AJP - Heart and Circulatory Physiology, Vol 248, Issue 3 360-H365, Copyright © 1985 by American Physiological Society
Effect of controlled ventilation on renal and splanchnic blood flows during nicotine
M. T. Bedran de Castro, H. F. Downey, G. J. Crystal and F. A. Bashour
The present study was undertaken to evaluate the influence of respiratory
condition [free breathing (FB) vs. controlled ventilation (CV)] and of
anesthetic [pentobarbital (PA) vs. chloralose (CA)] on nicotine-induced
vasomotor responses in the renal cortex and splanchnic beds. Nicotine (36
micrograms . kg-1 . min-1 iv) was infused in four groups of dogs: group I,
PA and CV; group II, PA and FB; group III, CA and CV; group IV, CA and FB.
Regional vascular conductances (VC) were calculated from regional blood
flows measured with 15-microns radioactive microspheres. In group I, VC
fell in renal cortex (-22%) and pancreas (-52%), increased in liver
(hepatic arterial bed +130%), and did not change significantly in duodenum
and spleen. In group III, VC fell to a greater extent in renal cortex,
pancreas, duodenum, and spleen than in group I; VC in hepatic arterial bed
did not change. In FB dogs (groups II and IV), nicotine caused marked
hyperventilation, but decreases in VC in renal cortex, pancreas, and
duodenum were similar to those in CV dogs. Results indicate that during
intravenous infusion of nicotine 1) hyperventilation does not attenuate or
reverse vasoconstriction in renal cortex, pancreas, or duodenum under
either PA or CA, although it does in spleen under CA; 2) vasodilator
mechanisms predominate over vasoconstrictor mechanisms in the hepatic
arterial bed; and 3) vasoconstrictor responses in renal cortex, pancreas,
duodenum, spleen, and liver are more pronounced under CA than under PA.
