Gastrointestinal Loss Research Articles

Varioliform gastritis and duodenitis associated with protein-losing gastroenteropathy, treated with omeprazole

A 44-year-old female with varioliform gastritis and duodenitis had gastrointestinal protein loss revealed by 111indium chloride scintigraphy. Treatment with omeprazole, a proton pump inhibitor, for 2 months, followed by famotidine, resulted in clinical improvement with resolution of the gastroduodenal lesions and protein loss. Colonization of the stomach with Helicobacter pylori was found before and after the treatment. The results in this patient suggest that omeprazole can be of value for the treatment of varioliform gastritis associated with protein-losing gastroenteropathy. The role of Helicobacter pylori in the pathogenesis of this disease is unclear.

Acute renal failure in Eastern India

The present study included 426 patients with acute renal failure age range 7 months to 85 years, during 8-year period (1984-1992). Medical, surgical and obstetric causes were responsible for ARF in 68.3, 17.8, and 14% of cases respectively. The main aetiological factors encountered were volume depletion secondary to gastrointestinal fluid loss (35.2%), acute glomerulonephritis (10.3%), nephrotoxin (8.6%), falciparum malaria (4.2%), obstructive uropathy (13%), post-abortal (10.5%), and miscellaneous factors (1.4%) of patients. The overall mortality was 19.2%. Thus our observation revealed that diarrhoeal diseases (35.2%), obstructive uropathy (13.3%), and septic abortion (10.5%) were the main causes for ARF in medical, surgical, and obstetric groups respectively. In contrast to our studies, acute renal failure associated with diarrhoeal diseases, septicaemia, falciparum malaria and septic abortion are rare in European countries.

Preweaning losses of piglets on a state farm in Bosnia and Herzegovina

The objective of a 3 year pilot survey of preweaning mortality on a large swine farm in Bosnia and Herzegovina was to provide producers and/or veterinarians with information about causes of piglet losses, their occurrence and frequency at the herd (regional) level. This may also serve as a model for an assessment at the national level. The SNOVET system, a part of the National Animal Health Monitoring System (launched in the USA in 1985), was applied for the classification of causes of deaths among suckling piglets based on postmortem findings. To assess the incidences of causes of preweaning losses, 354094 piglets born in 34 648 litters were monitored daily from June 1985 to May 1988. Respective information from 20 682 (or 5.8%) stillborns and those piglets that died from birth to weaning (49 058 or 14.7%) was given. Among piglets born alive, overlaying was the most frequent cause of death (6%), followed by mortality due to gastrointestinal syndrome (3.9%), cachexia/inanitio neonatorum (2.2%), and losses of small or deformed piglets (1.6%). The incidence of pneumonia was very low (0.02%). A relatively high proportion of causes of mortality remained unknown (0.9%) partly owing to savaging or losing piglet corpses in the sewers. The use of recorded information on type, extent, and incidence of piglet mortality (gathered on the sample of appropriate size) on a long-term basis may help in the development of effective strategies to reduce/control losses until weaning.

Intramural Gastric Actinomycosis

We report a case of intramural gastric actinomycosis and review the features of the additional 16 cases of this uncommon infection reported in the literature. The patient had gastrointestinal symptoms, weight loss, and fever after gastric operation. At laparotomy, an infiltrating gastric tumor-like lesion was found. Histology revealed actinomycosis, and the patient was successfully treated with oral penicillin. Because of its rarity, intramural actinomycosis is an entity overlooked by most surgeons. Reporting of such cases may help increase the awareness of this important and curable disease.

