THORACIC DUCT LYMPH FLOW CHANGES SECONDARY TO ALTERATIONS IN SERUM CALCIUM LEVELS: A PROPOSED MECHANISM OF ACTION

Abstract

The mechanism behind the dose-related increase in
thoracic duct lymph flow (TDLF) produced by an
injection of calcium gluconate was investigated in
parathyroidectomized dogs divided into groups
composed of three animals each. After skeletal
muscle paralysis was induced by succinylcholine
chloride, calcium produced a highly significant rise
in TDLF (P < 0.001). This rules out skeletal muscle
contractility as a factor in the response to calcium.
Blocking the parasympathetic system with atropine
also failed to inhibit the TDLF response to calcium.
Levarterenol augmented both TDLF and aortic blood
pressure (ABP) while the fall in ABP produced by
Isoproterenol was accompanied by a rise in TDLF.
Sympathetic inhibition attempted by a combination
of adrenalectomy, reserpinization, phenoxybenzamine
hydrochloride and propanolol significantly diminished
TDLF after calcium (P < 0.001). An infusion of
angiotensin completely abolished TDLF, probably
by precapillary vasoconstriction. While angiotensin
was still being infused, calcium significantly increased
TDLF (P < 0.001). Papaverine was the only drug
able to completely block the action of calcium on
TDLF. These experiments suggest that lymph propulsion
changes after calcium may be due to the action
of this ion on the lymphatic channel wall.