UMLS:C0021843 - FACTA Search

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Query: UMLS:C0021843 (bowel obstruction)
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Intestinal obstruction, as a rule, is associated with an increasing amount of non-coagulable nitrogen in the blood. With acute intoxication the rise in non-coagulable nitrogen may be rapid and reach as high as three or even ten times normal. With more chronic intoxication there may be little or no rise in the blood non-coagulable nitrogen. Closed intestinal loops show exactly the same picture, and, when combined with obstruction, may give very high nitrogen readings. Acute proteose intoxication due to injection of a pure proteose will show a prompt rise in blood non-coagulable nitrogen, even an increase of 100 per cent within 3 or 4 hours. These intoxications also show a high blood content of creatinine and urea. The residual or undetermined nitrogen may be very high. A human case of intestinal obstruction with autopsy presents blood findings exactly similar to those observed in many animal experiments. Clinically the non-coagulable nitrogen of the blood may give information of value in intestinal obstruction. A high reading means a grave intoxication, but a low reading may be observed in some fatal cases and gives no assurance that a fatal intoxication may not supervene. The kidneys in practically all these experiments are normal in all respects. It is possible that protein or tissue destruction rather than impaired eliminative function is responsible for the rise in non-coagulable nitrogen of the blood in these acute intoxications. Transfusions of dextrose solutions often benefit intestinal obstruction, and may depress the level of the non-coagulable nitrogen in the blood. Some cases show no change in non-coagulable nitrogen following transfusions and diuresis, and, as a rule, such cases present the most severe intoxication.
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PMID:INTESTINAL OBSTRUCTION : VI. A STUDY OF NON-COAGULABLE NITROGEN OF THE BLOOD. 1986 19

1. In experimental wounds, made by removing various sized pieces of skin from the frog, there is a rapid coagulation of the blood plasma and lymph to form a coagulation tissue which fills the wound cavity. 2. The observations on the living animals show that the coagulation a grave intoxication, but a low reading may be observed in some fatal cases and gives no assurance that a fatal intoxication may not supervene. The kidneys in practically all these experiments are normal in all respects. It is possible that protein or tissue destruction rather than impaired eliminative function is responsible for the rise in non-coagulable nitrogen of the blood in these acute intoxications. Transfusions of dextrose solutions often benefit intestinal obstruction, and may depress the level of the non-coagulable nitrogen in the blood. Some cases show no change in non-coagulable nitrogen following transfusions and diuresis, and, as a rule, such cases present the most severe intoxication.
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PMID:THE ORIGIN AND STRUCTURE OF A FIBROUS TISSUE FORMED IN WOUND HEALING. 1986 20

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.
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PMID:PROTEOSE INTOXICATIONS AND INJURY OF BODY PROTEIN : I. THE METABOLISM OF FASTING DOGS FOLLOWING PROTEOSE INJECTIONS. 1986 1

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.
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PMID:PROTEOSE INTOXICATIONS AND INJURY OF BODY PROTEIN : II. THE METABOLISM OF DOGS WITH DUODENAL OBSTRUCTION AND ISOLATED LOOPS OF INTESTINE. 1986 2

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.
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PMID:PROTEOSE INTOXICATIONS AND INJURY OF BODY PROTEIN : V. THE INCREASE IN NON-PROTEIN NITROGEN OF THE BLOOD IN ACUTE INFLAMMATORY PROCESSES AND ACUTE INTOXICATIONS. 1986 53

Associated with the intoxication of intestinal obstruction there exists a definite impairment of the excretory function of the kidneys. The degree of functional depression corresponds roughly with the intensity of the clinical intoxication. The decrease in the urea ratio and in the capacity of the kidneys to excrete sodium chloride is more marked than is the percentage decrease of phenolsulfonephthalein elimination. The great increase in the non-protein nitrogen of the blood usually observed in acute intestinal obstruction, which has hitherto been explained as being due entirely to an increased rate of protein catabolism, is due in part to retention of the products released from the injured cell protein. It is probable that the impaired renal function is due to direct action of the toxic substances upon the renal epithelium. The actual demonstration of this renal injury is perhaps the strongest evidence so far obtained to prove the presence of an actual toxic substance in the blood during intestinal obstruction. This obscure disability of the kidneys during the height of the intoxication of acute ileus should always be considered in the clinical management of this condition. It may also serve as a guide to indicate the degree of intoxication.
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PMID:I. RENAL FUNCTION INFLUENCED BY INTESTINAL OBSTRUCTION. 1986 27

A study of the non-protein nitrogen, urea nitrogen, uric acid, creatinine, amino-acid nitrogen, sugar, and chlorides of the blood and the CO(2)-combining power of the plasma in normal dogs, and in dogs after different types of intestinal obstruction, is reported. Following ligation of the duodenum, ligation of the duodenum with gastroenterostomy, and ligation of the upper half of the ileum, a fall in chlorides and a rise in the non-protein nitrogen and urea nitrogen of the blood and in the CO(2)-combining power of the plasma occur. The uric acid, creatinine, amino-acid nitrogen, and sugar show no significant changes. The fundamental change is a fall in chlorides followed by an alkalosis. The degree of alkalosis depends upon the rate of formation of carbonate, rate of excretion by the kidneys, and extent of neutralization of the carbonate by acid bodies formed during the intoxication. The fall in chlorides is probably due to a utilization of the chlorine ion in the course of the intoxication. It is suggested that this use of chlorine is a protective measure on the part of the body. There are indications that high intestinal obstruction should not be treated by the administration of alkalies. The urea nitrogen is a good index of the protein destruction. Ligation of the ileum at the ileocecal valve is followed by little increase in nitrogen and no change in the chlorides or CO(2)-combining power of the plasma. The close similarity of the blood findings in intestinal obstruction, acute lobar pneumonia, and serum disease suggests that these widely different conditions may have a common chemical basis.
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PMID:CHEMICAL CHANGES IN THE BLOOD OF THE DOG AFTER INTESTINAL OBSTRUCTION. 1986 32

