The Initial Blood Glucose Concentration in Patients with Isolated Traumatic Brain Injury

2006 ◽  
Vol 18 (4) ◽  
pp. 304-305
Author(s):  
B Wolcke ◽  
U Abu-Tair ◽  
S Schaefer ◽  
W Rommel ◽  
C Lott ◽  
...  
1997 ◽  
Vol 17 (1) ◽  
pp. 50-53 ◽  
Author(s):  
Robert Vink ◽  
Elke M. Golding ◽  
John P. Williams ◽  
Tracy K. McIntosh

Effects of blood glucose concentration on biochemical and neurologic outcome following lateral fluid percussion-induced traumatic injury of moderate severity (2.8 atm) in rats were studied using radioactive phosphorus (31P) magnetic resonance spectroscopy (MRS) and a battery of tests designed to evaluate posttraumatic neurologic motor function. Prior to injury, male Sprague-Dawley rats (n = 18) were randomly assigned to receive either dextrose, 2 ml 50% (wt/vol), zinc insulin (10 IU/kg) or no treatment, thus dividing the animals into hyperglycemic, hypoglycemic, and normoglycemic groups, respectively. Animals were then injured, monitored for 4 h by 31P MRS before being allowed to recover, and assessed for posttraumatic motor function. Following brain injury, there was no difference in brain intracellular pH between groups over the 4-h posttraumatic MRS monitoring period. Similarly, intracellular free magnesium, cytosolic phosphorylation potential, and neurologic outcome posttrauma were not significantly different between groups. We conclude that, unlike models of ischemia, blood glucose concentration may not be a significant factor affecting outcome in traumatic brain injury.


1970 ◽  
Vol 65 (3) ◽  
pp. 481-489
Author(s):  
F. A. László ◽  
I. Szijj ◽  
F. Durszt ◽  
K. Kovács

ABSTRACT The hypoglycaemic action of synthetic human 1,39-corticotrophin was determined in mice and its effectiveness compared with highly purified porcine corticotrophin. Synthetic human 1,39-corticotrophin (0.01 mg = 1.0 IU) and porcine corticotrophin (1.0 IU) induced a transient hypoglycaemia. After the administration of the porcine corticotrophin the decrease in the blood glucose concentration was somewhat more marked and prolonged. Adrenocortical activity was not necessary for the development of hypoglycaemia. In adrenalectomized mice, dexamethasone substitution by increasing the initial blood glucose content, made the effect more pronounced. Pretreatment with corticotrophin reduced the extent of the alloxan-induced transitory hyperglycaemia. On the other hand, it did not influence the high blood glucose values in manifest alloxan diabetic animals. It is possible that corticotrophin induces hypoglycaemia through insulin release. This is an extra-adrenal effect of corticotrophin as it is also observed in adrenalectomized mice.


2014 ◽  
Vol 307 (4) ◽  
pp. H587-H597 ◽  
Author(s):  
Mark W. Sims ◽  
James Winter ◽  
Sean Brennan ◽  
Robert I. Norman ◽  
G. André Ng ◽  
...  

While it is well established that mortality risk after myocardial infarction (MI) increases in proportion to blood glucose concentration at the time of admission, it is unclear whether there is a direct, causal relationship. We investigated potential mechanisms by which increased blood glucose may exert cardiotoxicity. Using a Wistar rat or guinea-pig isolated cardiomyocyte model, we investigated the effects on cardiomyocyte function and electrical stability of alterations in extracellular glucose concentration. Contractile function studies using electric field stimulation (EFS), patch-clamp recording, and Ca2+ imaging were used to determine the effects of increased extracellular glucose concentration on cardiomyocyte function. Increasing glucose from 5 to 20 mM caused prolongation of the action potential and increased both basal Ca2+ and variability of the Ca2+ transient amplitude. Elevated extracellular glucose concentration also attenuated the protection afforded by ischemic preconditioning (IPC), as assessed using a simulated ischemia and reperfusion model. Inhibition of PKCα and β, using Gö6976 or specific inhibitor peptides, attenuated the detrimental effects of glucose and restored the cardioprotected phenotype to IPC cells. Increased glucose concentration did not attenuate the cardioprotective role of PKCε, but rather activation of PKCα and β masked its beneficial effect. Elevated extracellular glucose concentration exerts acute cardiotoxicity mediated via PKCα and β. Inhibition of these PKC isoenzymes abolishes the cardiotoxic effects and restores IPC-mediated cardioprotection. These data support a direct link between hyperglycemia and adverse outcome after MI. Cardiac-specific PKCα and β inhibition may be of clinical benefit in this setting.


2014 ◽  
Vol 19 (3) ◽  
pp. 527-533 ◽  
Author(s):  
Miho Senda ◽  
Susumu Ogawa ◽  
Kazuhiro Nako ◽  
Masashi Okamura ◽  
Takuya Sakamoto ◽  
...  

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