THORACIC DUCT LYMPH FLOW CHANGES SECONDARY TO ALTERATIONS IN SERUM CALCIUM LEVELS: A PROPOSED MECHANISM OF ACTION
- M Deysine
- M Mader
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.
How to Cite:
Deysine, M. & Mader, M., (1980) “THORACIC DUCT LYMPH FLOW CHANGES SECONDARY TO ALTERATIONS IN SERUM CALCIUM LEVELS: A PROPOSED MECHANISM OF ACTION”, Lymphology 13(1), 1-8.