Potassium homeostasis and its disturbances in children

Although only 2% of the body potassium is present in the extracellular space, its concentration is finely regulated by the internal balance, or distribution of potassium between the intracellular and extracellular compartments, and by the external balance, or difference between intake and output of potassium. Internal balance is modulated by a host of factors, including insulin, epinephrine, extracellular pH and plasma tonicity. Potassium output from the body is mainly determined by renal excretion. Renal secretion of potassium takes place predominantly in the principal cells of late distal and cortical collecting tubules, by a process involving the accumulation of potassium in the cell by the activity of the basolateral Na+,K(+)-ATPase and its exit through luminal conductive channels. The factors regulating renal potassium secretion are potassium intake, rate of tubular fluid flow, distal sodium delivery, acid-base status and aldosterone. Hypokalaemia may result from a low potassium intake, excessive gastrointestinal, cutaneous or renal losses and altered body distribution. Aetiological diagnosis and therapy are best accomplished when the acid-base status is assessed at the same time. Before establishing the diagnosis of hyperkalaemia, spurious hyperkalaemia due to haemolysis or release of potassium from cells during clot retraction (pseudohyperkalaemia) should be ruled out. Hyperkalaemia may result from exogenous or endogenous loading, decreased renal output and altered body distribution. Acute hyperkalaemia represents an emergency situation which requires immediate therapy.

Disturbances of Potassium Homeostasis in Poisoning

Unless renal function is impaired or rhabdomyolysis is severe, hyperkalemia is a relatively uncommon metabolic complication of poisoning. In contrast, marked hypokalemia is a more common problem and may have serious sequelae. Most potassium disturbances in acute poisoning are due to disruption of extra-renal control mechanisms, notably the activity of Na+/K+ ATPase and K+ channels. Hypokalemia occurs because of increased Na+/K+ ATPase activity (e.g. beta 2 agonist, theophylline or insulin poisoning), competitive blockade of K+ channels (e.g. barium or chloroquine poisoning), gastrointestinal losses and/or alkalosis. Hyperkalemia follows inhibition of Na+/K+ ATPase activity (e.g. by digoxin), increased uptake of potassium salts, disruption of intermediary metabolism (e.g. cyanide poisoning), activation of K+ channels (e.g. fluoride poisoning), and the presence of acidosis and rhabdomyolysis, particularly if the latter is complicated by renal failure. Hypokalemia results in generalized muscle weakness, paralytic ileus, ECG changes (flat or inverted T waves, prominent U waves, ST segment depression) and cardiac arrhythmias (atrial tachycardia +/- block, AV dissociation, VT, VF). Hyperkalemia is associated with abdominal pain, diarrhea, muscle pain and weakness, ECG changes (tall peaked T waves, ST segment depression, prolonged PR interval, QRS prolongation) and cardiac arrhythmias (VT, VF). Significant disturbances of potassium homeostasis are often unrecognized and may cause considerable morbidity and mortality. Prompt recognition and appropriate treatment of these disturbances could be life-saving.

The mechanisms of gastrointestinal loss of iron

The purpose of this article is to demonstrate the usefulness of erythrokinetic studies in the evaluation of difficult cases of hypoferremia. Thorough search for causes of chronic blood loss and nutritional history taking are mandatory in these patients before undertaking the erythrokinetic studies. Using erythrokinetic studies in six hypoferremic women, the hypoferremia was the result of incomplete iron absorption in five and complete iron malabsorption in one. The results of the iron absorption studies of these hypoferremic patients were compared to the results of similar studies of patients with simple iron deficiency due to chronic blood loss or to poor nutrition where iron absorption is high. Three of the five patients with incomplete iron malabsorption had in addition, excessive transferrin (Tf) fecal iron loss. Two patients of this group had also increased fecal blood loss. Five patients out of the six responded well to iron therapy but they had to receive it indefinitely, otherwise their hypoferremia would relapse.

