Irreversible hemorrhagic shock in dogs: problem of onset of irreversibility

1961 ◽  
Vol 200 (2) ◽  
pp. 269-273 ◽  
Author(s):  
H. Hift ◽  
J. G. Strawitz
Keyword(s):  
Blood Glucose ◽  
Hemorrhagic Shock ◽  
Phase Contrast ◽  
Time Course ◽  
Blood Glucose Concentration ◽  
Morphological Changes ◽  
Liver Glycogen ◽  
Liver Mitochondria ◽  
Glycogen Level ◽  
Pattern Characteristic

Various time course studies were conducted in dogs subjected to a modified Wiggers procedure in an effort to ascertain whether the first reinfusion demand (the earliest overt sign of cardiovascular instability) could be associated with any other measurable biological change. The biphasic blood glucose pattern characteristic of irreversible hemorrhagic shock was thus shown generally to reach its hyperglycemic peak shortly before or at the time of first reinfusion, typically preceded by or coinciding with the earliest morphological changes in liver mitochondria (phase contrast, electron micrographs) and followed by progressive lengthening of the prothrombin time. The declining phase in blood glucose concentration was apparently not associated with any critical liver glycogen level or with any unusual rises in blood lactate, etc. The suggestion is therefore made that the sugar is used metabolically because of a liver shutdown induced by some extrahepatic agent(s) and that these events may, in turn, elicit malfunction elsewhere, e.g. the heart.

Hepatic handling of pancreatic glucagon and glucose during meals in rats

1984 ◽  
Vol 247 (5) ◽  
pp. R827-R832 ◽  
Author(s):  
W. Langhans ◽  
K. Pantel ◽  
W. Muller-Schell ◽  
E. Eggenberger ◽  
E. Scharrer
Keyword(s):  
Blood Glucose ◽  
Portal Vein ◽  
Hepatic Vein ◽  
Blood Glucose Concentration ◽  
Glucagon Secretion ◽  
Liver Glycogen ◽  
Pancreatic Glucagon ◽  
Hepatic Portal Vein ◽  
Hepatic Portal ◽  
Induced Changes

Prandial changes in plasma pancreatic glucagon, blood glucose, and liver glycogen levels were studied during the first meal after 12 h of food deprivation in rats. To determine whether pancreatic glucagon secretion is influenced by the composition of the diet, the experiments were performed in rats fed high-carbohydrate (HC), high-fat (HF), or high-protein (HP) diets. Plasma glucagon levels in the hepatic portal vein increased about 100% during meals in all feeding groups, whereas glucagon levels in the hepatic vein changed very little. Blood glucose concentration in the hepatic portal vein increased during meals in HC diet-fed rats but decreased in HF and in HP diet-fed rats. Blood glucose in the hepatic vein also increased in HC and HP diet-fed rats. In addition, liver glycogen content decreased during meals in HC and HP diet-fed rats and by 14 min after the meal in HF diet-fed rats. These results demonstrate that a considerable amount of the glucagon released during meals in HC, HF, and HP diet-fed rats remains in the liver. This is consistent with the hypothesis that the liver is important for the satiety effect of glucagon. The results also suggest that glucagon contributes to the meal-induced changes in hepatic carbohydrate metabolism observed in all groups.

THE EFFECTS OF HORMONES ON THE CARBOHYDRATE METABOLISM OF THE LAMPREY LAMPETRA FLUVIATILIS

1965 ◽  
Vol 31 (2) ◽  
pp. 127-137 ◽  
Author(s):  
P. J. BENTLEY ◽  
B. K. FOLLETT
Keyword(s):  
Blood Glucose ◽  
Blood Glucose Level ◽  
Carbohydrate Metabolism ◽  
Glucose Concentration ◽  
Skeletal Muscles ◽  
Blood Glucose Concentration ◽  
Liver Glycogen ◽  
Arginine Vasotocin ◽  
Glycogen Concentration ◽  
Muscle Glycogen Concentration

SUMMARY River lampreys regulated their blood glucose concentration when injected with glucose. Mammalian insulin decreased the blood glucose concentration in the lamprey while adrenaline, cortisol and arginine vasotocin increased it. Glucagon had no effect initially but after a delay of 4 hr. decreased the blood glucose level. Insulin and cortisol increased the liver glycogen concentration. Adrenaline decreased the muscle glycogen concentration; vasotocin increased it. Treatment with alloxan increased the blood glucose concentration. Fat and glycogen in the lamprey are stored mainly in the skeletal muscles and their histochemical distribution in muscle is described. The results are discussed in relation to the metabolism of the migrating lamprey and the evolution of the control of carbohydrate metabolism in vertebrates.

