• U Orlinska, J W Olson, and M N Gillespie.
• University of Kentucky College of Pharmacy, Division of Pharmacology and Toxicology, Lexington 40536.
• Res. Commun. Chem. Pathol. Pharmacol. 1988 Nov 1; 62 (2): 187-94.

AbstractBased on the documented role of polyamines in regulation of cell growth and differentiation, we have proposed that these organic cations are essential for hypertrophic and hyperplastic responses of pulmonary vascular cells which underlie development of hypertensive pulmonary vascular disease. In support of this contention, we have shown in rat models of monocrotaline (MCT)- and chronic hypoxia-induced pulmonary hypertension that whole-lung polyamine contents are elevated and that blockade of polyamine synthesis forestalls development of hypertensive pulmonary vascular remodeling and sustained pulmonary hypertension. To determine if the involvement of polyamines in pulmonary hypertension could be ascribed to events occurring in cells of the vascular wall, as opposed to parenchymal or airways cells, the present study measured polyamine contents as a function of time in macroscopic pulmonary arteries from MCT-treated rats. Rats were given MCT or its vehicle and, at 1,4,7, and 21 days post-treatment, the contents of putrescine, spermidine, and spermine were assessed in whole right lung and in an arterial segment from the left lung consisting of the first and extending to the sixth intrapulmonary branch. Relative to control animals, contents of putrescine and spermidine were elevated in whole lung at 4, 7 and 21 days post MCT while the content of spermine was elevated above control at 21 days. In pulmonary arterial segments, contents of putrescine and spermidine were augmented significantly at 7 and 21 days after MCT treatment. Spermine content in arterial segments was increased at 21 days. Right ventricular hypertrophy indicative of sustained pulmonary hypertension was not evident until 21 days post-treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

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