Humoral pulmonary vasoregulation in conscious dogs after left lung autotransplantation

P. M. Desai, K. Nishiwaki, R. S. Stuart, Daniel Nyhan, P. A. Murray

Research output: Contribution to journalArticle

Abstract

We investigated the roles of cyclooxygenase metabolites, arginine vasopressin (AVP) and angiotensin II (ANG II), as mediators of the chronic increase in pulmonary vascular resistance associated with left lung autotransplantation (LLA) in conscious dogs. Continuous left pulmonary vascular pressure-flow (LP-Q) plots were generated in conscious dogs 2- to 5- wk post-LLA and in sham-operated control conscious dogs. LLA resulted in a marked shift (P <0.01) in the LP-Q relationship as reflected by an approximate doubling of the pulmonary vascular pressure gradient at each common value of left pulmonary blood flow compared with the control group. Cyclooxygenase pathway inhibition (indomethacin) and AVP V1-receptor block had no effect on the LP-Q relationship post-LLA. Angiotensin-converting enzyme inhibition (captopril) also failed to reverse the increase in pulmonary vascular resistance post-LLA. Because captopril has the dual effect of inhibiting the production of ANG II and the degradation of bradykinin, additional studies utilizing a selective ANG II receptor antagonist were performed. ANG II receptor block (saralasin) significantly altered the LP-Q relationship post-LLA to cause active pulmonary vasodilation (P <0.01). Thus, the chronic increase in pulmonary vascular resistance post-LLA is not mediated by metabolites of the cyclooxygenase pathway or AVP V1-receptor activation. A significant component of the increase in pulmonary vascular resistance resulting from LLA is mediated by ANG II. The differential responses to captopril and saralasin may imply a pulmonary vasoregulatory role for bradykinin post-LLA.

Original languageEnglish (US)
Pages (from-to)902-908
Number of pages7
JournalJournal of Applied Physiology
Volume76
Issue number2
StatePublished - 1994

Fingerprint

Autologous Transplantation
Dogs
Lung
Vasopressin Receptors
Vascular Resistance
Captopril
Prostaglandin-Endoperoxide Synthases
Angiotensin II
Saralasin
Bradykinin
Blood Vessels
Angiotensin II Type 1 Receptor Blockers
Pressure
Angiotensin Receptors
Arginine Vasopressin
Peptidyl-Dipeptidase A
Vasodilation
Indomethacin

Keywords

  • angiotensin II
  • arginine vasopressin
  • captopril
  • chronic instrumentation
  • cyclooxygenase metabolites
  • indomethacin
  • lung transplantation
  • pressure-flow plots
  • pulmonary circulation
  • saralasin
  • V-receptor block

ASJC Scopus subject areas

  • Endocrinology
  • Physiology
  • Orthopedics and Sports Medicine
  • Physical Therapy, Sports Therapy and Rehabilitation

Cite this

Desai, P. M., Nishiwaki, K., Stuart, R. S., Nyhan, D., & Murray, P. A. (1994). Humoral pulmonary vasoregulation in conscious dogs after left lung autotransplantation. Journal of Applied Physiology, 76(2), 902-908.

Humoral pulmonary vasoregulation in conscious dogs after left lung autotransplantation. / Desai, P. M.; Nishiwaki, K.; Stuart, R. S.; Nyhan, Daniel; Murray, P. A.

In: Journal of Applied Physiology, Vol. 76, No. 2, 1994, p. 902-908.

Research output: Contribution to journalArticle

Desai, PM, Nishiwaki, K, Stuart, RS, Nyhan, D & Murray, PA 1994, 'Humoral pulmonary vasoregulation in conscious dogs after left lung autotransplantation', Journal of Applied Physiology, vol. 76, no. 2, pp. 902-908.
Desai, P. M. ; Nishiwaki, K. ; Stuart, R. S. ; Nyhan, Daniel ; Murray, P. A. / Humoral pulmonary vasoregulation in conscious dogs after left lung autotransplantation. In: Journal of Applied Physiology. 1994 ; Vol. 76, No. 2. pp. 902-908.
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