scholarly journals PROTEOSE INTOXICATIONS AND INJURY OF BODY PROTEIN

1917 ◽  
Vol 25 (3) ◽  
pp. 461-477 ◽  
Author(s):  
G. H. Whipple ◽  
J. V. Cooke
Keyword(s):  
Intestinal Obstruction ◽  
Cell Injury ◽  
Lethal Dose ◽  
Complete Recovery ◽  
Base Line ◽  
Protein Nitrogen ◽  
Body Protein ◽  
Unit Dose ◽  
Nitrogen Elimination ◽  
Urinary Nitrogen

Proteose injections in dogs cause vomiting, diarrhea, temperature reactions, low blood pressure, prostration, and, after large doses, an excess of antithrombin with incoagulable blood. A single proteose injection, for example one-half a lethal dose, causes abrupt clinical reactions in a normal dog with apparent complete recovery within 24 to 48 hours. The nitrogen elimination curve in a fasting dog under such conditions shows a great rise in total urinary nitrogen. The apex of the curve usually falls during the second 24 hour period following the injection. This rise may be over 100 per cent increase above the mean base-line nitrogen level. It does not fall promptly to normal but declines slowly in 3 to 5 days or more toward the original base-line (Text-fig. 1). This speaks for a definite cell injury with destruction of considerable protein substance due to a single proteose injection. The disturbance of cell equilibrium is not rapidly or promptly restored to normal. A dog which has received previous proteose injections is partially immune or tolerant to subsequent injections of proteose. These dogs, as a rule, show less intense clinical reactions and less rise in the curve of nitrogen elimination following a unit dose of standard proteose as compared with normal or non-immune controls. The proteose used in these experiments was prepared as described from material obtained in cases of intestinal obstruction or of closed intestinal loops. These experiments explain the sharp rise in blood non-protein nitrogen which follows within a few hours the injection of a toxic proteose. They also point to the correct explanation of the high non-protein nitrogen of the blood found in intestinal obstruction or with closed intestinal loops.

scholarly journals PROTEOSE INTOXICATIONS AND INJURY OF BODY PROTEIN

1918 ◽  
Vol 28 (2) ◽  
pp. 243-252
Author(s):  
J. V. Cooke ◽  
G. H. Whipple
Keyword(s):  
Intestinal Obstruction ◽  
Clinical Analysis ◽  
Abscess Formation ◽  
Protein Nitrogen ◽  
Urea Nitrogen ◽  
Body Protein ◽  
Acute Infections ◽  
Pathological Conditions ◽  
Septic Inflammation ◽  
Urinary Nitrogen

Sterile abscess formation in the dog is accompanied by a large increase in output of urinary nitrogen and also by a small but definite increase in the blood non-protein nitrogen. All this nitrogenous material of course is derived from body protein injury and autolysis. Septic inflammation in the dog (pleurisy, pneumonia, peritonitis, etc.) likewise shows a distinct rise in the blood non-protein nitrogen. This rise is not often so great as that frequently observed in the intoxication of intestinal obstruction. Many acute infections in man (septicemia, peritonitis, pneumonia, etc.) show a definite rise in the non-protein nitrogen and urea nitrogen of the blood; some cases show a very great rise above normal (over 100 mg. of non-protein nitrogen per 100 cc. of blood). There may be no anatomical change in the kidney beyond the familiar picture of cloudy swelling. This does not exclude the possibility of some transient functional derangement of the kidney epithelium. Certain obscure intoxications in man may show a considerable rise in the non-protein nitrogen of the blood, indicating a large amount of protein disintegration. These findings must be taken into account in any clinical analysis and interpretation of high non-protein nitrogen of the blood in pathological conditions.

scholarly journals PROTEOSE INTOXICATIONS AND INJURY OF BODY PROTEIN

1917 ◽  
Vol 25 (3) ◽  
pp. 479-494 ◽  
Author(s):  
G. H. Whipple ◽  
J. V. Cooke ◽  
T. Stearns
Keyword(s):  
Total Nitrogen ◽  
Duodenal Obstruction ◽  
The Body ◽  
Intestinal Loop ◽  
Base Line ◽  
General Reaction ◽  
Protein Nitrogen ◽  
Body Protein ◽  
Nitrogen Elimination ◽  
Elimination Curve

