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Positive inotropic action of insulin on piglet heart
Insights
Insulin directly enhances newborn piglet heart contractility during hypoglycemia. This cardiac stimulation, independent of central nervous system or beta-adrenergic activity, may involve calcium fluxes, but did not improve hypoxia resistance.
Area of Science:
- Cardiovascular Physiology
- Neonatal Metabolism
- Endocrinology
Background:
- Hypoglycemia poses significant risks to neonatal cardiac function.
- Insulin's direct effects on the myocardium are not fully understood.
- Neonatal hypoxia resistance is influenced by glycogen stores.
Purpose of the Study:
- To investigate the impact of insulin-induced hypoglycemia on cardiac performance in newborn piglets.
- To determine if insulin has a direct positive inotropic effect on the neonatal myocardium.
- To assess insulin's influence on myocardial resistance to hypoxia.
Main Methods:
- Insulin was administered to newborn piglets to induce hypoglycemia.
- Cardiac performance was assessed by measuring dP/dt max, with heart rate, aortic pressure, and flow held constant.
- Central nervous system and beta-adrenergic activity were eliminated using vessel ligation and beta-blocker administration (practolol).
Main Results:
- A significant positive inotropic response was observed, with dP/dt max increasing to 138% of control values.
- This cardiac stimulation occurred independently of central nervous system or beta-adrenergic influences.
- Pretreatment with insulin did not alter the rate of cardiac function deterioration during hypoxia.
Conclusions:
- Insulin directly stimulates myocardial contractility in newborn piglets during hypoglycemia.
- The mechanism of insulin-induced cardiac stimulation is likely independent of glucagon and may involve calcium fluxes.
- Insulin does not appear to enhance myocardial resistance to hypoxia under these experimental conditions.
Abstract:
This study was designed to investigate changes in cardiac performance during hypoglycemia produced by the administration of insulin in the newborn piglet. With heart rate, aortic pressure, and aortic flow held constant, the treated group demonstrated a pronounced positive inotropic response manifested by an increase of dP/dt max to 138% of control values. Central nervous system function and beta adrenergic activity were excluded from the preparation by ligation of the brachiocephalic vessels and administration of practolol. For reasons discussed, it is unlikely that the findings can be ascribed to glucagon contamination. Therefore, the increase in contractility presumably resulted from a direct effect of insulin upon the myocardium. Clinical and laboratory data suggest that the resistance of the neonate to hypoxia is modified by glycogen stores. Insulin is known to increase glycogen synthesis, and this effect might be expected to augment myocardial resistance to hypoxia. Under the conditions of these experiments, however, pretreatment with insulin had no demonstrable influence on the rate of deterioration of cardiac function during hypoxia. The mechanism of cardiac stimulation by insulin is unknown but may involve calcium fluxes.