Irreversible hemorrhagic shock in dogs: structure and function of liver mitochondria

1961 ◽  
Vol 200 (2) ◽  
pp. 264-268 ◽  
Author(s):  
H. Hift ◽  
J. G. Strawitz
Keyword(s):  
Hemorrhagic Shock ◽  
Membrane Structure ◽  
Phase Contrast ◽  
Krebs Cycle ◽  
Liver Mitochondria ◽  
Structure And Function ◽  
Absorbing Material ◽  
Krebs Cycle Enzymes ◽  
And Function ◽  
Normal Controls

Paired experiments were conducted with dogs dying in irreversible hemorrhagic shock and with normal controls. Examined under the electron microscope the liver cells from the experimental dogs were found to contain enlarged mitochondria characterized by a swollen matrix, rather than an altered double-membrane structure. Swollen, abnormal particles were also observed under phase contrast in whole-tissue blendorates and purified mitochondrial suspensions derived from such livers. Simultaneously, slices and purified suspensions prepared from those livers yielded higher than normal oxygen uptakes but normal P/O ratios and the purified mitochondria were found to contain normal proportions but excessive amounts of proteinous, nitrogenous and UV-absorbing material. It is suggested that liver mitochondria adjust to the stress imposed by the prolonged oligemia and hypoxia by enlarging and acquiring an extra complement of Krebs' cycle enzymes. The liver may thus be in a state of potential hyperactivity at a time when the animal as a whole is succumbing to the effects of irreversible hemorrhagic shock.

Liver fructose 2,6-bisphosphate in rats running at different treadmill speeds

1988 ◽  
Vol 255 (1) ◽  
pp. R38-R41
Author(s):  
W. W. Winder ◽  
H. T. Yang ◽  
J. Arogyasami
Keyword(s):  
Blood Glucose ◽  
Time Course ◽  
Liver Glycogen ◽  
Work Rate ◽  
Rapid Decline ◽  
Cyclic Monophosphate ◽  
Significant Change ◽  
Rate Of Decline ◽  
All Speeds

To determine the effect of work rate on liver fructose 2,6-bisphosphate (fructose 2,6-P2), rats were run for 5 min on a treadmill up a 15% grade at 16, 21, 26, 31, and 36 m/min. The liver content of fructose 2,6-P2 decreased 25, 42, 50, 62, and 71% from resting values after 5 min of running at these work rates. The time course of the decline in liver fructose 2,6-P2 was also studied in rats run at 16 m/min for times ranging from 5 to 100 min, at 23 m/min for times ranging from 5 to 60 min, and at 31 m/min for times of 5, 10, and 20 min. The hepatic content of fructose 2,6-P2 declined significantly after 5 min in all three groups of rats. The rate of decline was greatest in rats run at 31 m/min. After 100 min of running, fructose 2,6-P2 in livers of rats running at 16 m/min declined to levels seen in rats run at 31 m/min for 20 min. Changes in fructose 2,6-P2 occurred before a detectable decline in liver glycogen and in the absence of any significant change in blood glucose. Liver adenosine 3',5'-cyclic monophosphate (cAMP) was elevated after 5 min of exercise in rats running at 23 and 31 m/min but not in rats running at 16 m/min. By the end of exercise, hepatic cAMP was elevated in rats running at all speeds. The rapid decline in fructose 2,6-P2 probably plays a role in decreasing hepatic glycolysis, thereby ensuring that glucose 6-phosphate derived from glycogenolysis is diverted to blood glucose.

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

1961 ◽  
Vol 200 (2) ◽  
pp. 261-263 ◽  
Author(s):  
J. G. Strawitz ◽  
H. Hift ◽  
A. Ehrhardt ◽  
D. W. Cline
Keyword(s):  
Blood Glucose ◽  
Hemorrhagic Shock ◽  
Survival Time ◽  
Recovery Period ◽  
Liver Glycogen ◽  
Mortality Rates ◽  
Blood Stream ◽  
Survival Times ◽  
Sugar Levels ◽  
Fasted Rats

Paired fed and fasted rats were subjected to the standard shock procedure consisting of a combination of tail bleeding and heart puncture with an intervening recovery period of 90 minutes. Mortality rates in the two groups were similar but the survival times were shortened in the fasted group. Following tail bleeding all animals mobilized glucose into the blood stream and developed severe hyperglycemia. In those individuals in either group which ultimately died, the blood sugar levels were further reduced following heart puncture; the rates of glucose loss were inversely proportional to survival time; the results were terminal hypoglycemias and near exhaustion of liver glycogen. In contrast, the survivors in either group, examined 4 hours after heart puncture, were found to be hyperglycemic and engaged in glycogen neogenesis. It is concluded that the ultimate death or survival of an animal in hemorrhagic shock is independent of its initial glucose reserves, but seems somehow to be related to its ability to maintain itself in a hyperglycemic state.