Dogs with isolated loops of small intestine show many evidences of intoxication. A study of the total nitrogen elimination shows a great rise above the normal base-line minimum of the fasting period (Table II). This means that the intoxication is associated with a great destruction of body protein, and explains the high non-protein nitrogen of the blood which was observed and reported previously (2). Injection of a proteose obtained from a closed intestinal loop will cause a similar rise in the nitrogen elimination curve. This furnishes more evidence that the intoxication observed in association with a closed intestinal loop is in reality a proteose intoxication. Dogs injected with sublethal doses of proteose will show a definite tolerance to subsequent injection, and will show much less acute intoxication after the isolation of a closed intestinal loop (Table 1). These immune or tolerant dogs show a much less pronounced rise in the nitrogen elimination curve during proteose intoxication of any type. This indicates that the tolerance or immunity to proteose gives more protection for the body proteins against the injury which these toxic proteoses inflict upon the body cells. Complete duodenal obstruction combined with a gastrojejunostomy gives a chronic type of intestinal obstruction associated with little vomiting, which is peculiarly suited to metabolism study (Table IV). Such duodenal obstructions show a definite and sustained rise in the curve of nitrogen elimination above the normal base-line level. These dogs, too, are tolerant to injections of standard toxic proteoses. Control ether anesthesia experiments show little if any rise in the curve of nitrogen elimination (Table VI). Control laparotomy experiments show a definite rise in the curve of nitrogen elimination, but a rise which is small compared with the rise noted in the intoxication of duodenal obstruction or of isolated intestinal loops. It is probable that the tissue injury and disintegration associated with the wound reaction are responsible for the general reaction. We may assume that protein split products from the wound area are absorbed and are responsible for the general reaction observed. We propose to assume that the intoxications here studied are associated with a definite proteose intoxication, which is capable of initiating and continuing a profound injury of tissue protein. One index of this protein injury is the great and sustained rise in the curve of total nitrogen elimination.

scholarly journals PROTEIN METABOLISM AND PROTEIN RESERVES DURING ACUTE STERILE INFLAMMATION

1945 ◽  
Vol 82 (1) ◽  
pp. 65-76 ◽  
Author(s):  
S. C. Madden ◽  
W. A. Clay
Keyword(s):  
Amino Acids ◽  
Nitrogen Balance ◽  
Protein Intake ◽  
Oral Feeding ◽  
Nitrogen Excretion ◽  
Protein Nitrogen ◽  
Body Protein ◽  
Low Protein ◽  
Positive Balance ◽  
Urinary Nitrogen

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.

Resistance training reduces whole-body protein turnover and improves net protein retention in untrained young males

2006 ◽  
Vol 31 (5) ◽  
pp. 557-564 ◽  
Author(s):  
Joseph W. Hartman ◽  
Daniel R. Moore ◽  
Stuart M. Phillips
Keyword(s):  
Resistance Training ◽  
Resistance Exercise ◽  
Nitrogen Balance ◽  
Protein Turnover ◽  
Whole Body ◽  
Body Protein ◽  
Protein Retention ◽  
The Impact ◽  
Net Protein ◽  
Urinary Nitrogen

