We are analyzing https://link.springer.com/article/10.1186/s12933-017-0527-5.

Title:
Glycemia and the cardioprotective effects of insulin pre-conditioning in the isolated rat heart | Cardiovascular Diabetology
Description:
While acute hyperglycemia has been shown to mitigate the beneficial effects of ischemic preconditioning, its effect on insulin-induced preconditioning remains unclear. The study was designed to test the hypothesis that acute hyperglycemia diminishes the cardioprotective effects following a 20-min pre-ischemic pre-conditioning with insulin in the isolated rat heart using the Langendorff system. Forty hearts were assigned to receive modified Krebs–Henseleit (KH) buffer containing 0.5 U/L insulin and 100 mg/dL glucose (InsG100, n = 10), KH buffer with 100 mg/dL glucose (G100, n = 10), KH buffer supplemented with 0.5 U/L insulin and 600 mg/dL glucose (InsG600, n = 10), or with 600 mg/dL glucose (G600, n = 10). To match the osmotic pressure of the InsG600 group, 27.5 mmol/L of mannitol was added to KH solution in the InsG100 and G100 group. The four groups were perfused with each solution for 20 min prior to 15 min of no-flow ischemia, and during 20 min of reperfusion. Only during the ischemic period the heart was paced at 222 beats/min. Measurements of heart rate, coronary flow and maximum of LV derivative of pressure development (dP/dt max) were recorded. Myocardial phospho-protein kinase B (p-Akt) and tumor necrosis factor-α (TNF-α) levels were assayed by enzyme-linked immunosorbent assay and sandwich ELISA, respectively following reperfusion. After reperfusion, LV dP/dt max and heart rate in the InsG100 group was significantly higher than that in the other three groups. The myocardial p-Akt level in the InsG100 group was significantly elevated when compared to the InsG600 group at the end of reperfusion. The p-Akt levels in the InsG600 and InsG100 group were significantly higher than in the corresponding non-insulin groups. Acute hyperglycemia diminishes the cardioprotective effects of insulin preconditioning in the isolated rat heart, possibly mediated through the suppression of myocardial Akt phosphorylation.
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Keywords {🔍}

insulin, group, insg, article, heart, min, preconditioning, hyperglycemia, myocardial, pubmed, reperfusion, glucose, google, scholar, data, ischemia, ischemic, mgdl, groups, study, pressure, akt, rat, pakt, cas, coronary, tnfα, cardioprotective, effects, acute, buffer, mmoll, significantly, fig, manuscript, rate, max, isolated, flow, cardiac, access, full, dpdt, kinase, elisa, higher, table, size, open, sato,

Topics {✒️}

myocardial phospho-protein kinase measure p-akt/total-akt myocardial p-akt/total-akt pre-ischemic insulin pre-conditioning phospho-protein kinase 20-min pre-ischemic pre-conditioning enzyme-linked immunosorbent assay tumor necrosis factor-α lv dp/dt max myocardial pre-conditioning aimed called counter-regulatory hormones intra-operative glucose management lv end-diastolic pressure article download pdf myocardial p-akt level cold modified krebs–henseleit p-akt/total-akt 600 mg/dl glucose prior isolated rat heart 60 mg/kg body weight akt signalling cascade receive modified krebs–henseleit invitrogen rat tnf related subjects dp/dt max full access myocardial ischemia–reperfusion susceptibility 100 mg/dl glucose 600 mg/dl glucose insulin-induced preservation myocardial akt phosphorylation pre-conditioning techniques blood glucose concentration blood glucose control ischemic pre-conditioning ischemic pre-conditioning [10] ischemic pre-conditioning [1] left ventricular derivative acute hyperglycemia blunts privacy choices/manage cookies krebs–henseleit lv total-akt level acute hyperglycemia diminishes akt-mtor system [12 protein kinase cardiac contractility insulin pre-conditioning insulin-pre-conditioning langendorff system micro homogenizing system

Questions {❓}

How does blood glucose control with insulin save lives in intensive care?