Magnesium Deficiency in Alcoholism: Possible Contribution to Osteoporosis and Cardiovascular Disease in Alcoholics

Magnesium (Mg) deficiency occurs frequently in chronic alcoholism and may contribute to the increased incidence of osteoporosis and cardiovascular disease seen in this population. Mg deficiency is primarily due to renal Mg-wasting and is exacerbated by dietary Mg deprivation, gastrointestinal losses with diarrhea or vomiting, as well as concomitant use of drugs such as diuretics and aminoglycosides. Osteoporosis is prevalent in the alcoholic population. Mg deficiency may contribute to increased bone loss by its effects on mineral homeostasis. In Mg depletion, there is often hypocalcemia due to impaired parathyroid hormone (PTH) secretion, as well as renal and skeletal resistance to PTH action. Serum concentrations of 1,25-vitamin D are also low. These changes are seen with even mild degrees of Mg deficiency and may contribute to the metabolic bone disease seen in chronic alcoholics. Hypomagnesemia in alcoholics may also contribute to increased cardiovascular disease by altering platelet function. Mg deficiency has been demonstrated to enhance platelet reactivity. In these studies, Mg was shown to inhibit platelet aggregation against various aggregation agents. Patients with Mg deficiency were shown to have increased platelet aggregation that was normalized with Mg therapy. The antiplatelet effect of Mg may be related to the finding that Mg inhibits the synthesis of thromboxane A2 and 12-hydroxyeicosatetraenoic acid, eicosanoids thought to be involved in platelet aggregation. Mg also inhibits the thrombin-induced Ca2+ influx in platelets, as well as stimulates synthesis of prostaglandin I2, the potent antiaggregatory eicosanoid. Therefore, Mg deficiency may increase platelet aggregation and cause increased hypertension and atherosclerotic cardiovascular disease in alcoholics.

Amino acid losses in ileostomy fluid on a protein-free diet

The contribution of losses via the gastrointestinal tract to maintenance amino acid requirements was assessed by collecting the ileostomy fluid of volunteers given a protein-free diet for 5 d. The subjects were eight adult men and women with terminal ileum ileostomies after ulcerative colitis. Four consecutive 24-h collections of both digesta and urine were made. On the last 2 d an antibiotic was given that suppressed microbial activity in the digesta and slightly reduced ileostomy outflow. Mean daily amino acid excretion in ileostomy fluid ranged from 32 mg/d for methionine to approximately 330 mg/d for aspartate and glutamate. These losses were compared with current international estimates of amino acid requirements. For most essential amino acids gastrointestinal losses accounted for 14-33% of daily maintenance requirements but for threonine the contribution was 61%.

