Journal of Applied Physiology, Vol 63, Issue 3 988-995, Copyright © 1987 by American Physiological Society
Chemical control of tracheal vascular resistance in dogs
G. Sahin, S. E. Webber and J. G. Widdicombe
Department of Physiology, St. George's Hospital Medical School, London, United Kingdom.
With anesthetized dogs we have measured upper tracheal vascular resistance
on both sides of the trachea simultaneously by perfusing the cranial
tracheal arteries and measuring inflow pressures at constant flows. The
ratio of pressure to flow gave vascular resistance (Rtv). Lung airflow,
blood pressure (BP), heart rate, and pressure in a cervical tracheal
balloon (Ptr) were also measured. In paralyzed dogs, systemic hypoxia due
to artificial ventilation with 10% O2-90% N2 increased Rtv by +8.1 +/- 1.0%
(SE), Ptr by +76 +/- 22.8%, and BP by +18.9 +/- 24%. After bilateral
cervical vagosympathectomy the increases in Rtv and BP were present (+8.8
+/- 0.9 and +22.3 +/- 0.3%, respectively). After carotid body denervation
Rtv, Ptr, and BP increased (+6.4 +/- 1.3, +58.6 +/- 31.6, and +14.6 +/-
3.3%, respectively). After vagotomy Rtv and BP increased (+14.1 +/- 1.7 and
+22.4 +/- 10.1%, respectively). Tracheal perfusion with hypoxic blood
caused a small vasodilation (-2.2 +/- 1.1%). Systemic hypercapnia due to
artificial ventilation with 8% CO2-92% air increased Rtv by +16.7 +/- 3.8%,
Ptr by +67 +/- 2.0%, and BP by +12.9 +/- 9.9%. Tracheal perfusion with
hypercapnic blood caused a small vasodilation (-2.5 +/- 1.2%). Stimulation
of the carotid body chemoreceptors with KCN caused a small increase in Rtv
(+1.2 +/- 0.5%) and increases in Ptr (+49.8 +/- 13.6%) and BP (+11.1 +/-
2.1%). Systemic hypoxia and hypercapnia caused tracheal vasoconstriction
mainly by an action on the central nervous system.
