The injection of 0.05-0.2 mg/kg adrenaline hydrochloride into the systemic vein of the cat at first retards the lymph flow from the thoracic duct transiently and then accelerates it. The degree of this acceleration is definitely weaker than that in the dog but it is rather close to that in the rabbit. The protein content in lymph is increased when the acceleration of lymph flow is less but it is reduced when the acceleration is greater. Judging from changes in arterial and portal blood pressures, the initial decrease in the lymph flow seems to be correlated to the temporary anemia occurring in the splanchnic area at the ascending stage of arterial blood pressure and the subsequent increase of the flow seems to be correlated to the congestion in the same area at the descending stage of arterial pressure.
Since the increase of protein in lymph is preventable by the prior ligature of periportal lymphatics, the majority of protein rich lymph may originate from the liver. In the cat portal blood pressure is not decreased by adrenaline as in the rabbit but it is increased as in the dog. This seems in all probability to be due to the fact that the constrictor response of intrahepatic vessels to this drug is more like in the dog than in the rabbit. The acceleration in the rate of lymph flow coincides with the rise in portal pressure rather than with that in arterial pressure. The administration of 0.5-3 mg/kg nicotine tartrate likewise accelerates the thoracic lymph in the cat a little less than that in the dog but close to that in the rabbit. Following this acceleration, there has been observed some retardation. As for the changes in arterial pressure and portal and jugular venous pressures, with an exception of an initial temporary fall in the arterial pressure, in every respect all of them present the reactions similar to those observed in the case of adrenaline administration. The lymphagogic effect and rise in the portal pressure due to nicotine are reduced in the adrenalectomized cat. The administration of 0.5-2 mg/kg acetylcholine chloride on 0.1-2 mg/kg pilocarpine hydrochloride also accelerates the flow of highly proteinized thoracic lymph in the cat. This action is rather marked in the case of the latter drug Portal blood pressure has been elevated by either one of these drugs, but in the case of acetylcholine a rather marked fall can be observed preceding the elevation. It seems that the lymph rich in protein is mainly produced in the liver, and the other portion of the lymph is formed by the increased plasma filtration resulting from the temporary congestion occurring in other abdominal area including intestines. The administration of 4 mg/kg atropine sulfate inhibits the lymphagogic effect and cardiovascular effects of these two drugs to quite a marked extent; while adrenalectomy partially suppresses these effects.
Generally cardiovascular responses what are believed to be associated with the lymphagogic effect of the drugs mentioned above in the cat resemble more closely to those in the dog rather than in the rabbit. The reason why lymphagogic effect in the cat is less than in the dog in spite of this seems to be due to a small capacity of tissue spaces where produced lymph is stored up until it is taken into lymphatic vessels. This can be readily understood even from the previously reported observations that the duration of the acceleration in lymph flow due to the obstruction of short period in hepatic vein or in portal vein is shorter in the cat than in the dog (Mitsufuji, Okayama-Igakkai-Zasshi, 71, 7II, 4113, 1959). Atropine in the cat inhibits the thoracic lymph flow just as in the case of the dog and rabbit, and decreases the protein content in lymph. This may be caused by the decrease in circulating blood volume in the portal vascular area.