We examined whether nitric oxide (NO) or prostaglandins modulate the presser response to serotonin (5-HT) in the isolated dog lung during hypothermia Right lower lung lobes were removed, ventilated and perfused with autologous blood at a constant flow (8.32±0.03 ml/min/g lobe weight) and a venous pressure of 4 cmH2O After stabilization at 37°C, hypothermia was induced by cooling the blood perfusing the lobe to 23, 19, and 13°C. At each temperature, 50 μg 5-HT was injected into the arterial cannula. At the peak pressor response lobar vascular resistance was partitioned into arterial and venous segments with double occlusion techniques Lobes were studied under control conditions (n=5), after inhibition of NO synthesis with 2 mM NG-nitro-L-arginine methyl ester (L-NAME) (n=5), and after cyclooxygenase inhibition (COI) with 45 μM meclofenamate (n=4) Hypothermia altered the pressor response to 5-HT (P<0.05), with an increase in resistance at 25°C, no change at 19°C, and a decrease at 13°C L-NAME did not alter the 5-HT pressor response from control lobes, but COI increased the pressor response to 5-HT at all temperatures (P<0.05) Our results suggest that vasodilator prostaglandins, but not NO, modulate the pressor response to 5-HT during hypothermia in the dog lung.
|Original language||English (US)|
|State||Published - Dec 1 1997|
ASJC Scopus subject areas
- Molecular Biology