I propose a combined experimental-theoretical approach to (1) study pulsatile pulmonary hemodynamics on-line under a variety of physiological and pathological conditions and (2) to improve and correlate two existing methods of investigation in hemodynamics. The long-term objective of this project is two-fold: (1) scientifically, to understand the behavior of the pulmonary vasculature under pulsatile flow conditions and to limit the body of information which has been obtained with steady flow to the results from the pulsatile flow experiments; (2) practically, to establish distinct patterns of the impedance spectra under different conditions and use such information as a means of online evaluation of the state of pulmonary hemodynamics. Experiments will be performed in dogs with two basic preparations: (1) intact right heart and cannulated left lung, either open chest or closed chest; (2) isolated left lower lobe, either in situ or in vitro, perfused by a pulsatile pump. In the first preparation instantaneous pressure-flow relationships will be recorded accurately and pulmonary vascular input impedance will be computed on-line. In the second preparation, arterial and venous occlusion (AVO) will be applied with precision and input impedance measurements will also be made. These data will be analyzed both on-line and off-line. Since the AVO technique elicits the impulse responses of the vascular system in the time-domain and input impedance characterizes the vascular system in the frequency-domain, an attempt will be made to correlate the results obtained from these two methods. In the intact right heart experiments, the pressure-flow relationship during the brief period when the pulmonary vascular bed discharges passively will be examined in particular. The effect of the left atrium on the pulsatility in the entire pulmonary vascular bed will also be investigated. The pathophysiological conditions to be studied in this project include lung inflation, hypoxia, effects on serotonin, isoproterenol and norepinephrine infusion, hemodilution, pulmonary embolism, acute lung injury with permeability edema, hydrostatic edema, endotoxic shock, hemorrhagic shock, and effects of IPPB ventilation and PEEP.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Research Project (R01)
Project #
5R01HL036908-03
Application #
3352271
Study Section
Respiratory and Applied Physiology Study Section (RAP)
Project Start
1986-07-01
Project End
1990-06-30
Budget Start
1988-07-01
Budget End
1990-06-30
Support Year
3
Fiscal Year
1988
Total Cost
Indirect Cost
Name
University of Southern California
Department
Type
DUNS #
041544081
City
Los Angeles
State
CA
Country
United States
Zip Code
90033
Maarek, J M; Grimbert, F (1994) Segmental pulmonary vascular resistances during oleic acid lung injury in rabbits. Respir Physiol 98:179-91
Maarek, J M; Chang, H K (1991) Pulsatile pulmonary microvascular pressure measured with vascular occlusion techniques. J Appl Physiol 70:998-1005
Maarek, J M; Hakim, T S; Chang, H K (1990) Analysis of pulmonary arterial pressure profile after occlusion of pulsatile blood flow. J Appl Physiol 68:761-9
Chartrand, D A; Maarek, J M; Ye, T H et al. (1990) Lung and chest wall mechanics in rabbits during high-frequency body-surface oscillation. J Appl Physiol 68:1722-6
Maarek, J M; Chartrand, D A; Ye, T H et al. (1990) Pulmonary lobar vascular resistances during constant and pulsatile flows. Respir Physiol 82:149-59
Hakim, T S; Maarek, J M; Chang, H K (1989) Estimation of pulmonary capillary pressure in intact dog lungs using the arterial occlusion technique. Am Rev Respir Dis 140:217-24