A patient with diarrhea, arthralgias, and fever

A 28-year-old carpenter presented with diarrhea and abdominal pain for the past 4 months. He reported the passage of 4-6 loose stools daily, associated with crampy midabdominal pain and bloating. He also reported a 5-year history of fever. This occurred primarily in the evenings, with temperatures sometimes reaching 103’F associated with drenching sweats. In addition, there was a 5-year history of fatigue and migratory arthralgias involving the proximal interphalangeal joints, wrists, elbows, knees, ankles, tarsal areas, and metatarsophalangeal joints. The arthralgias would usually only involve a single joint at a time with pain lasting 1-4 days in a given joint area. He had been treated with enteric-coated aspirin up to 4 g/day, as wel1 as with prednisone in a dose ranging from 5 to 10 mg daily, with excellent suppression of the arthralgias, although not complete relief of the fevers. He denied use of other medications. He was married, and there was no history of sexually transmitted disease or illicit drug use. His father was Italian and mother German; there was no family history of gastrointestina1 disease. The review of systems revealed no history of gastrointestinal bleeding, weight loss, skin rash, or other symptoms. On examination, his temperature was 36.9”C. He was muscular and healthy appearing. The vita1 signs were normal. The skin and mucous membrane examinations did not reveal any abnormalities. NO pallor or clubbing was noted. Abdominal examination revealed no masses or tenderness, and recta1 examination was normal. There were several smal1 nontender axillary nodes bilaterally and several less prominent inguinal nodes, but no cervical lymphadenopathy. On cardiac auscultation, an inconstant soft systolic click was heard, but no murmurs or rubs were detected. Neurological examination was normal. Laboratory results were as fellows (normal values in parentheses): hemoglobin, 9.1 g/dL (12.9-16.6); mean corpus9.2 X lO”/L (4.1-10.9) with normal differential; platelet count, 593 X 109/L (184-370); erythrocyte sedimentation rate, 52 mm/h (0-22); reticulocytes, 1.1% (0.6-1.8); periphera1 blood smear showed microcytic red blood cells and slight abnormalities including regenerating macrocytes, schizocytes, keratocytes and stomatocytes; hemoglobin electrophoresis normal; serum iron, 9 pg/dL (50-150); total iron binding capacity, 266 pg/dL (250-400); iron saturation, 3% (14-50); vitamin B,,, 367 ng/L (281-1079); serum folate, 7.0 pg/L (2-20); sodium, 137 mEq/L (135145); potassium, 4.9 mEq/L (3.6-4.8); calcium, 9 mg/dL (8.9-10.1); phosph orus, 4.6 mg/dL (2.5-4.5); total protein, 6.1 g/dL (6.3-7.9); glucose, 78 mg/dL (70-100); alkaline phosphatase, 159 U/L (98-25 1); aspartate aminotransferase, 25 u/L (12-31); total bilirubin, 0.4 mg/dL (0.1-1.1); direct bilirubin, 0.1 mg/dL (0.0-0.3); uric acid, 4.2 mg/dL (4.3-8.0); creatinine, 1.0 mg/dL (0.8-1.2); albumin, 3.3 g/ dL (3.5-5.0); total thyroxine, 6.5 pg/dL (5.0-12.5); fecal hemoglobin, 1.6 mg/g stool (0-2); rheumatoid factor, ~30 IU/mL (0-39); antinuclear antibody negative; anti-double stranded DNA, 53 U (0-70); and rapid plasma reagin nonreactive. Stool for parasites was negative; there were some fatty crystals. Cultures of urine and blood were negative. Chest and spine radiographs were normal. An upper gastrointestinal barium series showed a normal esophagus and stomach but minimally thickened duodenal and proximal jejunal folds. A barium enema showed slightly prominent “lymphoid follicles” in the cecum and ascending colon.

Relative specificity for active inflammatory bowel disease of plasma-derived proteins in gut lavage fluid

Objective: Whole gut lavage with isotonic non-absorbable fluid is essentially a whole gut perfusion; whole gut lavage fluid (WGLF) can be used for clinical evaluation of intestinal immunity. High concentrations of WGLF immunoglobulin (lg) G, albumin and α-1-antitripsin (A1AT; probably reflecting plasma leakage) are characteristics of active inflammatory bowel disease. We aimed to establish reference values for concentrations of these proteins in WGLF and to assess the extent of high concentrations in conditions other than active inflammatory bowel disease. Methods: Gut lavage was performed on 63 immunologically normal patients or volunteers and on 254 occasions in patients with gastrointestinal symptoms or disease. After filtration and addition of protease inhibitors, WGLF content of IgG was assayed by enzyme-linked immunosorbent assay; albumin and A1AT by immunoturbidimetry. Results: Normal ranges were established: IgG < 1–10 μg/ml; albumin <1–26 μg/ml and A1AT < 1–19 μg/ml WGLF. In 102 tests on patients with inflammatory bowel disease of varying activity, high concentrations of WGLF IgG were present in 64%, of albumin in 52% and of A1AT in 36%. High concentrations of one or more proteins were present in 15 out of 152 patients with other conditions. In the majority, the existence of gastrointestinal protein loss was consistent with the clinical picture (one lymphangiectasia, seven colorectal cancers, one gut lymphoma, one perforated diverticulitis, one pouchitis and one lymphocytic colitis). Conclusion: Studies of gut lavage fluid proteins provide a new approach to screening of clinically complex patients with inflammatory bowel disease and other ulcerating and inflammatory lesions. This simple technique offers an alternative to faecal isotope excretion in the diagnosis of protein-losing enteropathy.

