Role of the sympathetic nervous system in the ischemic and reperfused heart

Hara, Akiyoshi; Abiko, Yasushi

doi:10.1007/978-3-0348-8988-9_17

Cited by 8 publications

(11 citation statements)

References 41 publications

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“…Additionally, the widespread clinical use of beta-blockers for treatment of hypertension and cardioprotection may alter catecholamine responsiveness. 5 Furthermore, victims of trauma are unique in that they are often subjected to serial insults because the initial trauma that results in hospitalization followed by a subsequent operation to treat their trauma-related injuries. It is in this period of altered catecholamine levels that traumatic and operative wounds must heal.…”

mentioning

confidence: 99%

Norepinephrine Modulates the Inflammatory and Proliferative Phases of Wound Healing

Gosain

Jones

Shankar

et al. 2006

The Journal of Trauma: Injury, Infection, and Critical Care

132

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mentioning

confidence: 99%

Norepinephrine Modulates the Inflammatory and Proliferative Phases of Wound Healing

Gosain

Jones

Shankar

et al. 2006

The Journal of Trauma: Injury, Infection, and Critical Care

132

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“…[1][2][3][4] Prolonged myocardial ischemia causes a large amount of NE to be released from the sympathetic nerve terminals via non-exocytotic local metabolic mechanism independently of central sympathetic activation, and this excessive NE may promote myocardial injury. 5 Reperfusion following prolonged ischemia would prevent progression of ischemic cell necrosis, whereas reperfusion itself causes myocardial injury, the phenomenon known as reperfusion injury.…”

mentioning

confidence: 99%

Ischemia-Induced Norepinephrine Release, but not Norepinephrine-Derived Free Radicals, Contributes to Myocardial Ischemia - Reperfusion Injury

Nonomura

Nozawa

Matsuki

et al. 2005

Circ J

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t is generally accepted that excess levels of norepinephrine (NE) could lead to myocardial injury. [1][2][3][4] Prolonged myocardial ischemia causes a large amount of NE to be released from the sympathetic nerve terminals via non-exocytotic local metabolic mechanism independently of central sympathetic activation, and this excessive NE may promote myocardial injury. 5 Reperfusion following prolonged ischemia would prevent progression of ischemic cell necrosis, whereas reperfusion itself causes myocardial injury, the phenomenon known as reperfusion injury. [6][7][8][9][10] Increased interstitial concentration of NE during ischemia may be involved in the pathogenesis of reperfusion injury, because NE is a source of free radicals. [11][12][13] Previous studies have shown that auto-oxidation of NE results in the generation of highly reactive ·OH radicals. 12,13 Thus, the pathogenesis of catecholamine-induced myocardial injury in the setting of reperfusion following prolonged ischemia is multifactorial, but the relative role of this NE-derived free radical formation in increasing the size of the infarct after reperfusion remains unclear. Accordingly, we studied the effects of cardiac denervation on free radical formation and infarct size in rats with reperfusion following prolonged ischemia and compared them with those of -adrenoceptor blockade. Methods Experimental AnimalThe experimental procedures were approved by the guidelines for animal experimentation at Toyama Medical and Pharmaceutical University. A total of 48 male Wistar rats weighing 300-350 g were used for induction of myocardial ischemia as described previously. 14 Briefly, the rats were anesthetized with sodium pentobarbital (30 mg/kg, ip), and a left thoracotomy was performed to exteriorize the heart. The left coronary artery was ligated 2-3 mm from its origin with a suture of 5-0 prolene (Ethicon, Inc, Somerville, NJ, USA) for 30 min, and then the ligature was released.The animals were divided into 3 groups: control, phenol, and atenolol. The following protocols were performed: (i) determination of hemodynamics and infarct size (control = 8, phenol =6, atenolol =6), (ii) determination of interstitial NE concentrations during ischemia and reperfusion (control =7, phenol =4, atenolol =4), and (iii) electron paramagnetic resonance (EPR) study (control =6, phenol =7). One week before coronary ligation, regional cardiac denervation was performed by painting a solution of 10% phenol in ethanol on the left ventricular (LV) epicardium around the proximal region of the left coronary artery. 15 The 1-selective adrenoceptor blockade, atenolol (0.5 mg/kg), was Background Norepinephrine (NE)-derived free radicals may contribute to myocyte injury after ischemiareperfusion, so the influence of sympathetic denervation on myocardial ischemia -reperfusion injury was investigated in the present study. Methods and ResultsCardiac sympathetic denervation was produced in Wistar rats by a solution of 10% phenol 1 week before ischemia. Atenolol (0.5 mg/kg) was intravenously a...

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“…Neufcld et al [7] have shown that lidocaine reduces the incidence of ventricular fibrillation induced by exogenous lysophosphatidylcholine. These actions of lidocaine may also contribute to its protective action on the myocardium from ischemia-reperfusion damage, because catecholamines [8], reactive oxygen species [9] and lysophospholipids [10. 11] are factors involved in the production of ischemia-reperfusion damage.…”

Section: Introductionmentioning

confidence: 99%

Lidocaine Attenuates Mechanical and Metabolic Derangements Induced by Palmitoyl-L-Carnitine in the Isolated Perfused Rat Heart

1997

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The effect of lidocaine on the palmitoyl-L-carnitine (PAL-CAR)-induced mechanical and metabolic derangements was studied in Langendorff rat hearts, perfused aerobically at a constant flow rate and paced electrically. PALCAR (5 µmol/l) increased the left ventricular end-diastolic pressure, decreased the left ventricular developed pressure (i.e., mechanical dysfunction), and decreased the tissue levels of adenosine triphosphate and creatine phosphate (i.e., metabolic change). These mechanical and metabolic alterations induced by PALCAR were concentration-dependently attenuated by lidocaine (20, 50 or 100 µmol/l). Nevertheless, lidocaine (20, 50 or 100 µmol/l) did not affect the mechanical function and energy metabolism of the normal (PALCAR-untreated) heart. These results indicate that lidocaine has a cardioprotective action against the PALCAR-induced mechanical and metabolic derangements.

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Role of the sympathetic nervous system in the ischemic and reperfused heart

Cited by 8 publications

References 41 publications

Norepinephrine Modulates the Inflammatory and Proliferative Phases of Wound Healing

Norepinephrine Modulates the Inflammatory and Proliferative Phases of Wound Healing

Ischemia-Induced Norepinephrine Release, but not Norepinephrine-Derived Free Radicals, Contributes to Myocardial Ischemia - Reperfusion Injury

Lidocaine Attenuates Mechanical and Metabolic Derangements Induced by Palmitoyl-L-Carnitine in the Isolated Perfused Rat Heart

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