title: PROTEIN METABOLISM AND PROTEIN RESERVES DURING ACUTE STERILE INFLAMMATION : HIGH PROTEIN INTAKE COMPENSATES FOR INCREASED CATABOLISM.
abstract: Adult dogs were given a proteinless diet plus casein, 80 calories/kilo, 0.4 gm. nitrogen/kilo/day. Sterile controlled inflammation was produced by subcutaneous injection of turpentine. The reaction is characterized by local swelling, induration, and abscess formation, terminated by rupture or incision after 3 to 5 days and by general reactions of malaise, fever, leucocytosis, and increased urinary nitrogen. For 3 to 6 days after turpentine the nitrogen intake was provided in seven experiments by amino acids given parenterally (a solution of the ten essential amino acids (Rose) plus glycine). A normal dog with a normal protein intake showed a negative nitrogen balance after turpentine-urinary nitrogen doubled even as in inflammation during fasting. A protein-depleted dog (low protein reserves produced by very low protein intake) given a normal protein intake after turpentine maintained nitrogen balance-urinary nitrogen rose only slightly. With a high (doubled) protein intake the depleted dog showed strongly positive balance. Normal dogs with high (doubled) protein intakes react to turpentine with doubled urinary nitrogen outputs on individual days and therefore are maintained in approximate nitrogen balance and weight balance. This end may be achieved equally well or better by oral feeding, when such is possible and absorption unimpaired. The increased nitrogen excretion after injury is again shown directly related to the state of body protein reserves. Increased catabolism not inhibition of anabolism best explains the excess urinary nitrogen. Protection during injury of valuable protein reserves appears possible through an adequate intake of protein nitrogen.
authors.affiliation: Department of Pathology, The University of Rochester School of Medicine and Dentistry, Rochester, New York.
authors.forename: S C
authors.initials: SC
authors.lastname: Madden
authors.forename: W A
authors.initials: WA
authors.lastname: Clay