Hyponatremia in hospitalized patients with the acquired immunodeficiency syndrome (AIDS) and the AIDS-Related complex

Study objective: To determine the frequency, etiology, and clinical association of hyponatremia in patients with the acquired immunodeficiency syndrome (AIDS) and AIDS-related complex (ARC). Patients and methods: A prospective analysis of 167 patients with AIDS and 45 patients with ARC admitted on 269 occasions to a large metropolitan teaching hospital during a 3-month period. Results: Eighty-three patients (39%) with hyponatremia (serum sodium concentration less than 135 mmol/L) were observed during 99 hospitalisations, for a frequency of 38%. The mean (± standard error) of the lowest serum sodium concentration was 128 ± 1 mmol/L in the hyponatremic patients and 138 ± 1 mmol/L in the normonatremic patients. Hyponatremia was present on admission during 57 hospitalizations and was associated with gastrointestinal losses and hypovolemia in 43%. When hyponatremia developed during hospitalisation, 68% of the patients were clinically euvolemic and had a syndrome consistent with inappropriate secretion of antidiuretic hormone (SIADH). Patients with hyponatremia were hospitalized longer than those with normal serum sodium concentrations (17 ± 1 versus 9 ± 1 days, p < 0.001). In addition, the mortality rate in the hyponatremic group was higher than that in the normonatremic group (36.5% versus 19.7%, p < 0.01). Conclusion: Hyponatremia is a common electrolyte disorder in patients hospitalized with AIDS or ARC and is frequently associated with gastrointestinal losses or SIADH as well as increased morbidity and mortality.

Gastrointestinal Protein Loss in Elderly Patients with Cardiac Cachexia

Journal Article Gastrointestinal Protein Loss in Elderly Patients with Cardiac Cachexia Get access D King, D King University Department of Geriatric MedicineLiverpool Search for other works by this author on: Oxford Academic PubMed Google Scholar M L Smith, M L Smith University Department of Geriatric MedicineLiverpool Search for other works by this author on: Oxford Academic PubMed Google Scholar E Noonan, E Noonan University Department of Geriatric MedicineLiverpool Search for other works by this author on: Oxford Academic PubMed Google Scholar J H Silas, J H Silas University Department of Geriatric MedicineLiverpool Search for other works by this author on: Oxford Academic PubMed Google Scholar M Lye M Lye University Department of Geriatric MedicineLiverpool Search for other works by this author on: Oxford Academic PubMed Google Scholar Age and Ageing, Volume 22, Issue suppl_3, 1993, Pages P16-d–P17, https://doi.org/10.1093/ageing/22.suppl_3.P16-d Published: 01 September 1993

A Hypothesis: The Role of Magnesium and Possibly Copper Deficiency in the Pathogenesis of the Adult or Acute Respiratory Distress Syndrome (ARDS) as it Occurs in Infants, Children, and Adults