It is thought that resistance exercise results in an increased need for dietary protein; however, data also exists to support the opposite conclusion. The purpose of this study was to determine the impact of resistance exercise training on protein metabolism in novices with the hypothesis that resistance training would reduce protein turnover and improve whole-body protein retention. Healthy males (n = 8, 22 ± 1 y, BMI = 25.3 ± 1.8 kg·m–2) participated in a progressive whole-body split routine resistance-training program 5d/week for 12 weeks. Before (PRE) and after (POST) the training, oral [15N]-glycine ingestion was used to assess nitrogen flux (Q), protein synthesis (PS), protein breakdown (PB), and net protein balance (NPB = PS – PB). Macronutrient intake was controlled over a 5d period PRE and POST, while estimates of protein turnover and urinary nitrogen balance (Nbal = Nin – urine Nout) were conducted. Bench press and leg press increased 40% and 50%, respectively (p < 0.01). Fat- and bone-free mass (i.e., lean muscle mass) increased from PRE to POST (2.5 ± 0.8 kg, p < 0.05). Significant PRE to POST decreases (p <0.05) occurred in Q (0.9 ± 0.1 vs. 0.6 ± 0.1 g N·kg–1·d–1), PS (4.6 ± 0.7 vs. 2.9 ± 0.3 g·kg–1·d–1), and PB (4.3 ± 0.7 vs. 2.4 ± 0.2 g·kg–1·d–1). Significant training-induced increases in both NPB (PRE = 0.22 ± 0.13 g·kg–1·d–1; POST = 0.54 ± 0.08 g·kg–1·d–1) and urinary nitrogen balance (PRE = 2.8 ± 1.7 g N·d–1; POST = 6.5 ± 0.9 g N·d–1) were observed. A program of resistance training that induced significant muscle hypertrophy resulted in reductions of both whole-body PS and PB, but an improved NPB, which favoured the accretion of skeletal muscle protein. Urinary nitrogen balance increased after training. The reduction in PS and PB and a higher NPB in combination with an increased nitrogen balance after training suggest that dietary requirements for protein in novice resistance-trained athletes are not higher, but lower, after resistance training.

scholarly journals CHEMICAL CHANGES IN THE BLOOD OF THE DOG AFTER PYLORIC OBSTRUCTION

1923 ◽  
Vol 37 (3) ◽  
pp. 377-381 ◽  
Author(s):  
Russell L. Haden ◽  
Thomas G. Orr
Keyword(s):  
Intestinal Obstruction ◽  
Protein Metabolism ◽  
Close Relation ◽  
Inorganic Salts ◽  
Pyloric Obstruction ◽  
Marked Rise ◽  
Protein Nitrogen ◽  
Chemical Changes ◽  
Chemical Studies ◽  
High Intestinal Obstruction

Chemical studies of the blood and urine of four dogs following pyloric obstruction are reported. The observations of other workers that a fall in chlorides and a rise in CO2-combining power of the plasma occur, are confirmed. There is also a marked rise in the non-protein nitrogen of the blood, consisting mainly of urea nitrogen and undetermined nitrogen. The fall in chlorides is not due to the loss of chlorides in the gastric juice. The chlorine is probably bound somewhere in the process of protein destruction. There is a close relation between the fall in chlorides and the protein destruction. A study of tetany should include the protein metabolism as well as that of the inorganic salts, since it seems possible that the tetany is due to protein split-products and not to the alkalosis. The chemical changes following pyloric obstruction are essentially the same as those following high intestinal obstruction.

scholarly journals Water Hemlock (Cicuta Douglasii) Toxicoses in Sheep: Pathologic Description and Prevention of Lesions and Death

1996 ◽  
Vol 8 (4) ◽  
pp. 474-480 ◽  
Author(s):  
Kip E. Panter ◽  
Dale C. Baker ◽  
Phil O. Kechele
Keyword(s):  
Body Weight ◽  
North America ◽  
Intravenous Administration ◽  
Seizure Activity ◽  
Lethal Dose ◽  
Complete Recovery ◽  
Sodium Pentobarbital ◽  
Excessive Salivation ◽  
Grand Mal ◽  
Serum Biochemical

Water hemlock causes numerous livestock losses in North America every year. Description of pathologic and serum biochemical changes has been lacking in the literature. Tubers of western water hemlock ( Cicuta douglasii) induced excessive salivation, tremors, grand mal seizures, skeletal and cardiac myodegeneration, and death in sheep given 1.2–2.7 g fresh tuber/kg body weight by gavage. Seizures were intermittent with periods of relaxation until death occurred from anoxia during seizure activity. In sheep given 1.5–2.5 times the lethal dose of water hemlock by gavage, intravenous administration of sodium pentobarbital at the onset of the first seizure prevented further seizure activity and skeletal and cardiac myodegeneration and resulted in rapid and complete recovery.

