The intrinsic and interactive effects of RO 15-4513 and ethanol on locomotor activity, body temperature, and blood glucose concentration

Life Sciences ◽  
1989 ◽  
Vol 45 (16) ◽  
pp. 1467-1473 ◽  
Author(s):  
Angela L. Wood ◽  
Philip A. Healey ◽  
JoséA. Menéndez ◽  
Sarah L. Verne ◽  
Dale M. Atrens
1991 ◽  
Vol 69 (8) ◽  
pp. 1168-1177 ◽  
Author(s):  
David G. Penney ◽  
C. Clough Helfman ◽  
Joseph C. Dunbar Jr. ◽  
Lowell E. McCoy

Human and animal studies suggest a poorer outcome in the presence of abnormal blood glucose concentration during cerebral hypoxia–ischemia. It is unknown whether this is also the case in acute severe carbon monoxide poisoning. Using Levine-prepared rats, three groups were established and exposed to CO to answer this question: (1) hyperglycemics resulting from the administration of a 50% glucose solution, (2) hypoglycemics resulting from the administration of normal saline, and (3) untreated controls. The rats inhaled 2400 ppm CO for 90 min in the absence of anesthesia. Blood glucose was raised to a mean value of 402 mg/dL just prior to CO exposure in group 1. This resulted in an increased mortality rate (i.e., 54%), and during 4 h of room air recovery an impaired ability to regain body temperature, an increased plasma lactate dehydrogenase activity, and an increased neurologic deficit as compared with group 3. Hypoglycemia, which developed during CO exposure in group 2 (mean minimum glucose after 90 min, 44 mg/dL), resulted in an increased mortality rate (i.e., 46%), and during 4 h of room air recovery an impaired ability to regain body temperature and an increased neurologic deficit as compared with group 3. Blood glucose concentration in the rats in groups 2 and 3 that died during or shortly after CO exposure was significantly depressed relative to the survivors of those groups. Plasma insulin activity was elevated during CO exposure in group 1 as compared with group 3, but fell during recovery; insulin remained low throughout CO exposure and recovery in group 2. The results demonstrate the deleterious effects of both a very high and a very low blood glucose concentration during acute CO exposure.Key words: blood pressure, body temperature, carbon monoxide, glucose, heart rate, hematocrit, hyperglycemia, hypoglycemia, insulin, lactate dehydrogenase, mortality, morbidity, neurologic deficit.


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 ◽  
...  

Author(s):  
Li-Nong Ji ◽  
Li-Xin Guo ◽  
Li-Bin Liu

AbstractBlood glucose self-monitoring by individuals with diabetes is essential in controlling blood glucose levels. The International Organization for Standardization (ISO) introduced new standards for blood glucose monitoring systems (BGMS) in 2013 (ISO 15197: 2013). The CONTOUR PLUSThis study evaluated the accuracy and precision of CONTOUR PLUS BGMS in quantitative glucose testing of capillary and venous whole blood samples obtained from 363 patients at three different hospitals.Results of fingertip and venous blood glucose measurements by the CONTOUR PLUS system were compared with laboratory reference values to determine accuracy. Accuracy was 98.1% (96.06%–99.22%) for fingertip blood tests and 98.1% (96.02%–99.21%) for venous blood tests. Precision was evaluated across a wide range of blood glucose values (5.1–17.2 mmol/L), testing three blood samples repeatedly 15 times with the CONTOUR PLUS blood glucose meter using test strips from three lots. All within-lot results met ISO criteria (i.e., SD<0.42 mmol/L for blood glucose concentration <5.55 mmol/L; CV<7.5% for blood glucose concentration ≥5.55 mmol/L). Between-lot variations were 1.5% for low blood glucose concentration, 2.4% for normal and 3.4% for high.Accuracy of both fingertip and venous blood glucose measurements by the CONTOUR PLUS system was >95%, confirming that the system meets ISO 15197: 2013 requirements.


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