This is a hypothesis that magnesium (Mg) deficiency, often with associated copper (Cu) deficiency, contributes to the pathogenesis of the adult or acute respiratory distress syndrome (ARDS). ARDS occurs at all ages and is particularly lethal to infants and children. ARDS is an acute, life-threatening respiratory failure after widely diverse insults in patients with no prior history of cardiopulmonary dysfunction. The multiple predisposing factors include shock, sepsis, alcoholism, burns, gastroenteritis, and trauma. These are often treated with Mg-poor sodium-rich infusions, which increase renal excretion of Mg, or with multiple emergency transfusions of citrated blood, which temporarily binds Mg. Glucose or amino acid-rich infusates may result in translocation of Mg into intracellular space. Gastrointestinal loss of both Mg and Cu may be high. Unless specifically repleted, there may be major Mg and Cu losses. Within four d, about 1% of such patients in intensive care units, or 200,000 Americans a year, develop acute respiratory distress, with a survival rate of only 35%. The common denominator of injury is damage to the alveolar endothelium and epithelium, leading to increased permeability to protein, protein-rich alveolar edema, microatelectasis, and hyaline membranes. The pathogenesis is unknown. This hypothesis focuses on one aspect of this complex syndrome: The possible role of Mg deficiency and possibly Cu deficiency in the pathogenesis of ARDS. Deficiency of Mg leads to increased intracellular calcium (Ca), enhanced platelet aggregation, and increased secretion of thromboxane A2 (TXA2) from aggregated platelets. TXA2 is pro-aggregratory, and is a potent vasoconstrictor and bronchoconstrictor. As more platelets aggregate and are activated, there may be waves of exaggerated release of major vasoconstrictors that include TXA2, serotonin, and epinephrine, leading to pulmonary hypertension. Platelets release histamine which contributes to increased vascular permeability. Microvascular thrombosis of platelets, leukocytes, and thrombin lead to microatelectasis. Intrapulmonary shunting causes hypoxemia that is refractive to oxygen therapy. Cu is required for enzymes such as CuZn-superoxide dismutase (CuZnSOD) that provide major defense against damaging oxygen radicals. Mg and Cu are each required for normal immune response against infection and for oxidative phosphorylation (energy metabolism). Mg is required for protein synthesis, Cu for collagen and elastin synthesis. It appears to be of critical importance to investigate the roles of Mg and Cu in ARDS.

Tc-99m albumin scintigraphy in the localization of protein loss in the gut.

Scintigraphic localization of gastrointestinal protein loss has been recently reported. A noninvasive method for the localization of protein loss in the gut using Tc-99m labeled albumin seems encouraging and is described here. In six patients studied for protein-losing enteropathy, scintigraphic results of four were positive.

CT evaluation of active adrenal histoplasmosis

We describe three patients with puzzling systemic illnesses in whom computed tomography (CT) led to the diagnosis of active adrenal histoplasmosis. CT was performed in two patients because of gastrointestinal symptoms and weight loss and in the third because of fever developing 2 years after an apparent cure of histoplasmosis. All three patients had adrenal enlargement on CT with features of granulomatous adrenal disease in two. Hormone assays performed after CT supported the diagnosis of adrenal insufficiency and fine-needle adrenal aspiration biopsy with special stains of the aspirates showed histoplasma organisms in all three patients. The combination of adrenal enlargement on CT and laboratory findings of adrenal insufficiency should suggest the diagnosis of histoplasmosis, especially in endemic areas.

Gastrointestinal protein loss in children recovering from burns

Qualitative gastrointestinal protein loss was evaluated in 10 children with second- and/or third-degree burns covering 10% or more of their body surface area (BSA) by using fecal α-1-antitrypsin (FA-1-AT) as a marker. Patients were subdivided according to the extent of the burned area: group I (5 patients) had burns covering less than 20% of BSA; group II (5 patients) had burns covering more than 20% of BSA (mean, 37.2% = 24.9%). Results were compared with those of 12 healthy normal controls. Mean maximal FA-1-AT excretion in group II patients (2.71 ± 1.35 mg/g) was significantly greater than that found in group I children (0.43 ± 0.26 mg/g; P = .006) and in the controls (0.62 ± 0.25 mg/g; P = .004). The mean maximal FA-1-AT excretion positively correlated to the percent of BSA covered with burns ( r = 0.83). Although the mean septic score (SS) of group I patients (7 ± 2.9) was significantly greater than that calculated for group II children (3 ± 2.45; P = .047), only 2 patients in group II had positive microbiological caltures. Patients in both groups had received more than the recommended enteral caloric and protein allowance during the 96 hours prior to the maximal FA-1-AT measurements. Within this range, no correlation was found between the amount of FA-1-AT and the number of calories per kilogram protein consumed. By using the method of FA-1-AT quantification, this study provides the first report on postburn intestinal protein loss in children.

