The Effects of Somatostatin upon the Thoracic Duct Lymph and Triglyceride Homeostasis

the Relation between the Lymph Flow and the Vagus Nerve

Abstract

The role of circulating somatostatin in triglyceride (TG) homeostasis, especially in TG entry from the gastrointestinal tract, was evaluated on the lymph of the canine thoracic duct in fasting and postprandial states.
Cyclic somatostatin at a near physiologic (50 ng/min) and a pharmacologic (5μg/min) dosis was infused through either the portal or the femoral vein, and the lymph were collected at every 10 min through a cannula inserted into the thoracic duct under neuroleptanalgesia.
The results were as follows :
1) The levels of the lymph flow rates in the fasting state were significantly reduced to a mean of 87.0 ± 2.7, 91.0 ± 0.9% of the preinfusion values during somatostatin infusions at the rate of 50 ng/min through the portal and femoral veins, respectively, and to a mean of 78.0 ± 2.3, 80.3 ± 1.9% at the rate of 5 μg/min, respectively. The somatostatin infusions at these rates through either the portal or the femoral vein induced almost identical attenuating effects on the lymph flow rate whereas no significant changes in the flow were observed during saline infusion.
2) The effects of the somatostatin infusions on the lymph of fasting subjects at both rates through either the portal or the femoral vein were abolished by the vagotomy at the level of the diaphragm performed 1 hr prior to the infusions.
3) The levels of the flow rate, TG concentration, and TG content (flow×TG concentration) of the lymph which were obtained 3 hrs after the ingestion of a fat-protein rich meal were reduced to a mean of 80.9 ± 4.1, 80.0 ± 4.2, and 66.1 ± 5.3% of the basal values during the intraportal somatostatin infusion at the rate of 50ng/min, respectively, and to a mean of 91.1 ± 0.9, 84.4 ± 8.8, and 79.1 ± 8.0% during the intrafemoral infusion, respectively. These values were significant except changes of TG concentration. Whereas, somatostatin infusion at the rate of 5 μg/min into the portal vein induced significant reductions of the flow, TG concentration and TG content to a mean of 81.0 ± 10.1, 77.9 ± 5.9, and 62.3 ± 3.5%, respectively, and into the femoral vein to a mean of 84.7 ± 4.0, 66.1 ± 7.7, and 56.2 ± 7.3%, respectively. On the postprandial lymph, somatostatin infusions at these rates through either the portal or the femoral vein also induced almost identical levels of the attenuating effects on those parameters.
4) The pressures in the portal vein and the abdominal aorta and heart rate showed no changes during somatostatin infusions both at the rate of 50 ng/min and 5 μg/min through either the portal or the femoral vein in the fasting state of normal and vagotomized dogs.
These results indicate that somatostatin could retain almost the same potency on the thoracic duct lymph even though it passes through the liver both at a near physiologic and at a pharmacologic dose in the face of the vagus nerve and suggest the possibility that circulating somatostatin from the pancreas or other splanchnic organs might have a physiologic influence upon TG entry from the gut through altering dynamics of the splanchnic lymph system.