scholarly journals EFFECTS OF BACTERIAL ENDOTOXINS ON METABOLISM

1962 ◽  
Vol 116 (6) ◽  
pp. 897-911 ◽  
Author(s):  
L. Joe Berry ◽  
Dorothy S. Smythe ◽  
Susannah McC. Kolbye
Keyword(s):  
Nitrogen Excretion ◽  
Protein Nitrogen ◽  
Bacterial Endotoxins ◽  
Small Change ◽  
The Moment ◽  
Lower Ratio ◽  
Urinary Nitrogen Excretion ◽  
Urinary Nitrogen

The greater susceptibility to the lethal effects of bacterial endotoxin (heat-killed Salmonella typhimurium or Escherichia coli lipopolysaccharide, in mice infected with an attenuated strain of Mycobacterium tuberculosis (BCG) was confirmed. It reached a maximum at 2 weeks postinfection and gradually diminished for an additional 6 weeks. At the time of maximum susceptibility several metabolic and physiological differences became apparent. BCG-infected mice die sooner (4 to 12 hours) and without the diarrhea, conjunctivitis, and general symptomatology associated with endotoxin deaths of normal animals. Reticuloendothelial blockade results in only a small change in reactivity to endotoxin, in contrast to normal mice. Subcutaneous injection of 2 units of ACTH is followed by no significant increase in urinary nitrogen excretion while in control animals it more than doubles. Plasma clearance of intravenously administered inulin is approximately normal in BCG-infected mice 17 hours after an LD50 dose of endotoxin but control mice similarly treated show renal impairment. In line with this result is the absence of elevated carcass non-protein nitrogen (NPN) following endotoxin poisoning or at the moment of death from endotoxemia in the hyperreactive animals in contrast to the two- to threefold increase in carcass NPN in normal mice under similar conditions. Body carbohydrate is at a minimum and becomes depleted to a level approximating that found at death more rapidly in BCG-infected mice given endotoxin than in controls. There is also a lower ratio of carbohydrate anabolized to protein catabolized following cortisone administration to BCG-infected mice than in control mice. This is found in adrenalectomized mice and in stressed animals and is reported elsewhere. Some of the differences just described can be attributed to a refractory adrenal cortex. There is less depletion of adrenal cholesterol in vivo and lower corticoid synthesis in vitro than in normal mice yet this is not fundamentally responsible for the greater susceptibility of BCG-infected animals to endotoxin since adrenalectomized mice, which are even more susceptible, are metabolically and physiologically more comparable to normal mice than to BCG-infected mice. One can conclude, therefore, that the hyperreactivity of BCG-infected mice is more than an intensification of the normal response to endotoxin.

Enteral hyperalimentation in head injury

1985 ◽  
Vol 62 (2) ◽  
pp. 186-193 ◽  
Author(s):  
Guy L. Clifton ◽  
Claudia S. Robertson ◽  
Charles F. Contant
Keyword(s):  
Head Injury ◽  
Nitrogen Balance ◽  
Severe Head Injury ◽  
Nitrogen Excretion ◽  
Metabolic Complications ◽  
Protein Nitrogen ◽  
Enteral Hyperalimentation ◽  
Lower Protein ◽  
Protein Group ◽  
Urinary Nitrogen

