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W Schumer

Publications and source records attributed to W Schumer.

At least 55 records · Page 3Linked to original sources
PubMed1981

Glucocorticoid effect on glycolytic intermediates in septic rat heart.

Glycolytic intermediates in rat liver show similar changes in both endotoxic and peritonitis shock models suggesting a common etiology. To determine if this parallelism exists for other organs, adult rat hearts were analyzed 5 hours after E. coli endotoxin injection (2 mg/100 gm rat weight) or after sepsis produced by cecal incision. Tissue obtained by freeze-clamp biopsy was deproteinized and the metabolites were enzymatically assayed. Glucocorticoids were injected IV: 1 mg dexamethasone sodium phosphate (DMS) and 3 mg methylprednisolone sodium succinate (MPS) per 100 gm rat weight at time of operation. Glucose-6-phosphate (G6P) and fructose-6-phosphate (F6P) in septic hearts (N = 10) declined 36% and 37% from sham-operated control values (N = 11) of 640 nmole and 136 nmole per gm wet tissue. This finding is consistent with accelerated glycolysis. No changes of other metabolites indicative of severe hypoxic conditions were noted. A 2.5-fold increase in lactate was observed. This may reflect a shift to anaerobiosis in peripheral muscle and greater extraction by heart. Confirming earlier endotoxin rat heart data, glucocorticoids did not prevent decreases in G6P and F6P in septic hearts which declined 37% and 36% below sham controls (N = 10 for pooled glucocorticoid data). Hexose monophosphates in sham animals treated with GC alone were also found to be lowered. Glucocorticoids were synergistic with endotoxin in lowering beta-hydroxybutyrate in heart samples. It is concluded that endotoxin and sepsis produce identical responses on myocardial carbohydrate metabolites and that glucocorticoids do not counter these effects, which reflects the lack of gluconeogenic potential in this organ.

Animals↗
PubMed1981

Glucocorticoid action on rat hepatic glycolytic intermediates during experimental peritonitis.

Previous work demonstrated that glucose-6-phosphate (G6P) and fructose-6-phosphate (F6P) levels declined early in endotoxemic and septic livers. Since glucocorticoids are known to support hepatic gluconeogenesis in endotoxemia, these agents were tested in a peritonitis model produced by cecal incision in fasted adult male rats. Dexamethasone sodium phosphate (DMS) and methylprednisolone sodium succinate (MPS) were given in doses of 1 mg and 3 mg, respectively, per 100 gm rat weight at time of incision. Freeze-clamp biopsy samples obtained at 5 hr were enzymatically assayed. G6P and F6P in sepsis (N = 12) decreased 50% and 36%, respectively, below sham-operated control values (N = 15) of 236 and 61 nmole/gm wet tissue. The decrease with DMS was 20% and 16% and with MPS was 22% and 23%, showing partial restoration to normal levels. Phosphoenolpyruvate (PEP) did not decline in the moderate, non-terminal stage of peritonitis when compared to the control value (N = 19) of 209 nmole/gm. Treatment with glucocorticoids raised PEP to supernormal levels: DMS (N = 19) a 63% elevation, MPS (N = 12) a 51% elevation above controls in peritonitis rats. The glucocorticoid effect was similar in both rapid endotoxic and the slow peritonitis shock models. It is concluded that hexose monophosphate (HMP) increase is secondary to the support of PEP synthesis with glucocorticoid treatment. Changes in sham-operated control rat livers treated with glucocorticoids did not reach statistical significance.

Animals↗
PubMed1980

Glycolytic intermediates in rat heart after endotoxin treatment.

Glycolytic intermediates were determined in rat hearts five hours after an LD50 Escherichia coli endotoxin injection and glucose-6-phosphate (G6P) and fructose-6-phosphate (F6P) were decreased by 40% to 45% relative to control hearts. Levels of other intermediates which alter in severe hypoxia were unchanged. Adenosine triphosphate (ATP) and diphosphate (ADP) remained constant while glycogen was almost 50% depleted. A 30% fall in beta-hydroxybutyrate indicated that fatty acid utilization was decreased. The data were consistent with accelerated glycolysis. Pretreatment with the positive inotropic cardiac glycoside, ouabain, failed to maintain glycolytic intermediates in endotoxified heart at control levels. An identical fall in hexose monophosphates previously observed in rat livers may indicate that endotoxin has a similar action on enzymes regulating carbohydrate metabolism in different organs.

