Lung Tissue Resistance Measured in Saline-Filled Guinea Pig Lungs by Micropuncture
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© Springer-Verlag New York Inc. 1997
Lung Tissue Resistance Measured in Saline-Filled Guinea Pig Lungs by Micropuncture Y.-L. Lai,1,3 J. Wang,1 and S. J. Lai-Fook2 1
Division of Pharmacology and Experimental Therapeutics Division, College of Pharmacy, and 2Center for Biomedical Engineering, University of Kentucky, Lexington, Kentucky 40506, USA; 3Department of Physiology, College of Medicine, National Taiwan University, Taipei, Taiwan, Republic of China
Abstract. Lung tissue resistance (Rti) measured in air-filled guinea pig lungs by the alveolar capsule technique was a large part of total lung resistance (Rl), and we wondered whether similar results applied to saline-filled lungs. We used the micropuncture method to measure alveolar pressure (Palv) in saline-filled lungs of 21 guinea pigs. Palv and airway opening pressure (Pao) were measured before and after a sudden interruption of flow during an inflation or deflation maneuver. On stopping flow, there was an immediate large change in Pao followed by a smaller slower change in Pao. Palv was nearly constant immediately after flow interruption but followed the slower change in Pao. The initial change in Pao on flow interruption was interpreted as the resistive pressure loss in the airways. The small change in Pao and Palv was interpreted as the pressure loss caused by tissue stress adaptation. Airway resistance (Raw) and Rti were obtained by dividing the pressure losses by the flow before the interruption. Rl was the sum of Raw and Rti. The calcium blocker nifedipine reduced both Raw and Rti and abolished the difference in Rti between inflation and deflation. Values of Rti were 10–29% of Rl. However, with correction for viscosity, Rti predicted in air-filled lungs would dominate Rl. Key words: Airway resistance—Lung inflation or deflation—Liquid-filled lungs— Lung parenchyma. Introduction Lung tissue resistance (Rti) has been shown to contribute a significant part of the total pulmonary resistance (Rl) during air breathing [3, 11, 17, 21]. These studies either measured alveolar pressure directly with the alveolar capsule technique or separated Offprint requests to: Yih-Loong Lai.
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tissue from the airway resistance using the pressure response to interruption of flow [2]. As percent of Rl, the contribution of Rti was found to vary from 27% [11] to 93% [3]. During airway constriction caused by bronchoconstrictor agents, most of the increase in Rl was caused by an elevation in Rti [3, 20]. However, studies using tissue strips would predict much smaller increases in Rti [4], and there has been some question as to the mechanisms responsible for the increased Rti measured in constricted lungs [6]. The effects of alveolar surface tension and alveolar distortion caused by alveolar duct constriction have been proposed as reasons for the differences between in situ and in vitro measurements of Rti. A recent study has suggested that heterogeneity of small airway resistance might contribute the measurements of Rti [10]. Thus we wondered whether the effe
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