AJP - Heart and Circulatory Physiology, Vol 245, Issue 6 947-H956, Copyright © 1983 by American Physiological Society
Total body vascular capacitance changes during high intracranial pressure in dogs
P. M. Stein, C. L. MacAnespie and C. F. Rothe
The active capacitance response to increased intracranial pressure (Pic)
was studied in nine chloralose-anesthetized dogs. The vena cavae were
cannulated and drained into a reservoir as blood was pumped at a constant
flow (Q) into the right atrium. Central blood volume was determined as Q
times the mean transit time of dye from the right atrium to the aortic
root. Arterial compliance (Ca) was determined from the monoexponential
decay of systemic arterial pressure (SAP) during vagal cardiac arrest to
compute changes in arterial volume (delta SAP X Ca). Atropine was
administered to prevent bradycardia and dangerous, constant cardiac
output-induced increases in pulmonary arterial (PAP) and right and left
atrial pressures. Blood volume shifts indicative of active
venoconstriction, included changes in reservoir, central, and arterial
volumes during Pic of 100-200 mmHg. Raised Pic, after atropine, induced a
tachycardia, increased systemic and pulmonary resistances, and increased
SAP and PAP. Venoconstriction caused marked blood shifts between 125 and
200 mmHg Pic. The extrapolated response threshold was about 112 mmHg. In
the most sensitive range, venoconstriction amounted to 3.9 ml X kg-1 per
25-mmHg change in Pic. These results indicate that intense active
capacitance vessel constriction is an important part of cardiovascular
hemostasis during rapidly increased intracranial pressure.