Animals↗
PubMed1980

Endotoxin role in peritonitis septic shock in rats.

We attempted to clarify the role of endotoxin in septic shock by supporting the concept that endotoxin produces hemodynamic and metabolic alterations in a peritonitis septic shock model (PSM). In the control group I, each rat was sham-operated. In group II, each rat was etherized, subjected to laparotomy, and the appendix was resected, leaving a rent at the base of the cecum for stool to enter the peritoneum. In group III, each rat was injected intraperitoneally with a 4 ml suspension of its own feces containing equal amounts of bacteria as measured by colony count. In all groups, blood pressure, plasma glucose and lactate, as well as endotoxin, were measured hourly via polyethylene catheters in the right femoral arteries. In parallel studies, liver glycolytic intermediates were measured at five hours via freeze-clamp biopsies and compared with measurements determined in an endotoxic shock model in rats (ESM). The results showed similar glucoeogenic inhibitions in both PSM and ESM, the liver anti-gluconeogenic effect in PSM probably being produced by endotoxin.

Animals↗
PubMed1980

A time study of hepatic glycolytic intermediates in endotoxemic and septic rats and mice.

A time study was conducted on three key glycolytic intermediates in endotoxemic rat liver to determine which metabolite showed the earliest concentration changes. Glucose-6-phosphate (G6P) was found to be significantly decreased one hour after IV injection of endotoxin, whereas phosphoenolpyruvate (PEP) and fructose-1,6-diphosphate (FDP) were unaltered until three hours. In rat peritonitis produced by cecal incision, liver biopsy at five hours again revealed that only G6P levels were significantly influenced by the septic challenge. In a similar murine peritonitis model, which permitted longer survival times, analysis of liver samples at 12 and 18 hours supported the conclusion that G6P was the metabolite that responded first or most consistently to endotoxin and sepsis. Later changes in FDP and PEP appear to be secondary events. It is postulated that endotoxin may have a direct or indirect action on G6P regulating enzymes. Since rational therapy for septic shock must combat early changes, it would seem that measures that restore G6P levels might prevent the disturbed carbohydrate metabolism that characterizes late and severe sepsis.

Animals↗
PubMed1979

Septic shock.

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Emergencies↗
PubMed1979

Hypovolemic shock.

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Acid-Base Imbalance↗
PubMed1979

Phenothiazine effect on gastrointestinal tract function.

Clinical evidence indicates that phenothiazines, specifically chlorpromazine (CPZ), used extensively in the treatment of patients with mental and/or neurologic disorders produce an ileus characterized by pseudoobstruction with an extended barium transit time of eight to ten days. Postoperatively, these patients have a protracted ileus, lasting from ten to fourteen days. In our present study we investigated the mechanism of action by which phenothiazines block gastrointestinal tract function as well as the possible reversal of this effect by pharmacologic agents. Guinea pigs were injected intraperitoneally with CPZ at a dose of 30 mg/kg/day for five to seventeen days. This caused deleterious effects in the gastrointestinal tract, such as cessation of peristalsis of small intestine and colon, and marked distension of the cecum. In vitro pharmacologic studies were performed on the electrically stimulated longitudinal muscle-myenteric plexus of the guinea pigs. We found that phenothiazines interfered with the neuromuscular mechanism of the intestine, as exemplified by a lack of response to electrical current stimulation. The effect was protracted, lasting at least 24 hours. These effects were reversed by the administration of the anticholinesterase, physostigmine (PGM), provided the block was less than 80 per cent. The paralytic ileus produced was similar to that found in man.

Animals↗
PubMed1978

Endotoxin-challenged monkeys and rats.

Studies in our laboratory with both the monkey and the rat showed that, after three hours of endotoxemia, there was a significant decrease in the number of circulating platelets, total hemolytic complement (CH 50 units), and blood serotonin (5-HT) levels. Administration of dexamethasone sodium phosphate in the clinical dose range at the time of endotoxin challenge significantly attenuated the decrease in blood 5-HT levels when compared to the untreated groups in both the monkey and the rat experiments. In the monkey, CH 50 units remained at a higher level when dexamethasone was administered; however, the difference between the treated and untreated groups was not statistically significant. The number of circulating white blood cells and platelets did not appear to be significantly altered by corticosteroid treatment. It is suggested that glucocorticoids may interfere with lipopolysaccharide-induced alterations in complement components or factors regulating hemostasis that influence platelet 5-HT release.

