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Biomedical subjects

D R Strombeck

Publications and source records attributed to D R Strombeck.

At least 37 records · Page 2Linked to original sources
PubMed1984

Effects of catecholamines and ammonia on plasma and brain amino acids in dogs.

Investigations were made on the effects of catecholamine (Cat) infusions with and without ammonia (NH3) on plasma and brain amino acids (AA) and brain neurotransmitters in dogs. Groups of four dogs were infused for 5 h with epinephrine (E), epinephrine + norepinephrine (E + NE), epinephrine + norepinephrine with NH3 during h 4 and 5 (E + NE + NH3), epinephrine + norepinephrine + tryptophan with NH3 during h 4 and 5 (T + E + NE + NH3), or saline (C). Cat decreased (P less than 0.05) plasma Gly, Thr, Lys, Pro, Val, Ser, Arg, Leu, Trp, Phe, Asn, Tyr, Met, Ile, Cit, and Asp. The decreases at h 3 for all were to a mean of 45% of 0 h and were associated with no changes in plasma insulin or glucagon. Cat increased plasma Tau and Orn. Of the most abundant brain AA (82% of total), E + NE + NH3 had no effect (GABA, Asp, Gly, Ala, p-ethanolamine) or increased (Glu, Gln, Tau) brain levels. These AA were unchanged by Cat alone. Of the remaining brain AA, most were decreased by Cat (7 of 16, P less than 0.05) and E + NE + NH3 increased brain Trp but had no effect on brain serotonin, 5-hydroxyindoleacetic acid, or NE. Cat changed plasma AA in a way similar to changes produced by NH3 infusion and seen with hepatic insufficiency due to portacaval shunts and nitrosamine-induced pathology. Cat reduced brain AA levels, and this was partially restored by NH3.

Amino Acids↗
PubMed1984

Model of chronic pancreatitis in the dog.

A model of chronic pancreatitis was developed and characterized in the dog. Pancreatitis was produced by infusion of oleic acid through a cannula in the accessory pancreatic duct. Biochemical changes included early and marked increases in serum amylase and lipase activities which returned to base line within 3 weeks, at which time the dogs were clinically normal. In dogs euthanatized within 2 weeks, pathologic changes included massive necrosis and hemorrhage, cystic spaces filled with fluid, and abscesses. Histologic features revealed acute exudative pancreatitis with pancreatic atrophy and fibrosis. In dogs killed between weeks 3 to 12, changes included: marked atrophy with remaining acini surrounded by remnants consisting of collapsed stroma, blood vessels, and pancreatic ducts; marked coarse fibrosis with scattered inflammatory cells and occasional acinar tissue; and large irregular pseudocysts.

Animals↗
PubMed1983

Plasma amino acid, glucagon, and insulin concentrations in dogs with nitrosamine-induced hepatic disease.

Plasma amino acids, glucagon, and insulin concentrations were determined once a week in dogs that developed acute hepatic necrosis and chronic hepatic insufficiency after treatment with dimethylnitrosamine. During the acute phase, plasma concentrations of most amino acids increased, with the changes usually correlating with increased glucagon values. Insulin correlated with changes in 10 of 21 amino acids, but the latter were not the most abundant nor the branched-chain amino acids. During the chronic phase, plasma phenylalanine tyrosine, and methionine concentrations remained increased throughout the study. Plasma values of these amino acids did not correlate with plasma concentrations of either glucagon or insulin. The values of the most abundant amino acids were less than base-line levels during the chronic phase, and 9 of 10 of these correlated positively with glucagon concentrations, but not insulin. Only proline correlated positively with insulin. Isoleucine and valine showed a negative correlation with insulin. The low concentrations of the nonaromatic amino acids increased during the time from the early to late chronic phase, during which time plasma glucagon increased and insulin remained unchanged. This study shows that a significant positive correlation existed between glucagon and the most abundant plasma amino acids during the chronic phase of hepatic insufficiency, at which time most plasma amino acid concentrations were returning toward base line. Increased glucagon values did not correlate with any evidence for deterioration of hepatic function.

Amino Acids↗
PubMed1982

Evaluation of 60-minute blood p-aminobenzoic acid concentration in pancreatic function testing of dogs.

For evaluation of pancreatic function testing, a peptide that releases p-aminobenzoic acid (PABA) on digestion by chymotrypsin was given to clinically normal dogs and to dogs with unexplained diarrhea. Blood concentration of PABA and percentage of PABA excretion in the urine at 6 hours after oral administration were determined. One-hour blood values did not reflect pancreatic exocrine secretion as well as did the 6-hour urinary excretion values.

4-Aminobenzoic Acid↗
PubMed1982

Evaluation of treatment for pancreatic exocrine insufficiency in dogs with ligated pancreatic ducts.

Clinical evaluations and measurements of maldigestion and malabsorption were made in dogs before and after ligation of pancreatic ducts. Fecal wet and dry weights were 300% greater after duct ligation. Fecal fat excretion of dietary intake increased from 9% to 84%. An indirect test of pancreatic function revealed a disappearance of intestinal chymotrypsin activity. All values tested improved during replacement with 5 ml of enzyme powder/day. Little additional improvement was observed after doubling or quadrupling this dose. Little or no additional improvement was seen with the following additions to enzymes: 30-minute preincubation of enzymes with food, antacids, cimetidine (except high dose), neomycin, or bile acids. Enzymes in uncoated tablets were less effective, unless the tablets were crushed.

