Effect of hemorrhagic shock, fasting, and corticosterone administration on leucine oxidation and incorporation into protein by skeletal muscle

This study examined the effects of a nonselective beta-blocking agent on whole-body leucine metabolism in humans. Five normal, healthy subjects (4 male, 1 female) underwent a 6-h primed, constant-rate infusion of L-[1–13C]leucine after 5 days of twice daily oral use of 80 mg propranolol and a placebo. Leucine turnover was determined by tracer dilution and leucine oxidation by 13C enrichment of the expired CO2. Propranolol decreased the total daily energy expenditure from 1,945 +/- 177.5 to 1,619 +/- 92.5 kcal/day (P less than 0.05). A fasting associated decrease in blood glucose and an attenuated rise in free fatty acids and ketones were observed during beta-blockade. Propranolol also increased plasma leucine concentrations (73.1 +/- 8.7 to 103.4 +/- 7.3 mumol/l; P less than 0.05) and leucine oxidation (13.2 +/- 1.2 to 17.1 +/- 1.3 mumol.kg-1.h-1; P less than 0.05), although leucine turnover was not significantly altered (100.5 +/- 7.3 vs. 126.0 +/- 12.3 mumol.kg-1.h-1). In addition, the urinary urea nitrogen-to-creatinine ratio was greater during propranolol administration (0.24 +/- 0.04 vs. 0.34 +/- 0.02 mol/g; P less than 0.05). These data suggest that the beta-adrenergic system plays a role in the modulation of whole-body leucine metabolism in humans. Whether these changes are the result of a direct effect on skeletal muscle or an indirect effect mediated by altering the fuel supply to skeletal muscle cannot be discriminated by the present study.

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Prostaglandin modulation of adrenergic vascular control during hemorrhagic shock

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1981.241.1.h85 ◽

1981 ◽

Vol 241 (1) ◽

pp. H85-H90 ◽

Cited By ~ 1

Author(s):

R. F. Bond ◽

C. H. Bond ◽

L. C. Peissner ◽

E. S. Manning

Keyword(s):

Skeletal Muscle ◽

Hemorrhagic Shock ◽

Vascular Control ◽

Synthesis Inhibitor ◽

Muscle Perfusion ◽

System A ◽

In Series ◽

Adrenergic Nervous System ◽

Prostaglandin Synthesis Inhibitor ◽

Denervated Muscles

This study was designed to evaluate 1) whether the initial compensatory skeletal muscle vascular constriction induced by hemorrhagic hypotension is primarily the result of increased adrenergic neural tone rather than circulating vasoconstrictor agents, and 2) whether the secondary skeletal muscle decompensatory vasodilation is caused by inhibitory action of prostaglandins on peripheral adrenergic nervous system. A constant-flow vascularly isolated double canine gracilis muscle preparation in which one muscle served as innervated control for the contralateral muscle was used. Dogs were subjected to standard stepwise hemorrhagic shock protocol. In series 1, perfusion pressures of control muscles were compared to denervated muscles with the result that innervated muscle perfusion pressures increased initially from 105 to 175 mmHg but subsequently fell significantly (P less than 0.05) to 147 mmHg. Only modest increases in perfusion pressures with no significant secondary fall were noted in denervated muscles. Series 2 compared innervated control perfusion pressures to pressures perfusing muscles pretreated with prostaglandin-synthesis inhibitor sodium meclofenamate (MCF). The MCF-treated muscle perfusion pressures rose to 260 mmHg where they remained without the secondary fall noted in control muscles. These data support the two hypotheses tested.

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MONITORING SKELETAL MUSCLE AND SUBCUTANEOUS TISSUE ACID-BASE STATUS AND OXYGENATION DURING HEMORRHAGIC SHOCK AND RESUSCITATION

Shock ◽

10.1097/01.shk.0000172364.89128.28 ◽

2005 ◽

Vol 24 (3) ◽

pp. 270-275 ◽

Cited By ~ 22

Author(s):

Julio A Clavijo-Alvarez ◽

Carrie A Sims ◽

Michael R Pinsky ◽

Juan Carlos Puyana

Keyword(s):

Skeletal Muscle ◽

Hemorrhagic Shock ◽

Subcutaneous Tissue ◽

Acid Base ◽

Acid Base Status

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Glucose uptake by diaphragms from rats subjected to hemorrhagic shock

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1964.206.2.317 ◽

1964 ◽

Vol 206 (2) ◽

pp. 317-320 ◽

Cited By ~ 14

Author(s):

William R. Drucker ◽

John C. DeKiewiet

Keyword(s):

Skeletal Muscle ◽

Hemorrhagic Shock ◽

Glucose Uptake ◽

Anaerobic Metabolism ◽

Lactate Production ◽

Bicarbonate Buffer ◽

Metabolic Alterations ◽

Shock Models ◽

The Media ◽

Intracellular Energy

The marked metabolic alterations that occur in hemorrhagic shock have been ascribed to tissue anoxia occasioned by hypovolemia. Other investigators, utilizing different shock models, have explained the initial metabolic changes as secondary to humoral changes. In skeletal muscle, anoxia is known to cause an increased glucose uptake, whereas epinephrine causes a decreased uptake. The present work was undertaken to explore some alterations in carbohydrate metabolism during hemorrhagic shock in rats, when both tissue anoxia and an altered humoral state are present. Hemidiaphragms from rats subjected to a standardized hemorrhagic shock procedure and from control rats were excised and incubated aerobically in bicarbonate buffer containing glucose. After 1 hr of incubation aliquots of the media were analyzed for glucose and lactate. The results demonstrated a significantly greater glucose uptake and lactate production by the diaphragms from the bled rats. The data suggest that, during hemorrhagic shock in rats, tissue anoxia leads to a predominance of anaerobic metabolism and a severe depletion of intracellular energy, resulting in an increased uptake of glucose in skeletal muscle despite the concomitant altered humoral state which ordinarily would inhibit glucose uptake.

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