✓ The objectives of this study were to determine the ability of enteral hyperalimentation to meet the caloric and protein requirements in acute severe head injury, and to study the effect of increasing protein intake on nitrogen balance. This consecutive series of 20 patients suffered acute severe head injury and remained comatose for at least 24 hours. They were all without other major injuries, and were treated with steroids. These patients were randomly placed in two comparable treatment groups: one group was fed with an enteral formula containing 14% of its calories as protein and the other group received a formula containing 22% protein calories. Feedings were advanced to replace 140% of caloric expenditure measured by indirect calorimetry, averaging 3500 kcal/24 hr. Balance periods of the targeted intake were 7 days in duration, and were begun during the 1st week after injury for 65% of patients and in the 2nd week after injury for 35% of patients. The lower protein group received an average of 26.8 gm/24 hr of nitrogen, equivalent to 188 gm of protein, and the higher protein group 34.3 gm/24 hr, equivalent to 231 gm of protein. Nitrogen balance was −9.2 ± 6.7 gm/24 hr in the lower protein group and −5.3 ± 5.0 gm/24 hr in the higher protein group, but the difference did not reach statistical significance because of sample size and variability in extent of catabolism among patients. Despite the hyperalimentation, there was a mean negative cumulative nitrogen balance of 200 gm by the 2nd week after injury, and only three patients achieved net nitrogen equilibrium for the 7-day balance period. Despite enteral hyperalimentation, the patients' weight fell by 15% in the 2nd week, serum albumin was often decreased, and creatinine-height index decreased over time but remained in a normal range. Monitoring urinary urea nitrogen, which has been advocated as a generally available technique for measuring urinary nitrogen concentration, was found to be a poor measure of urinary nitrogen excretion. This work has demonstrated: 1) that high caloric and protein feedings may be delivered for prolonged periods enterally for most patients in the acute phase of head injury with few metabolic complications, and 2) that increasing the nitrogen content of feedings from 14% to 22% may somewhat improve nitrogen retention, although nitrogen equilibrium is seldom achieved.

scholarly journals Urinary Nitrogen Excretion of the Cockerels Fed Non-protein Nitrogen Diets

1974 ◽  
Vol 11 (5) ◽  
pp. 190-193 ◽  
Author(s):  
Yoshio NAKAHIRO ◽  
Yutaka ISSHIKI ◽  
Jun-ichi OKUMURA
Keyword(s):  
Nitrogen Excretion ◽  
Protein Nitrogen ◽  
Urinary Nitrogen Excretion ◽  
Urinary Nitrogen

scholarly journals ROENTGEN RAY INTOXICATION

1922 ◽  
Vol 35 (2) ◽  
pp. 187-202 ◽  
Author(s):  
S. L. Warren ◽  
G. H. Whipple
Keyword(s):  
Small Intestine ◽  
Clinical Evidence ◽  
Clinical Work ◽  
X Rays ◽  
Fatal Intoxication ◽  
Unit Dose ◽  
Slight Rise ◽  
Almost All ◽  
Proper Consideration ◽  
Urinary Nitrogen

Roentgen radiation of the thorax (abdomen shielded) in dogs, even with large doses (up to 512 milliampere minutes), gives no clinical evidence of intoxication. There may be a transient leucopenia and a slight rise in urinary nitrogen. Roentgen radiation of the abdomen (thorax shielded) in dogs, with a dose of 350 milliampere minutes, will almost certainly cause a fatal intoxication. Smaller doses may be survived but usually with signs of gastrointestinal intoxication. This lethal intoxication due to abdominal radiation presents a remarkably uniform clinical and anatomical picture. There is a latent period of 24 to 36 hours, during which the dog is perfectly normal clinically. The 2nd day usually shows the beginning of diarrhea and perhaps some vomitus. The 3rd and 4th days show progressive intoxication with increasing vomiting and bloody diarrhea until the dog becomes stuporous. Death is almost always on the 4th day. Anatomically the only lesions of significance are to be found in the small intestine. The epithelium of the crypts and villi shows more or less complete necrosis, and this condition may involve almost all of the small intestine. The epithelium may vanish completely except for a few cells here and there which have escaped and are often found in mitosis, probably an effort at repair and regeneration. We are forced to the conclusion that this remarkable injury of the epithelium of the small intestine is responsible for the various abnormal reactions and final lethal intoxication which follow a unit dose of Roentgen radiation over the abdomen of a normal dog. This sensitiveness of the intestinal epithelium to x-rays is not appreciated and should be given proper consideration in clinical work.

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