Schema {🗺️}

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         headline:Glycemia and the cardioprotective effects of insulin pre-conditioning in the isolated rat heart
         description:While acute hyperglycemia has been shown to mitigate the beneficial effects of ischemic preconditioning, its effect on insulin-induced preconditioning remains unclear. The study was designed to test the hypothesis that acute hyperglycemia diminishes the cardioprotective effects following a 20-min pre-ischemic pre-conditioning with insulin in the isolated rat heart using the Langendorff system. Forty hearts were assigned to receive modified Krebs–Henseleit (KH) buffer containing 0.5 U/L insulin and 100 mg/dL glucose (InsG100, n = 10), KH buffer with 100 mg/dL glucose (G100, n = 10), KH buffer supplemented with 0.5 U/L insulin and 600 mg/dL glucose (InsG600, n = 10), or with 600 mg/dL glucose (G600, n = 10). To match the osmotic pressure of the InsG600 group, 27.5 mmol/L of mannitol was added to KH solution in the InsG100 and G100 group. The four groups were perfused with each solution for 20 min prior to 15 min of no-flow ischemia, and during 20 min of reperfusion. Only during the ischemic period the heart was paced at 222 beats/min. Measurements of heart rate, coronary flow and maximum of LV derivative of pressure development (dP/dt max) were recorded. Myocardial phospho-protein kinase B (p-Akt) and tumor necrosis factor-α (TNF-α) levels were assayed by enzyme-linked immunosorbent assay and sandwich ELISA, respectively following reperfusion. After reperfusion, LV dP/dt max and heart rate in the InsG100 group was significantly higher than that in the other three groups. The myocardial p-Akt level in the InsG100 group was significantly elevated when compared to the InsG600 group at the end of reperfusion. The p-Akt levels in the InsG600 and InsG100 group were significantly higher than in the corresponding non-insulin groups. Acute hyperglycemia diminishes the cardioprotective effects of insulin preconditioning in the isolated rat heart, possibly mediated through the suppression of myocardial Akt phosphorylation.
         datePublished:2017-04-04T00:00:00Z
         dateModified:2017-04-04T00:00:00Z
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            Insulin-induced cardioprotection
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            Isolated rat heart
            Cardiac contractility
            Phospho-protein kinase B
            Tumor necrosis factor-α
            Diabetes
            Angiology
            Cardiology
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      headline:Glycemia and the cardioprotective effects of insulin pre-conditioning in the isolated rat heart
      description:While acute hyperglycemia has been shown to mitigate the beneficial effects of ischemic preconditioning, its effect on insulin-induced preconditioning remains unclear. The study was designed to test the hypothesis that acute hyperglycemia diminishes the cardioprotective effects following a 20-min pre-ischemic pre-conditioning with insulin in the isolated rat heart using the Langendorff system. Forty hearts were assigned to receive modified Krebs–Henseleit (KH) buffer containing 0.5 U/L insulin and 100 mg/dL glucose (InsG100, n = 10), KH buffer with 100 mg/dL glucose (G100, n = 10), KH buffer supplemented with 0.5 U/L insulin and 600 mg/dL glucose (InsG600, n = 10), or with 600 mg/dL glucose (G600, n = 10). To match the osmotic pressure of the InsG600 group, 27.5 mmol/L of mannitol was added to KH solution in the InsG100 and G100 group. The four groups were perfused with each solution for 20 min prior to 15 min of no-flow ischemia, and during 20 min of reperfusion. Only during the ischemic period the heart was paced at 222 beats/min. Measurements of heart rate, coronary flow and maximum of LV derivative of pressure development (dP/dt max) were recorded. Myocardial phospho-protein kinase B (p-Akt) and tumor necrosis factor-α (TNF-α) levels were assayed by enzyme-linked immunosorbent assay and sandwich ELISA, respectively following reperfusion. After reperfusion, LV dP/dt max and heart rate in the InsG100 group was significantly higher than that in the other three groups. The myocardial p-Akt level in the InsG100 group was significantly elevated when compared to the InsG600 group at the end of reperfusion. The p-Akt levels in the InsG600 and InsG100 group were significantly higher than in the corresponding non-insulin groups. Acute hyperglycemia diminishes the cardioprotective effects of insulin preconditioning in the isolated rat heart, possibly mediated through the suppression of myocardial Akt phosphorylation.
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         Acute hyperglycemia
         Insulin-induced cardioprotection
         Stunned myocardium
         Isolated rat heart
         Cardiac contractility
         Phospho-protein kinase B
         Tumor necrosis factor-α
         Diabetes
         Angiology
         Cardiology
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      name:Tadahiko Ishiyama
      affiliation:
            name:Yamanashi University Hospital
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PostalAddress:
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      name:Department of Anesthesia, McGill University Health Centre Glen Site, Royal Victoria Hospital, Montreal, Canada
      name:Department of Anesthesiology, University of Yamanashi, Chuo-city, Japan
      name:Department of Anesthesia, McGill University Health Centre Glen Site, Royal Victoria Hospital, Montreal, Canada
      name:Operating Theater, Yamanashi University Hospital, Chuo-city, Japan
      name:Operating Theater, Yamanashi University Hospital, Chuo-city, Japan
      name:Department of Anesthesiology, University of Yamanashi, Chuo-city, Japan
      name:Department of Anesthesia, McGill University Health Centre Glen Site, Royal Victoria Hospital, Montreal, Canada

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