Animals↗
PubMed1976

Glucocorticoid effect on hepatic carbohydrate metabolism in the endotoxin-shocked monkey.

This study investigated the effect of glucocorticoid treatment on survival, on hepatic carbohydrate metabolism, and on levels of hepatic adenine nucleotides in the endotoxin-shocked monkey. Dexamethasone sodium phosphate (DMP) administered either at the time of endotoxin challenge or up to 90 minutes afterward significantly increased the survival rates. Endotoxin administered alone caused profound hypoglycemia and lactic-acidemia, which were alleviated by the administration of DMP. Endotoxin administered alone significantly decreased the hepatic levels of glucose-6-phosphate, fructose-6-phosphate, phospho-enolpyruvate, adenosine triphosphate, adenosine diphosphate, and glycogen; and it significantly increased the hepatic levels of fructose-1,6-diphosphate, lactate, and adenosine mono-phosphate. The administration of DMP at the time of endotoxin challenge maintained the levels of all these metabolites at or near the control levels.

Adenosine Diphosphate↗
PubMed1976

Steroids in the treatment of clinical septic shock.

A prospective (Part I) and a retrospective (Part II) study were used to determine the safety and efficacy of corticosteroids in the treatment of septic shock. In Part I, 172 consecutive patients in septic shock admitted over an 8-year period were treated with either steroid or saline: 43 received dexamethasone (DMP), 43 received methylprednisolone (MPS), and 86 received saline. The study was double-blind and randomized, and the three groups were compared for age, severity of shock, presence of underlying disease, and year of study. In the 86 saline-treated patients, the mortality rate was 38.4% (33/86); in the steroid-treated patients, it was 10.4% (9/86). With MPS the mortality rate was 11.6% (5/43), and with DMP it was 9.3% (4/43). Thus, overall mortality was significantly less in the steroid-treated group than in the control group. Further, there was no significant difference in mortality rate between the DMP- and the MPS-treated patients. In Part II, 328 patients were studied retrospectively. One-hundred sixty were treated without steroid, and 168 were treated with either DMP or MPS. Again, the two groups of patients were compared for severity of shock, underlying disease, age, and year of study. Mortality among patients treated without steroid was 42.5% (68/160) and among patients treated with steroid was 14% (24/168); there was no significant difference in mortality rate between DMP- and MPS-treated patients. In Parts I and II combined, complications occurred in 6% of steroid-treated patients with no significant difference between DMP- and MPS-treated groups.

Adrenal Cortex Hormones↗
PubMed1976

Anaerobic Infections.

Oxygen-sensitive anaerobic bacteria comprise the largest group of organisms among the human endogenous microflora. The oral cavity, the vagina and the colon are areas where the obligate anaerobes are predominant and can be isolated in high numbers. Clinical clues that indicate anaerobic sepsis include a putrid odor of the exudate and evidence of abscess, necrosis or associated gas formation. A Gram stain is highly valuable in early identification. Surgical drainage and appropriate antibiotics are essential.

Abdomen↗
PubMed1975

Glucocorticoid and antibiotic effect on experimental gram-negative bacteremic shock.

This study was designed to answer the three following questions: (1) Are glucocorticoids as protective in Gram-negative bacteremic shock as they are in endotoxic shock? (2) Is there any difference in efficacy between a bacteriostatic and a bactericidal antibiotic in bacteremic shock? (3) Does the combination of glucocorticoid with antibiotic potentiate the individual protective effects of both? Bacteremia was induced in male Sprague-Dawley rats by a single intravenous injection of viable Escherichia coli. The results showed that dexamethasone sodium phosphate alone afforded significant protection against Gram-negative bacteremic shock up to eight hours after challenge. The choice of a bactericidal vs a bacteriostatic antibiotic did not influence the survival rates in this study. The survival rate was maximal when dexamethasone was used with both ampicillin sodium and gentamicin sulfate.

Ampicillin↗