Irreversible hemorrhagic shock in rats: changes in blood glucose and liver glycogen

Strawitz, Joseph G.; Hift, Helen; Ehrhardt, Anton F.; Cline, Dominique

doi:10.1152/ajplegacy.1961.200.2.261

Cited by 30 publications

(13 citation statements)

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“…Since there was a difference in the response in rats with similar initial glycogen levels, it can be concluded that the level of glycogen had no effect on the degree of the response. These results correlated with observations of Strawitz et al (1961), who stated that the ultimate death or survival of rats subjected to hemorrhagic shock did not depend on the initial glycogen present but was related to the ability of the rat to maintain the hyperglycemia.…”

Section: Discussionsupporting

confidence: 90%

“…To control for circadian variation in glycogen, many experiments utilized the control fed or starved rat model. Controlled feeding produces a prolonged hyperglycemia and hyperinsulinemia (Hammad et al, 1982), and rats that are starved do not survive shockrelated insults as well as fed rats (Strawitz et al, 1961;Dimlich, unpublished observation). Therefore, it was decided to allow each rat free access to food and water until the time of anesthesia.…”

Section: Discussionmentioning

confidence: 97%

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Effects of compound 48/80 on hepatic glycogen and glucose‐6‐phosphatase early in the diurnal cycle of the rat

Dimlich

Cardell

1984

Am. J. Anat.

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The amount and distribution of glycogen as well as the activity of glucose-6-phosphatase (G-6-Pase) in the livers of rats were analyzed by biochemical and/or histochemical techniques. During the first 5 hr of the light cycle, livers of rats were sampled prior to and 30 min following an injection of compound 48/80 or Ringer's solution. Glycogen decreased significantly in response to sampling; however, treatment with compound 48/80 provoked an additional significant decrease in hepatic glycogen. These differences occurred irrespective of the time during the 5 hr that this was studied. The livers of the majority of the rats treated with compound 48/80 displayed a periportal distribution of glycogen, while those treated with Ringer's showed a more uniform pattern. Hepatic G-6-Pase activity was unchanged in either the Ringer's or compound 48/80 treated rats. These results indicated that (1) the significant glycogenolytic response occurs independently of the amount of glycogen present, (2) G-6-Pase activity is not affected within 30 min following the stimulation of glycogenolysis, (3) variation in glycogen patterns during depletion depends on the nature of the stimulus and/or degree of response, and (4) the amount of glycogen available for release is limited.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 97%

Effects of compound 48/80 on hepatic glycogen and glucose‐6‐phosphatase early in the diurnal cycle of the rat

Dimlich

Cardell

1984

Am. J. Anat.

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“…In rats surviving drug treatment, blood glucose continued to increase over a 30 min or longer period, while in those rats which (26,27), differences in survival might be related to the maintenance of hyperglycemia.…”

Section: Discussionmentioning

confidence: 96%

“…Strawitz et al (26) have correlated hyperglycemia with survival in rats subjected to hemorrhagic shock. They reporLed that rats which died were not synthesizing glycogen.…”

Section: Discussionmentioning

confidence: 99%

Mast Cell Degranulation, Hepatic Glycogen Depletion, and Hyperglycemia in Compound 48/80 or Pilocarpine-Treated Rats

2007

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Blood glucose, hepatic glycogen, and mean carotid blood pressure were determined in anesthetized Sprague-Dawley rats receiving an i.v. infusion of Compound 48/80, pilocarpine, or Ringer's solution as a control. Histochemical determinations of the integrity and number of hepatic mast cells and hepatic glycogen content also were performed at the light microscopic level, and the results compared to those from rats whose livers were treated topically with each of these compounds. Compound 48/80 produced a marked decrease in mean carotid blood pressure, while pilocarpine produced a slight increase in this parameter. Injection of either Compound 48/80 or pilocarpine provoked an increase in blood glucose and a decrease in hepatic glycogen as well as in the number of hepatic mast cells. Infusion produced no change in glycogen within cardiac or skeletal muscle. The application of Compound 48/80 or pilocarpine to the surface of the liver evoked no alteration in the histochemical appearance of hepatic glycogen. However, the topical application of these substances elicited a significant decrease in the number of Falck-Hillarp-positive hepatic mast cells. Blood glucose was higher in rats that survived 30 min or more after injection of either compound. However, glucose levels were significantly higher in rats that survived 30 min or longer following Compound 48/80 infusion than in those surviving pilocarpine treatment. These results provide evidence that the i.v. injection of Compound 48/80 or pilocarpine causes: (a) hyperglycemia; (b) depletion of hepatic glycogen, and (c) a concomitant decrease in the number of Falck-Hillarppositive mast cells. The degree of hyperglycemia appeared to correlate with the length of survival of the rats and to be independent of the hyper-or hypotensive effects elicited by either chemical.A recent study of mast cells, and their role in hepatic microvascular regulatory mechanisms, revealed that i.v. and topical administration of Compound 48/80 or pilocarpine evokes mast cell degranulation and a decrease in blood flow through the liver of the rat (1-3). Compound 48/80 also was found histochemically to provoke a decrease in hepatic glycogen content following i.v. administration. Rat mast cells contain histamine, serotonin, and heparin (4-8). Of these constituents, serotonin has been reported to produce glycogenolysis and hyperglycemia when infused into rat liver (9). The present study was designed as part of investigations to test the hypothesis that Compound 48/80 or pilocarpine-induced degranulation of hepatic mast cells causes hyperglycemia and depletion of hepatic glycogen. Blood glucose was Received March 16, 1981; accepted February 3,1982. However, since the glycolytic response elicited by Compound 48/80 and pilocarpine-induced degranulation mimicked that evoked by serotonin (9), it is hypothesized that the hyperglycemia and glycogenolysis are mediated by neuroendocrine mechanisms which are related to the degranulation of extrahepatic mast cells. MATERIALS AND METHODS ANIMALS A N D PHARMAC...

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“…The signs of damaged glycid metabolism include Ihe lowering of gly cogen reserves in the liver and muscles (6, 8, i), 10), the heightening of the blood sugar level with a gradual lowering afterwards (4,15,17), the higher level of lactic and pyruvic acid in the blood (1,4,5,14,22) and the lower glycolytic activity of the blood (20).Factors which cause these changes are not exactly defined. Therefore we estimated in this work changes in the utilization of glucose by the red blood cells and tried to find out Ihe cause of these changes.…”

mentioning

confidence: 99%

The Influence of Acidosis on the Utilization of Glucose by the Red Blood Cells in Shock

Triner¹,

Kypson²,

Mráz³

et al. 1964

Pharmacology

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Irreversible hemorrhagic shock in rats: changes in blood glucose and liver glycogen

Cited by 30 publications

References 0 publications

Effects of compound 48/80 on hepatic glycogen and glucose‐6‐phosphatase early in the diurnal cycle of the rat

Effects of compound 48/80 on hepatic glycogen and glucose‐6‐phosphatase early in the diurnal cycle of the rat

Mast Cell Degranulation, Hepatic Glycogen Depletion, and Hyperglycemia in Compound 48/80 or Pilocarpine-Treated Rats

The Influence of Acidosis on the Utilization of Glucose by the Red Blood Cells in Shock

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