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ARTICLE |

Endotoxin Disrupts β-Adrenergic Signal Transduction in the Heart

Denis D. Bensard, MD; Anirban Banerjee, PhD; Robert C. McIntyre Jr, MD; Randolph L. Berens, PhD; Alden H. Harken, MD
Arch Surg. 1994;129(2):198-205. doi:10.1001/archsurg.1994.01420260094013.
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Background:  Nonsurvivors of septic shock demonstrate impaired myocardial function refractory to the administration of β-agonists.

Methods:  Using the isolated rat heart preparation, the integrity of the β-adrenergic transduction pathway was tested (rate pressure product, rate of contraction, rate of relaxation, and cyclic adenosine monophosphate content) using isoproterenol hydrochloride (β-receptor agonist) or colforsin (forskolin) (adenylyl cyclase activator) stimulation following intracoronary endotoxin infusion.

Results:  Basal rate pressure product, rate of contraction, rate of relaxation, and cyclic adenosine monophosphate concentrations were unaffected by endotoxin infusion. Endotoxin impaired increases in rate pressure product, rates of contraction and relaxation, and cyclic adenosine monophosphate to isoproterenol (P<.05), but the response to colforsin was unaffected by endotoxin.

Conclusions:  Endotoxin disrupts the myocardial response to direct β-receptor stimulation but not to adenylyl cyclase stimulation in the isolated rat heart.

Clinical Relevance:  Alteration of the proximal β-adrenoreceptor complex by endotoxin suggests that therapy of the failing heart during refractory septic shock may be directed to intact sites distal in the β-adrenergic pathway.(Arch Surg. 1994;129:198-205)

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