Animals↗
PubMed1981

Effects of an anticholinergic and a corticosteroid on acute pancreatitis in experimental dogs.

In a model developed to study acute pancreatitis in the dog, the disease process was comparable with the spontaneously occurring disease. Infusion of oleic acid into the accessory pancreatic duct induced, grossly and microscopically, acute hemorrhagic pancreatitis with pancreatic atrophy, fibrosis, fat necrosis, and edema. Clinical changes included persistent fever and tachycardia in all dogs and abdominal pain, vomiting, and diarrhea in most. Serum amylase and lipase activities increased markedly as did activities of alkaline phosphatase, aspartate aminotransferase, and alanine aminotransferase. Hematologic alterations included hemoconcentration (despite intensive fluid therapy) and leukocytosis due primarily to neutrophilia and monocytosis. Neither corticosteroid nor anticholinergic therapy begun 24 to 32 hours after oleic acid infusion altered the course of the disease. Dogs survived 8 days and appeared clinically normal when the study was terminated.

Amylases↗
PubMed1981

Serum amylase and lipase activities in the diagnosis of pancreatitis in dogs.

To determine the usefulness of information provided by measurement of serum amylase activity in the evaluation of dogs for pancreatitis, the relationship of amylase activity to lipase activity in 713 paired serum samples was investigated by statistical analysis. Little change in mean amylase concentration was found until lipase values exceeded 800 U/L. The ranges of amylase activity (mean +/- 2 SD) were essentially the same for dogs with no pancreatitis (0 to 100 U of lipase activity/L) as for dogs with a high probability for the disease (700 to 799 U of lipase activity/L), 0 to 4,029 U/L and 857 to 4,869 U/L, respectively. Pathologic findings from biopsy and necropsy reports from 92 dogs for which serum lipase determinations were done indicated that serum lipase increased not only with pancreatitis, but also with other medical problems, such as renal and hepatic disease. It was concluded that determination of serum amylase activity without knowledge of serum lipase activity was of little value to diagnose pancreatitis. High amylase activity was not specific for pancreatitis and low amylase activity could not rule out the disease. The results of this study also showed that low serum lipase values almost always eliminated the possibility of pancreatitis and that high values were often, but not always, diagnostic for pancreatitis.

Amylases↗
PubMed1981

Effects of ammonia infusion on plasma glucagon, insulin, and amino acids in intact, pancreatectomized, and adrenalectomized dogs.

Ammonium salts were infused in intact, pancreatectomized, and adrenalectomized dogs to produce coma-inducing amounts of plasma ammonia. Changes in intact dogs included hyperglycemia, hyperglucagonemia, hyperinsulinemia, and decreases in plasma concentrations of glutamine, alanine, threonine, glycine, lysine, valine, proline, serine, arginine, leucine, isoleucine, and methionine. Urinary excretion of catecholamines increased more than 20-fold, whereas plasma hydrocortisone concentrations were essentially unchanged. In pancreatectomized dogs, ammonia infusions caused hyperglycemia, a mild hyperglucagonemia, and no changes in plasma amino acid concentrations, other than a decrease in alanine and an increase in taurine. In adrenalectomized dogs, ammonia infusion resulted in normoglycemia, hyperglucagonemia (comparable with that seen in intact dogs), hyperinsulinemia (2 to 3 times that seen in intact dogs), and decreased plasma concentrations of alanine, isoleucine, leucine, and valine. Finally, propranolol administration did not affect ammonia-induced glucagon and insulin release. The endocrine portion of the pancreas appears to mediate the major effects of ammonia on plasma amino acid values. The effect of ammonia in stimulating glucagon release may occur by an alpha-adrenergic pathway or by direct stimulation of pancreatic islet cells.

Adrenal Glands↗
PubMed1981

Biochemical and coagulation changes in a canine model of acute necrotizing pancreatitis.

Acute necrotizing (hemorrhagic) pancreatitis was induced in 12 dogs by infusing oleic acid into their pancreatic ducts. There were decreases in blood pH, complement, antithrombin III, blood platelets, 24- and 48-hour plasminogen, and 24-hour haptoglobin and modest decreases in serum albumin. There were increases in fibrinogen, 48- to 120-hour haptoglobin, and 96-hour and 120-hour plasminogen and prolongations of prothrombin and activated partial thromboplastin times. The latter 2 changes together with decreases in antithrombin III, platelet numbers, and complement were indicative of consumption coagulopathy. A clinically innocuous but statistically significant decrease in serum total and ionized calcium despite significant acidosis was noted. This indicates that serum total and ionized calcium is helpful in making the diagnosis of acute necrotizing pancreatitis. Methemalbuminemia of 6 mg/dl at 24 hours and 7 mg/dl at 48 hours indicates that methemalbuminemia is a valuable diagnostic and prognostic finding in association with acute necrotizing pancreatitis.

Acute Disease↗
PubMed1978

Ammonia tolerance test in clinically normal dogs and in dogs with portosystemic shunts.

The oral ammonia tolerance test was investigated in 20 clinically normal dogs and in 6 dogs with naturally occurring portosystemic shunts. The dogs with portosystemic shunting had a marked rise in venous blood ammonia following the administration of ammonium chloride, as compared with the control dogs. Fasting venous blood ammonia content was not uniformly reliable in separating the dogs with portosystemic shunting from the clinically normal dogs.

Ammonia↗