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 CO(2)-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.
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PMID:CHEMICAL CHANGES IN THE BLOOD OF THE DOG AFTER PYLORIC OBSTRUCTION. 1986 33

Experiments to determine the effect of furnishing an ample supply of sodium chloride on the toxemia of pyloric and intestinal obstruction are reported. A fall in chlorides is the first and seemingly most significant change to take place in the blood after pyloric and intestinal obstruction. The chloride is apparently utilized by the body as a protective measure against the primary toxic substance. Two dogs with pyloric obstruction were given 50 cc. of 10 per cent NaCl subcutaneously daily. One lived 3 days, the other 4. The blood showed little change, except a marked terminal rise in chlorides. Animals given a like amount of distilled water or 25 per cent glucose showed the changes typical of untreated animals. The obstruction of the pylorus was released in six dogs 48 to 72 hours after the initial operation. Two died within 24 hours after the second operation with a high non-protein nitrogen in the blood. Two survived but showed a high level of non-protein nitrogen in the blood and a high nitrogen excretion in the urine, low blood chlorides, and a marked alkalosis. One dog in such a state died on the 13th day from peritonitis, arising in a wound infection. The other showed a marked fall in non-protein nitrogen in the blood following the administration of 10 gm. of sodium chloride by mouth, but died following the intravenous injection of 25 per cent sodium chloride. Two animals were given 50 cc. of 10 per cent NaCl subcutaneously, at the time of the second operation. The blood rapidly returned to normal and complete recovery followed. Two dogs with the duodenum obstructed by section and inversion of the cut ends were treated with 10 per cent sodium chloride after the obstruction had existed for 48 hours and the characteristic blood changes had developed. The non-protein nitrogen returned to normal within 48 hours after treatment was begun. One dog died following a lateral anastomosis for relief of the obstruction. A second operation was not attempted in the other animal. Two dogs in which the duodenum was obstructed by section and inversion of the cut ends were given 500 cc. of 0.85 per cent NaCl subcutaneously on the day of operation and each day thereafter until death. One dog lived 21 days, the other 28. Both dogs showed a marked alkalosis, but never any rise in the non-protein nitrogen of the blood. The animals at autopsy showed intussusception of the ileum with extensive ulceration. In one there was a perforation and terminal peritonitis. The operation wounds healed normally. Three dogs with section of the duodenum were given 500 cc. of distilled water every day. One died in 24 hours, one in 48 hours, and the third in 72 hours. Autopsy showed no cause for death other than toxemia. One dog with section of the duodenum was given 500 cc. of 2 per cent glucose every day. The blood showed a rapid rise in non-protein nitrogen and carbon dioxide-combining power, and a fall in chlorides. The animal died 72 hours after operation. Three dogs with section of the duodenum were given 500 cc. of 1 per cent sodium bicarbonate every day. One dog died in 72 hours, one lived 7 days, and the third lived 9 days. All developed a high non-protein nitrogen in the blood and two showed marked clinical symptoms of an alkalosis. These results demonstrate that solutions of sodium chloride have a marked effect in preventing and controlling the toxemia of pyloric and intestinal obstruction as shown in clinical symptoms and in chemical changes in the blood. Dogs given an abundant supply of distilled water died more quickly than untreated control animals. Solutions of glucose have no specific value, and sodium bicarbonate solutions prolong life only a short while. Good therapeutic results have been obtained with very concentrated sodium chloride solutions, and with dry sodium chloride given by mouth. It seems evident that sodium chloride has a specific action in preventing and possibly in controlling the changes produced by the toxic body. Sodium chloride is a valuable therapeutic agent in pyloric and high intestinal obstruction.
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PMID:THE EFFECT OF SODIUM CHLORIDE ON THE CHEMICAL CHANGES IN THE BLOOD OF THE DOG AFTER PYLORIC AND INTESTINAL OBSTRUCTION. 1986 71

The chemical changes in the blood of dogs treated with various inorganic salts after obstruction of the duodenum are reported. Two dogs treated with sodium chloride survived approximately six times as long as the average untreated animal, one living 22 days, the other 24 days. Ammonium chloride was found to produce an acidosis. The administration of potassium chloride, calcium chloride, and magnesium chloride did not prevent the usual rise in non-protein nitrogen and fall in chlorides, and the fatal outcome. Iodides seemingly hasten the toxic process. Sodium bromide appears to have an inhibitory action upon it, but much less than that of sodium chloride. Sodium sulfate, magnesium sulfate, sodium citrate, monosodium phosphate, and disodium phosphate failed to alter the course of the intoxication. Atropine and pilocarpine were without therapeutic value in preventing the changes characteristic of intestinal obstruction.
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PMID:THE EFFECT OF INORGANIC SALTS ON THE CHEMICAL CHANGES IN THE BLOOD OF THE DOG AFTER OBSTRUCTION OF THE DUODENUM. 1986 47

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