Tissue resistance and the contractile state of lung parenchyma.
When challenged with a contractile agonist in increasing graded concentrations, lung parenchymal tissue assumes a sequence of mechanical states. That sequence is mapped here. Isolated lung parenchymal strips from male Hartley guinea pigs were mounted in a bath containing Krebs solution at 37 degrees C, aerated with 95% O2-5% CO2. One end was attached to a force transducer and the other to a servo-controlled lever arm. After stress adaptation, sinusoidal length oscillations (1% strain at 0.31 Hz) yielded force-length loops from which we computed induced changes in active tension (F), tissue stiffness (E), and hysteresivity (eta) (J. J. Fredberg and D. Stamenović. J. Appl. Physiol. 67:2408-2419, 1989). Changes of tissue resistance (R) were, by definition, governed by those of eta and E. Histamine (10(-6) -10(-3) M), prostaglandin D2 (10(-5) -10(-4) M), and prostaglandin F2 alpha (10(-5) -10(-4) M) caused dose-related increases of F, eta, and E. Plotting induced changes of E vs. those of F revealed a unique relationship that was identical for these as well as a wider panel of contractile agonists; changes of E and F were closely associated. However, plotting induced changes of E vs. those of eta revealed relationships that differed distinctly between agonists; changes of eta were dissociated from those of F and E. This latter observation demonstrated the existence of distinct mechanical states that differed according to the specific agonist by which the tissue was stimulated. In producing agonist-induced changes in R, changes of E were of equal or greater importance compared with those of eta. We conclude that guinea pig lung parenchyma, viewed as an integrated physiological tissue system, exhibits different kinds as well as varying intensities of mechanical response according to the specific agonist present in the cellular microenvironment. These differences in contractile state reveal themselves principally in the hysteretic nature of the tissue.
Fredberg
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Harvard School of Public Health, Boston, Massachusetts 02115.
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D000222:Adaptation, Physiological; D000403:Airway Resistance / Q000187:drug effects / Q000502:physiology; D000818:Animals; D015237:Dinoprost / Q000494:pharmacology; D006168:Guinea Pigs; D006632:Histamine / Q000494:pharmacology; D066298:In Vitro Techniques; D008168:Lung / Q000187:drug effects / Q000502:physiology*; D008297:Male; D008970:Molecular Weight; D009119:Muscle Contraction / Q000187:drug effects / Q000502:physiology; D009130:Muscle, Smooth / Q000187:drug effects / Q000502:physiology*; D010812:Physical Stimulation; D015230:Prostaglandin D2 / Q000494:pharmacology
D006632:Histamine; D015237:Dinoprost; D015230:Prostaglandin D2