No abstract

One hundred sixty-three baboons ( Papio doguera were sacrificed and autopsied immediately after being trapped in their natural habitat in Kenya, British East Africa. Approximately three-fourths of the 67 adults had some degree of aortic intimal lipid deposition, as indicated by gross Sudan IV staining, and a few animals had extensive fatty streaks. These fatty streaks were more frequent with advancing age, but there was no sex difference. Electron microscopy disclosed most of the intimal lipid droplets to be intracellular. Fibrous plaques were infrequent and had a variable but usually low lipid content. One elderly male had fibrous plaques with hemorrhage into their bases. Histologic sections of the coronary arteries showed many small musculo-elastic intimal plaques in which lipid could only rarely be demonstrated. The aortic intimal lipid deposits cannot be attributed to the consumption of excessive animal fat or to hypercholesterolemia. These results indicate that the baboon, like man, is highly susceptible to arterial intimal lipid deposition and that it promises to be an excellent animal for the experimental investigation of atherosclerosis. They further more caution that adequate controls be used in all experimental work involving arterial lesions in primates.

When blood plasma proteins are depleted by bleeding and return of the washed red cells (plasmapheresis) the regeneration of new plasma proteins can be controlled at will by diet. The amount and character of protein intake is all important. Liver protein and casein are efficient proteins to promote rapid regeneration of plasma proteins but some vegetable proteins are also efficient. The blood plasma proteins are reduced by plasmapheresis close to the edema level (3.5–4.0 per cent) and kept at this level by suitable exchanges almost daily. The amount of plasma protein removed is credited to the given diet period. A basal ration is used which is poor in vegetable protein (potato) and contains no animal protein. The dog on this ration can be kept in nitrogen balance but can produce only about 2 gm. plasma protein per kilo body weight per week. With liver or casein feeding this production can be increased three- or fourfold. A reserve of protein building material can be demonstrated in the normal dog when its plasma proteins are depleted. In the first 3 weeks of depletion this reserve in excess of the final basal output may amount to 3–20 gm. protein. This may be stored at least in part in the liver. As much as 50 per cent of this reserve may be albumin or albumin producing material. A reversal of the albumin-globulin ratio may be observed on the basal diet alone. The reversal will always follow plasmapheresis with the dog on the basal diet and the total plasma protein output will consist approximately of 2 parts globulin and 1 part albumin. Liver diet will raise the production and output of albumin and bring the ratio back toward normal. Albumin production may actually exceed the globulin output during liver diet periods. The change is less conspicuous with casein but in the same direction.

Large amounts of normal blood plasma can be given intravenously to normal dogs over several weeks without causing any significant escape by way of the urine. There appears to be no renal threshold for plasma protein even with high plasma protein concentration (9.7 per cent). Dogs receiving sugar by mouth and plasma by vein can be kept practically in nitrogen equilibrium and it would seem that the injected protein must be utilized by the body. If this can happen in this emergency we may suspect that normally there is a certain amount of "give and take" between body protein and plasma protein. Plasma protein fed by mouth under identical conditions shows the same general reaction as noted with plasma by vein but the urinary nitrogen is a little higher and suggests that the injected protein is utilized a little more completely to form new protein. The difference may be explained as due to deaminization in the case of protein by mouth. During fasting periods the blood plasma proteins are used up and the total circulating protein may even decrease to one-half the normal level. The plasma protein concentration changes but little and the significant change is a shrinkage of plasma volume. All these facts point to a dynamic equilibrium between tissue protein and plasma protein depending upon the physiological needs of the moment. In the absence of food protein the body can use material coming from one body protein to fabricate badly needed protein material of different character.