TY - JOUR
T1 - Effect of hydralazine on vascular mechanics in a canine lobar preparation of pulmonary embolism
AU - Lupi-Herrera, Eulo
AU - Furuya, Maria Elena
AU - Sandoval, Julio
AU - Correa, Elma
AU - Leal, Maria Elena
AU - Quesada, Alejandro
AU - Palomar, Andres
AU - Barrios, Roberto
PY - 1992/1/1
Y1 - 1992/1/1
N2 - 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 < 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 < 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 < 0.01), QL and 1/Rp decreased (p < 0.05), and there was an increase in Ppai (p < 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 < 0.01) with no change in Ppa at flows below 100 ml/min. QL and 1/Rp increased (p < 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.
AB - 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 < 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 < 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 < 0.01), QL and 1/Rp decreased (p < 0.05), and there was an increase in Ppai (p < 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 < 0.01) with no change in Ppa at flows below 100 ml/min. QL and 1/Rp increased (p < 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.
KW - hydralazine
KW - isolated canine lobe
KW - lobar embolization
KW - mean closing pressure
KW - pulmonary circulation
KW - vascular conductance
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U2 - 10.1007/BF00566681
DO - 10.1007/BF00566681
M3 - Article
C2 - 1518300
AN - SCOPUS:0026739650
SN - 0341-2040
VL - 170
SP - 291
EP - 309
JO - Lung: An International Journal on Lungs, Airways and Breathing
JF - Lung: An International Journal on Lungs, Airways and Breathing
IS - 5
ER -