Journal of Applied Physiology, Vol 76, Issue 4 1589-1593, Copyright © 1994 by American Physiological Society

ARTICLES

Responses to pressure and vasoactive agents by isolated pulmonary arteries from monocrotaline-treated rats

J. A. Madden, P. A. Keller, R. M. Effros, C. Seavitte, J. S. Choy and A. D. Hacker
Research Service, Veterans Affairs Medical Center, Milwaukee, Wisconsin.

Intralobar and side branch pulmonary arteries removed from rats 7, 14, and 21 days after injection with monocrotaline (MCT) were cannulated and pressurized, and their responses to potassium chloride, norepinephrine, acetylcholine, and angiotensin II were measured. Static pressure-diameter curves were also performed, and arterial distensibility was calculated. Arteries from all three MCT-treated groups showed reduced responses to potassium chloride and angiotensin II compared with control arteries (P < 0.05). The norepinephrine response was significantly reduced in arteries from the 14- and 21-day groups (P < 0.05). Dilations in response to acetylcholine were similar in arteries from the control and 7-day groups but were reduced compared with those in control vessels from the 14- and 21-day groups (P < 0.05). Compared with control values, the slopes of the pressure-diameter curves and the arterial distensibility decreased significantly with time after MCT treatment (P < 0.05). Values for arterial distensibilities obtained in the isolated pulmonary arteries support the theory that structural changes that occur as a result of MCT administration contribute to vessel stiffness. The acetylcholine-induced dilation of vessels from MCT-treated rats indicates that endothelium-derived factors are still produced, but diminished vasodilation coupled with decreased distensibilities after MCT suggest that abnormal vascular remodeling rather than a change in agonist sensitivity may be responsible for the reduced responsiveness seen in these arteries.

This article has been cited by other articles:

				C. D. Fike, Y. Zhang, and M. R. Kaplowitz Thromboxane inhibition reduces an early stage of chronic hypoxia-induced pulmonary hypertension in piglets J Appl Physiol, August 1, 2005; 99(2): 670 - 676. [Abstract] [Full Text] [PDF]

				R. M. F. Berger, A. H. Cromme-Dijkhuis, W. C. J. Hop, M. N. Kruit, and J. Hess Pulmonary Arterial Wall Distensibility Assessed by Intravascular Ultrasound in Children With Congenital Heart Disease* : An Indicator for Pulmonary Vascular Disease? Chest, August 1, 2002; 122(2): 549 - 557. [Abstract] [Full Text] [PDF]

				C. D. Fike, S. L. Pfister, M. R. Kaplowitz, and J. A. Madden Cyclooxygenase contracting factors and altered pulmonary vascular responses in chronically hypoxic newborn pigs J Appl Physiol, January 1, 2002; 92(1): 67 - 74. [Abstract] [Full Text] [PDF]

				K. L. Karau, R. H. Johnson, R. C. Molthen, A. H. Dhyani, S. T. Haworth, C. C. Hanger, D. L. Roerig, and C. A. Dawson Microfocal X-ray CT imaging and pulmonary arterial distensibility in excised rat lungs Am J Physiol Heart Circ Physiol, September 1, 2001; 281(3): H1447 - H1457. [Abstract] [Full Text] [PDF]

				K. M. Ito, M. Sato, K. Ushijima, M. Nakai, and K. Ito Alterations of endothelium and smooth muscle function in monocrotaline-induced pulmonary hypertensive arteries Am J Physiol Heart Circ Physiol, October 1, 2000; 279(4): H1786 - H1795. [Abstract] [Full Text] [PDF]

				R.M.F. Berger Possibilities and impossibilities in the evaluation of pulmonary vascular disease in congenital heart defects Eur. Heart J., January 1, 2000; 21(1): 17 - 27. [PDF]

				R. Mathew, E. S. Gloster, T. Sundararajan, C. I. Thompson, G. A. Zeballos, and M. H. Gewitz Role of inhibition of nitric oxide production in monocrotaline-induced pulmonary hypertension J Appl Physiol, May 1, 1997; 82(5): 1493 - 1498. [Abstract] [Full Text] [PDF]