Hypokalemic Adrenal Crisis in a Patient With AIDS

Electrolyte disorders have been reported frequently in patients with AIDS. Adrenal insufficiency has been associated with hyponatremia in this group of patients. We have presented the case of a patient with AIDS whose early course was complicated by hyponatremia, hypoglycemia, and hyperkalemia. Shortly thereafter, hypokalemia developed due to gastrointestinal potassium losses from diarrhea. Although cosyntropin stimulation testing later confirmed the diagnosis of adrenal insufficiency, it was not considered because of coexistent hypokalemia. Diarrhea in patients with AIDS and diminished adrenal reserve may invalidate hypokalemia as an exclusion criterion for the diagnosis of adrenal crisis.

Metabolism of dietary sulphate: absorption and excretion in humans.

Dietary sulphate may affect colonic pathophysiology because sulphate availability determines in part the activity of sulphate reducing bacteria in the bowel. The main product of sulphate reducing bacterial oxidative metabolism, hydrogen sulphide, is potentially toxic. Although it is generally believed that the sulphate ion is poorly absorbed, there are no available data on how much sulphate reaches the colon nor on the relative contributions from diet and endogenous sources. To resolve these questions, balance studies were performed on six healthy ileostomists and three normal subjects chosen because they did not have detectable sulphate reducing bacteria in their faeces. The subjects were fed diets which varied in sulphate content from 1.6-16.6 mmol/day. Sulphate was measured in diets, faeces (ileal effluent in ileostomists), and urine by anion exchange chromatography with conductivity detection. Overall there was net absorption of dietary sulphate, with the absorptive capacity of the gastrointestinal tract plateauing at 5 mmol/day in the ileostomists and exceeding 16 mmol/day in the normal subjects. Endogenous secretion of sulphate in the upper gastrointestinal tract was from 0.96-2.6 mmol/day. The dietary contribution to the colonic sulphate pool ranged up to 9 mmol/day, there being linear identity between diet and upper gastrointestinal losses for intakes above 7 mmol/day. Faecal losses of sulphate were trivial (less than 0.5 mmol/day) in the normal subjects at all doses. It is concluded that diet and intestinal absorption are the principal factors affecting the amounts of sulphate reaching the colon. Endogenous secretion of sulphate by colonic mucosa may also be important in determining amounts of sulphate in the colon.

The mechanisms and prevention of intravascular fluid loss after occlusion of the supraceliac aorta in dogs

Mechanisms of intravascular fluid depletion after temporary occlusion of the supraceliac aorta were investigated in a canine model. During ischemia and reperfusion, hemodynamic parameters, superior mesenteric artery flow, intestinal mucosal perfusion, and mucosal permeability were monitored. After 12 hours of reperfusion, the volumes of intravenous electrolyte fluid required to maintain hemodynamic stability and fluid lost into the gastrointestinal tract and peritoneal cavity were measured. The distribution of total body water was analyzed by use of radionuclide dilution techniques. Group A animals underwent laparotomy only, group B had the supraceliac aorta occluded for 45 minutes, group C had superoxide dismutase administered after 45 minutes of aortic occlusion, and group D animals were exposed to mild hypothermia during a similar ischemia and reperfusion period. No significant difference was found in mean superior mesenteric artery flow or mucosal perfusion during ischemia among groups B, C, and D. During reperfusion superior mesenteric artery flow returned to values similar to control in all groups. Aortic occlusion increased mucosal permeability most significantly in group B (p < 0.01). Mean intravenous fluid requirements (ml/mg) were the following: group A, 80 ± 5; group B, 201 ± 9 (p < 0.01); group C, 116 ± 7 (p < 0.05); group D, 245 ± 24 (p < 0.05). Mean gastrointestinal fluid loss was highest in the hypothermic group and smallest if superoxide dismutase was given. Mean intracellular fluid volume was increased in groups B and D compared with group A (p < 0.01). We conclude that aortic occlusion and reperfusion results in increased requirement for intravenous fluid as fluid shifts into the intracellular space and is lost into the gastrointestinal tract. These fluid shifts are increased by hypothermia but can be minimized by superoxide dismutase.