title: Effect of hydralazine on vascular mechanics in a canine lobar preparation of pulmonary embolism.
abstract: We studied the effect of hydralazine (H) on pulmonary vascular mechanics in an isolated, in situ, canine lobe model of normal and increased pulmonary vascular resistance (Rp) produced by Gelfoam embolization (GE). Pulmonary pressure-flow (P-Q) curves from 24 lobes were obtained at baseline and after each intervention. Hemodynamic parameters for analysis included: the mean critical closing pressure (Ppai), vascular conductance (1/Rp), lobar flow (QL), and the pulmonary inflow pressure (Ppa) at different levels (50, 100, 200, 400, and 600 ml/min) of a fixed flow. After the preparation was stabilized, the 24 lobes were classified into 2 groups. For group 1 (n = 8) we studied the effect of H on the normal pulmonary vasculature. In group 2 (n = 16) we studied the effect of GE. Following GE, this group was further divided in half. For group 2A (n = 8) we followed the natural history of GE with measurements at 15 and 60 min. For group 2B (n = 8) measurements were done 15 min after GE and repeated again 15 min after the infusion of H. For group 1 lobes, H promoted a significant decrease (p less than 0.001) in Ppa at fixed flows of 200, 400, and 600 ml/min compared to baseline, with no change in Ppa for flows below 100 ml/min. QL and 1/Rp increased (p less than 0.01), and there was not any significant change in Ppai. In group 2A lobes, GE produced an increase in Ppa at all levels of flow (p less than 0.01), QL and 1/Rp decreased (p less than 0.05), and there was an increase in Ppai (p less than 0.05). These changes remained stable over the 60 min of observation. For group 2B lobes, GE produced the same hemodynamic changes as in group 2A, and the infusion of H caused a decrease in Ppa at flows between 100 and 300 ml/min. (p less than 0.01) with no change in Ppa at flows below 100 ml/min. QL and 1/Rp increased (p less than 0.01) and Ppai did not change compared to 15 min after GE. We conclude that in the normal canine pulmonary vasculature as well as in the model of GE, H decreased Rp and did not affect mean critical closing pressure, all of which may be explained by an increase in vascular conductance due to an increase in vascular distensibility.
authors.affiliation: Cardiopulmonary Department, National Institute of Cardiology Ignacio Chavez, Mexico D.F.
authors.forename: E
authors.initials: E
authors.lastname: Lupi-Herrera
authors.forename: M E
authors.initials: ME
authors.lastname: Furuya
authors.forename: J
authors.initials: J
authors.lastname: Sandoval
authors.forename: E
authors.initials: E
authors.lastname: Correa
authors.forename: M E
authors.initials: ME
authors.lastname: Leal
authors.forename: A
authors.initials: A
authors.lastname: Quesada
authors.forename: A
authors.initials: A
authors.lastname: Palomar
authors.forename: R
authors.initials: R
authors.lastname: Barrios
mesh_terms: D000818:Animals; D001784:Blood Gas Analysis; D004195:Disease Models, Animal; D004285:Dogs; D006439:Hemodynamics / Q000187:drug effects; D006830:Hydralazine / Q000627:therapeutic use*; D011655:Pulmonary Embolism / Q000097:blood / Q000188:drug therapy* / Q000503:physiopathology; D012123:Pulmonary Ventilation / Q000187:drug effects*
chemical_list: D006830:Hydralazine