Prospective randomized trial of glucose-insulin-potassium in acute myocardial infarction

Rogers, William J.; Segall, Peter H.; McDaniel, Huey G.; Mantle, John A.; Russell, Richard O.; Rackley, Charles E.

doi:10.1016/0002-9149(79)90081-x

Cited by 114 publications

(23 citation statements)

References 33 publications

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“…Several clinical trials have reported an improvement in hemodynamic measurements and reduced mortality in patients receiving intravenous glucose alone or in the form of a glucose infusion containing insulin and potassium during acute myocardial infarction (45)(46)(47)(48). It is well established that within minutes after acute coronary occlusion metabolic changes result that, if prolonged, adversely affect myocardial cell survival.…”

Section: Discussionmentioning

confidence: 99%

Hypoxia and glucose independently regulate the beta-adrenergic receptor-adenylate cyclase system in cardiac myocytes.

Rocha‐Singh¹,

Honbo²,

Karliner³

1991

J. Clin. Invest.

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We explored the effects of two components of ischemia, hypoxia and glucose deprivation, on the jl-adrenergic receptor (fiAR)-adenylate cyclase system in a model of hypoxic injury in cultured neonatal rat ventricular myocytes. After 2 h ofhypoxia in the presence of 5 mM glucose, cell surface #AR density (3H-CGP-12177) decreased from 54.8±8.4 to 39±63 (SE) fmol/mg protein (n = 10, P < 0.025), while cytosolic #AR density ('25I-iodocyanopindolol IICYPI) increased by 74% (n = 5, P < 0.05). Upon reexposure to oxygen cell surface IAR density returned toward control levels. Cells exposed to hypoxia and reoxygenation without glucose exhibited similar alterations in #AR density.In hypoxic cells incubated with 5 mM glucose, the addition of 1 MM (-)-norepinephrine (NE) increased cAMP generation from 29.3±10.6 to 54.2±16.1 pmol/35 mm plate (n = 5, P < 0.025); upon reoxygenation cAMP levels remained elevated above control (n = 5, P < 0.05). In contrast, NE-stimulated cAMP content in glucose-deprived hypoxic myocytes fell by 31% (n = 5, P < 0.05) and did not return to control levels with reoxygenation. ,AR-agonist affinity assessed by (-)-isoproterenol displacement curves was unaltered after 2 h of hypoxia irrespective of glucose content. Addition of forskolin (100 MM) to glucose-supplemented hypoxic cells increased cAMP generation by 60% (n = 5; P < 0.05), but in the absence of glucose this effect was not seen.In cells incubated in glucose-containing medium, the decline in intracellular ATP levels was attenuated after 2 h of hypoxia (21 vs. 40%, P < 0.05). Similarly, glucose supplementation prevented LDH release in hypoxic myocytes.We conclude that (a) oxygen and glucose independently regulate 6dAR density and agonist-stimulated cAMP accumulation; (b) hypoxia has no effect on ,BAR-agonist or antagonist affinity; (c) 5 mM glucose attenuates the rate ofdecline in cellular ATP levels during both hypoxia and reoxygenation; and (d) glucose prevents hypoxia-induced LDH release, a marker of cell injury. (J. Clin. Invest. 1991. 88:204-213.) Key words:

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Section: Discussionmentioning

confidence: 99%

Hypoxia and glucose independently regulate the beta-adrenergic receptor-adenylate cyclase system in cardiac myocytes.

