Alterations in the Myocardial β-adrenergic System During Experimental Endotoxemia

Overview

Journal J Anesth

Specialty Anesthesiology

Date 2013 Jul 11

PMID 23839552

Citations 1

Authors

Y Kadoi

S Saito

N Fujita

T Morita

T Fujita

Affiliations

Soon will be listed here.

Abstract

In this study to investigate whether β-adrenergic receptor systems in the heart are impaired during endotoxemia, we examined two models of septic shock in rats, each of which has a different time course for the shock state. Male Wistar rats were divided into two groups: (1) the LPS (lipopolysaccharide) iv group (Escherichia coli endotoxin 1.0 mg·kg(-1) iv bolus administration), and (2) the CLP (cecal ligation and puncture model) group. As a control group for each model, a 0.9% saline injection group and a sham-operated group were also prepared. At 3, 12, and 24 h after treatment, the rats were killed and their hearts were removed as rapidly as possible. In the LPS iv and CLP groups, an increase in the plasma epinephrine (E) and norepinephrine (NE) levels compared with the control and sham-operated groups was observed at both 3 and 12h after treatment (P<0.05). There was a decrease in myocardial tissue NE concentration at 3, 12 and 24h in the CLP group. This decrease was especially marked at 24h. In the LPS iv group, a decrease in β-receptor density was observed at 3 h (control, 87.07±4.59 fmol·mg(-1) protein; LPS iv, 60.73±3.51 fmol·mg(-1) protein), but was not observed at 24h. In contrast, a decrease in β-receptor density in the CLP group was observed at 24h (sham-operated, 80.9±3.65 fmol·mg(-1) protein; CLP, 66.1±4.08 fmol·mg(-1) protein), but was not observed at 3h. The β-receptor density in the hearts of LPS iv rats and the altered hemodynamics recovered in line with the decrease in plasma catecholamines (CA). However, in the CLP group the alteration in hemodynamics was not in line with plasma CA. The alteration in hemodynamics of septic-shock rats observed in this study was linked to the change in heart β-receptor density rather than the change in plasma CA. These observations suggested that the alterations which occur in the β-receptor system during endotoxemia depend upon the model of animal sepsis that is employed, and the time course of the septic-shock state. These alterations in the β-adrenergic system are thought to cause myocardial dysfunction during endotoxemia.

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References

Shepherd R, Lang C, McDonough K . Myocardial adrenergic responsiveness after lethal and nonlethal doses of endotoxin. Am J Physiol. 1987; 252(2 Pt 2):H410-6. DOI: 10.1152/ajpheart.1987.252.2.H410. View

Romano F, Jones S . Characteristics of myocardial beta-adrenergic receptors during endotoxicosis in the rat. Am J Physiol. 1986; 251(2 Pt 2):R359-64. DOI: 10.1152/ajpregu.1986.251.2.R359. View

Kovarik M, Jones S, Romano F . Plasma catecholamines following cecal ligation and puncture in the rat. Circ Shock. 1987; 22(4):281-90. View

Lurie K, Bristow M, Reitz B . Increased beta-adrenergic receptor density in an experimental model of cardiac transplantation. J Thorac Cardiovasc Surg. 1983; 86(2):195-201. View

Jones S, Romano F . Myocardial beta adrenergic receptor coupling to adenylate cyclase during developing septic shock. Circ Shock. 1990; 30(1):51-61. View

WEIL-MALHERBE H, Bone A . The chemical estimation of adrenaline-like substances in blood. Biochem J. 1952; 51(3):311-8. PMC: 1197847. DOI: 10.1042/bj0510311. View

Shepherd R, McDonough K, Burns A . Mechanism of cardiac dysfunction in hearts from endotoxin-treated rats. Circ Shock. 1986; 19(4):371-84. View

Wichterman K, Baue A, Chaudry I . Sepsis and septic shock--a review of laboratory models and a proposal. J Surg Res. 1980; 29(2):189-201. DOI: 10.1016/0022-4804(80)90037-2. View

Williams L, Lefkowitz R, Watanabe A, Hathaway D, Besch Jr H . Thyroid hormone regulation of beta-adrenergic receptor number. J Biol Chem. 1977; 252(8):2787-9. View

10.

Jones S, Kovarik M, Romano F . Cardiac and splenic norepinephrine turnover during septic peritonitis. Am J Physiol. 1986; 250(5 Pt 2):R892-7. DOI: 10.1152/ajpregu.1986.250.5.R892. View

11.

Benedict C, Rose J . Arterial norepinephrine changes in patients with septic shock. Circ Shock. 1992; 38(3):165-72. View

12.

Ghosh S, Latimer R, Gray B, Harwood R, Oduro A . Endotoxin-induced organ injury. Crit Care Med. 1993; 21(2 Suppl):S19-24. DOI: 10.1097/00003246-199302001-00005. View

13.

Pohorecky L, Wurtman R, Taam D, Fine J . Effects of endotoxin on monoamine metabolism in the rat. Proc Soc Exp Biol Med. 1972; 140(3):739-46. DOI: 10.3181/00379727-140-36543. View

14.

Jones S, Romano F . Dose- and time-dependent changes in plasma catecholamines in response to endotoxin in conscious rats. Circ Shock. 1989; 28(1):59-68. View

15.

Bradford M . A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye binding. Anal Biochem. 1976; 72:248-54. DOI: 10.1016/0003-2697(76)90527-3. View

16.

Parratt J . Myocardial and circulatory effects of E. coli endotoxin; modification of responses to catecholamines. Br J Pharmacol. 1973; 47(1):12-25. PMC: 1776526. DOI: 10.1111/j.1476-5381.1973.tb08154.x. View

17.

Silverman H, Lee N, El-Fakahany E . Effects of canine endotoxin shock on lymphocytic beta-adrenergic receptors. Circ Shock. 1990; 32(4):293-306. View

18.

Pardini B, Jones S, Filkins J . Cardiac and splenic norepinephrine turnovers in endotoxic rats. Am J Physiol. 1983; 245(2):H276-83. DOI: 10.1152/ajpheart.1983.245.2.H276. View

19.

Felice L, Felice J, Kissinger P . Determination of catecholamines in rat brain parts by reverse-phase ion-pair liquid chromatography. J Neurochem. 1978; 31(6):1461-5. DOI: 10.1111/j.1471-4159.1978.tb06573.x. View

20.

Rosenthal H . A graphic method for the determination and presentation of binding parameters in a complex system. Anal Biochem. 1967; 20(3):525-32. DOI: 10.1016/0003-2697(67)90297-7. View