Some effects of fasting on rats fed a choline-deficient diet

1960 ◽  
Vol 198 (2) ◽  
pp. 371-374 ◽  
Author(s):  
E. Douglas Rees ◽  
William W. Winternitz ◽  
William F. Lattanzi
Keyword(s):  
Blood Glucose ◽  
Ketone Bodies ◽  
Blood Glucose Concentration ◽  
Liver Glycogen ◽  
Control Group ◽  
Deficient Diet ◽  
Hepatic Fat ◽  
Blood Ketone Bodies ◽  
Deficient Group

The blood ketone body concentrations of fasted and nonfasted rats fed a diet deficient in choline were determined and found to be similar to the concentrations obtained from a control group fed the same diet supplemented with choline. However, the animals on the choline-deficient diet had an 18–20% greater mean liver mass, and this could account for the failure to demonstrate the depressed level of blood ketone bodies which was anticipated on the basis of previous in vitro studies. Other possible explanations of this discrepancy are discussed. Despite a high hepatic fat content, the choline-deficient group had a normal concentration of liver glycogen. The nonfasting blood glucose concentration of the choline-deficient group (91.5 ± 5 mg %) was lower than that of the control group (102 ± 3 mg %). After 24 hours of fasting, the values were 52 ± 3 mg % and 61 ± 5 mg % for the choline-deficient and control group, respectively. The 72-hour fasting values were 43 ± 2 mg %, and 49 ± 2 mg %, respectively. Data showing the effect of diet composition on ketonemia, liver glycogen and blood glucose are presented and are in accord with previous studies.

scholarly journals Effects of fasting and refeeding on the metabolic functions of the turtle Kinosternon scorpioides (Linnaeus, 1766) raised in captivity

2013 ◽  
Vol 33 (8) ◽  
pp. 1041-1044 ◽  
Author(s):  
Antonia S. Oliveira ◽  
Cinthia G. Candioto ◽  
Débora M.S. Santos ◽  
José G. Pereira ◽  
Alana L. Sousa ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Food Deprivation ◽  
Muscle Glycogen ◽  
Blood Glucose Concentration ◽  
Liver Lipid ◽  
Liver Glycogen ◽  
In Captivity ◽  
Fasting And Refeeding ◽  
The One ◽  
Muscle Lipids

The metabolic responses of adult and young freshwater Kinosternon scorpioides turtles raised in captivity were evaluated. Two experiments were performed: a) blood metabolite changes caused by food deprivation, and b) liver and muscle glycogen and total lipid differences after fasting and refeeding. Blood glucose concentration of young animals was susceptible to food deprivation. In both groups this metabolite decreased after 30 days of fasting. Feeding for 15 days did not recover blood glucose. Total seric proteins were not affected by food deprivation. Fasting decreased blood urea nitrogen and the highest difference was found around 30 days. Uric acid increased in young animals after 60 days of fasting. Triacylglicerol decreased after 15 days of fasting and refeeding for 15 days recovered the pre-fasting levels. Free fatty acid plasma tended to increase around 15 days of fasting. Liver glycogen decreased at day 15 of fasting, being stable thereafter while muscle glycogen decreased at a slower rate. Total liver lipid stabilized after 30 days and then decreased 70% after 60 days of fasting. Muscle lipids remained stable throughout fasting. It could be concluded that fasting of Kinosternon scorpioides led to metabolic adaptations similar to the one reported from reptiles and fish.

Metabolic responses to exercise after fasting

1986 ◽  
Vol 61 (4) ◽  
pp. 1363-1368 ◽  
Author(s):  
G. L. Dohm ◽  
R. T. Beeker ◽  
R. G. Israel ◽  
E. B. Tapscott
Keyword(s):  
Blood Glucose ◽  
Blood Glucose Concentration ◽  
Human Subjects ◽  
Plasma Concentrations ◽  
Exercise Bout ◽  
Liver Glycogen ◽  
Glycogen Depletion ◽  
Fat Mobilization ◽  
Blood Glucose Homeostasis ◽  
Beta Hydroxybutyrate

Fasting before exercise increases fat utilization and lowers the rate of muscle glycogen depletion. Since a 24-h fast also depletes liver glycogen, we were interested in blood glucose homeostasis during exercise after fasting. An experiment was conducted with human subjects to determine the effect of fasting on blood metabolite concentrations during exercise. Nine male subjects ran (70% maximum O2 consumption) two counterbalanced trials, once fed and once after a 23-h fast. Plasma glucose was elevated by exercise in the fasted trial but there was no difference between fed and fasted during exercise. Lactate was significantly higher (P less than 0.05) in fasted than fed throughout the exercise bout. Fat mobilization and utilization appeared to be greater in the fasted trial as evidenced by higher plasma concentrations of free fatty acids, glycerol, and beta-hydroxybutyrate as well as lower respiratory exchange ratio in the fasted trial during the first 30 min of exercise. These results demonstrate that in humans blood glucose concentration is maintained at normal levels during exercise after fasting despite the depletion of liver glycogen. Homeostasis is probably maintained as a result of increased gluconeogenesis and decreased utilization of glucose in the muscle as a result of lowered pyruvate dehydrogenase activity.

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