Rocha‐Singh¹,

Honbo²,

Karliner³

1991

J. Clin. Invest.

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“…This value distinctly exceeds the 13 % calculated by a shift of the ATP/ O ratio from 2.80 to 3.17 when myocardial metabolism is converted from lipid to glucose utilization. Nevertheless, because of hyperosmolality, side effects or toxicity (18,19,20,21,24,25) the clinically applicable substance to achieve this goal is as yet not found.…”

Section: Discussionmentioning

confidence: 99%

Changes in myocardial substrate and energy metabolism by S-(4)-hydroxyphenylglycine and an N-(6)-derivative of adenosine

et al. 1986

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In 15 mongrel open chest dogs oxidative myocardial carbohydrate utilization was stimulated by activation of pyruvatedehydrogenase with S-(4)-hydroxyphenylglycine (HPG) or by inhibition of lipolysis with N(6)-allyl-N(6)-cyclohexyladenosine (PAA). HPG and PAA shifted cardiac respiratory quotients (RQ) from 0.83 to 0.89 and 0.99, respectively. Oxygen extraction ratio of lactate was significantly increased by both interventions. Arterial nonesterified fatty acids (NEFA) concentration decreased significantly only by PAA. The oxygen saving potency of both interventions was quantified over a wide hemodynamic range by comparing the directly measured myocardial oxygen consumption (MVO2) with the myocardial energy requirements calculated from its hemodynamic determinants according to the Bretschneider formula during base conditions and beta-stimulation. Inhibition of peripheral lipolysis with PAA reduced MVO2 by 14%, enzyme activation with HPG by 8%. The results show that the efficiency of the myocardial energy supply can be influenced by manipulation of the oxidative substrate metabolism.

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“…In the pre treated group, no elevations in resting CF and resting LVP were observed during hypoper fusion (0.3±0.1 4g and -1.0±0. 3 dmmHg at the end of hypoperfusion, respectively). In the post-treated group, these elevations were similar to those in the non-treated group (3.1 ±0.4 4g and 10.1 ±4.4 dmmHg at the end of hypoperfusion, respectively).…”

Section: Animals and Treatmentmentioning

confidence: 96%

Improvement of Hypoperfusion with Norepinephrine Injury by Ex Vivo Insulin in Isolated Diabetic Rat Hearts

Ikema

Higuchi

Hirayama

et al. 1990

Japanese Journal of Pharmacology

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Abstract-Effects of insulin on contractile and energy metabolic dysfunctions during hypoperfusion (2 ml/min/g heart wt., 60 min) with 10-6 M norepinephrine were studied in paced hearts isolated from streptozotocin-diabetic rats. Insulin (2 mU/ min/g heart wt.) was infused 20 min before and during hypoperfusion (pre-treated group) or 30 min after the onset of hypoperfusion (post-treated group). Hearts in the non-treated group were hypoperfused without insulin and other hearts in the control group were not hypoperfused.In the non-treated group, resting con tractile force (CF) and resting left ventricular pressure (LVP) were significantly elevated to maximum levels within 30 min after hypoperfusion and these elevations were restored in the pre-treated group but not in the post-treated group. Developed CF was depressed in the non-treated group and improved significantly in the pre treated group but not in the post-treated group. Developed LVP was depressed in the non-treated group, and depression was slightly larger in the pre-treated group. In the non-treated group, ATP and creatine phosphate contents in the left ventricle significantly decreased. Decreases in ATP and creatine phosphate contents in the inner layer were partially restored in the pre-treated group but not in the post treated group. Lactate significantly increased in the non-treated group and increased even further in the insulin treated groups.These results indicate that contractile dysfunction during hypoperfusion with norepinephrine is improved by pre-treated insulin, as is partial recovery of energy metabolism.

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Prospective randomized trial of glucose-insulin-potassium in acute myocardial infarction

Cited by 114 publications

References 33 publications

Hypoxia and glucose independently regulate the beta-adrenergic receptor-adenylate cyclase system in cardiac myocytes.

Hypoxia and glucose independently regulate the beta-adrenergic receptor-adenylate cyclase system in cardiac myocytes.

Changes in myocardial substrate and energy metabolism by S-(4)-hydroxyphenylglycine and an N-(6)-derivative of adenosine

Improvement of Hypoperfusion with Norepinephrine Injury by Ex Vivo Insulin in Isolated Diabetic Rat Hearts

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