OBJECTIVES: Acute pulmonary hypertension following cardiac surgery can have a significant effect on postoperative morbidity and mortality. However, limited data are available on the efficacy and potency of clinically used systemic vasopressors on the pulmonary vasculature. The aim of this study was to use human pulmonary artery to characterize the pharmacological effects of clinically used vasopressors on the human pulmonary vasculature. METHODS: Fifty-seven pulmonary artery rings of internal diameter 2-4 mm and 2 mm long, mounted in a multiwire myograph system, were used to measure changes in isometric tension. We constructed concentration response curves by cumulative addition to the myograph chambers of KCl, noradrenaline (NA), adrenaline (AD), vasopressin, endothelin-1 (ET-1) and prostaglandin F2a (PGF2a). RESULTS: AD, NA, ET-1, PGF2a and KCl caused dose-dependent vasoconstriction in the pulmonary artery samples (EC50 246 nM [95% confidence interval, CI, 153-394 nM], 150 nM [95% CI 51-447 nM], 1.46 nM [95% CI 0.69-3.1 nM], 6.35 µM [95% CI 3.58-11.2 µM] and 17.24 mM [95% CI 12.43-24.07 mM], respectively), whereas vasopressin had no significant effect. The order of efficacy was KCl = PGF2a > AD > NA > ET-1 and the order of potency was ET-1 T-AD = NA > PGF2a > KCl. CONCLUSIONS: This study demonstrated the efficacy and potency of clinically used vasopressors and endogenous vasopressors on human pulmonary vascular tone. PGF2a and KCl equally caused maximal amounts of constriction, whereas ET-1 had less effect and vasopressin had no effect. These effects may need to be taken into account in the clinical setting because they might result in the development of pulmonary hypertension.
OBJECTIVES: Acute pulmonary hypertension following cardiac surgery can have a significant effect on postoperative morbidity and mortality. However, limited data are available on the efficacy and potency of clinically used systemic vasopressors on the pulmonary vasculature. The aim of this study was to use human pulmonary artery to characterize the pharmacological effects of clinically used vasopressors on the human pulmonary vasculature. METHODS: Fifty-seven pulmonary artery rings of internal diameter 2-4 mm and 2 mm long, mounted in a multiwire myograph system, were used to measure changes in isometric tension. We constructed concentration response curves by cumulative addition to the myograph chambers of KCl, noradrenaline (NA), adrenaline (AD), vasopressin, endothelin-1 (ET-1) and prostaglandin F2a (PGF2a). RESULTS:AD, NA, ET-1, PGF2a and KCl caused dose-dependent vasoconstriction in the pulmonary artery samples (EC50 246 nM [95% confidence interval, CI, 153-394 nM], 150 nM [95% CI 51-447 nM], 1.46 nM [95% CI 0.69-3.1 nM], 6.35 µM [95% CI 3.58-11.2 µM] and 17.24 mM [95% CI 12.43-24.07 mM], respectively), whereas vasopressin had no significant effect. The order of efficacy was KCl = PGF2a > AD > NA > ET-1 and the order of potency was ET-1 T-AD = NA > PGF2a > KCl. CONCLUSIONS: This study demonstrated the efficacy and potency of clinically used vasopressors and endogenous vasopressors on human pulmonary vascular tone. PGF2a and KCl equally caused maximal amounts of constriction, whereas ET-1 had less effect and vasopressin had no effect. These effects may need to be taken into account in the clinical setting because they might result in the development of pulmonary hypertension.
Authors: Azar Hussain; Robert T Bennett; Zaheer Tahir; Emmanuel Isaac; Mubarak A Chaudhry; Syed S Qadri; Mahmoud Loubani; Alyn H Morice Journal: World J Cardiol Date: 2019-10-26