypnea and death within 70 min. There was increase in pulmonary water content and decrease in PaO2/FiO2 ratio. HR and mean arterial pressure (MAP) showed progressive decrease. In vagotomized animals OA-induced tachypnea was not seen but OA-induced toxicity persisted. In indomethacin pretreated rats, OA produced an abrupt decrease in respiratory frequency, (RF) HR and MAP leading to death of the animals within 12 min. Pulmonary water content was increased in these animals. Bilateral vagotomy did not prevent the indomethacin-induced exacerbation of ARDS. However, vagotomy did not alter the OA-induced toxicity and the parameters were similar to OA only group.
Results of the present study indicate that vagally mediated mechanisms are not involved in indomethacin-induced exacerbation of ARDS; possibly involve chemically mediated mechanisms.
ARDS, Vagotomy, Pulmonary edema, Indomethacin, Oleic acid
