Inhibition of Norepinephrine Reuptake and Size of Myocardial Infarction during Focal Ischemia and after Preconditioning

Naumenko, S. E.; Latysheva, T. V.; Gilinskii, M. A.

doi:10.1007/s10517-010-1056-3

Cited by 3 publications

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“…The association of depression with MI is critical, as the mortality rate is increased three to four times in depressed MI patients compared to non-depressed MI patients ( 3 ) . As the level of non-responders is still high with antidepressant treatments ( 4 , 5 ) and that the treatment may interfere with myocardial infarct size ( 6 ) , new antidepressant strategies need to be identified for such cases.…”

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confidence: 99%

Attenuation of post-myocardial infarction depression in rats byn-3 fatty acids or probiotics starting after the onset of reperfusion

et al. 2012

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Proinflammatory cytokines play a central role in depression-like behaviour and apoptosis in the limbic system after myocardial infarction (MI). A PUFA n-3 diet or the combination of Lactobacillus helveticus R0052 and Bifidobacterium longum R0175 probiotics, when given before the ischaemic period, reduce circulating proinflammatory cytokines as well as apoptosis in the limbic system. The present study was designed to determine if the same nutritional interventions maintain their beneficial effects when started after the onset of the reperfusion period and attenuate depression-like behaviour observed after MI. MI was induced by the occlusion of the left anterior descending coronary artery for 40 min in rats. After the onset of reperfusion, animals were fed with a high-or low-PUFA n-3 diet, combined or not with one billion live bacteria of L. helveticus and B. longum. At 3 d post-MI, caspase-3 enzymatic activities and terminal 2 0 -deoxyuridine, 5 0 -triphosphate (dUTP) nick-end labelling (TUNEL)-positive cells were decreased in the CA1, dentate gyrus (DG) and amygdala with the high-PUFA n-3 diet, as compared to the three other diets. Probiotics attenuated caspase-3 activity and TUNEL-positive cells in the DG and the medial amygdala. At 2 weeks post-MI, depression-like behaviour was observed in the low-PUFA n-3 diet without probiotics-group, and this behaviour was attenuated with the high-PUFA n-3 diet or/and probiotics. These results indicate that a high-PUFA n-3 diet or the administration of probiotics, starting after the onset of reperfusion, are beneficial to attenuate apoptosis in the limbic system and post-MI depression in the rat.Key words: n-3 Fatty acids: Apoptosis: Limbic system: Diet: Behaviour: Hippocampus: Amygdala Depressive mood is common after myocardial infarction (MI) (1) and 20 % of MI patients develop an episode of major depression (2) . The association of depression with MI is critical, as the mortality rate is increased three to four times in depressed MI patients compared to non-depressed MI patients (3) . As the level of non-responders is still high with antidepressant treatments (4,5) and that the treatment may interfere with myocardial infarct size (6) , new antidepressant strategies need to be identified for such cases.The physiopathology of depression is complex and different mechanisms are involved (7) . Our previous work and that of others indicate that proinflammatory cytokines may play a key role in depression-like behaviour (8 -10) . Indeed, injection of proinflammatory cytokines is followed by depression-like behaviour (11) . Post-MI increased levels of proinflammatory cytokines are accompanied by apoptosis in the hippocampus and the amygdala, another physiopathological element of depression (8,9,12) .Dietary interventions can be used to prevent the post-MI elevation of proinflammatory cytokines. For example, we have shown that high-PUFA n-3 diets reduce the circulating level of TNFa after MI (13) . High-PUFA n-3 diets also reduce levels of monocyte chemotactic protein-1 (...

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Attenuation of post-myocardial infarction depression in rats byn-3 fatty acids or probiotics starting after the onset of reperfusion

et al. 2012

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“…At this stage, differences in the dynamics of neurotransmitters were also observed. If ischemic preconditioning largely prevents the increase in interstitial noradrenalin under conditions of long-term ischemia [1,2], the content of serotonin in the same conditions is reduced only during the fi rst 20 min of ischemia in comparison with the control. Probably prolonged ischemia signifi cantly limits the effective time of the serotonin transporter functioning.…”

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“…The dynamics and effects of some of them, such as norepinephrine, are fairly well known [1,2]. The data on the role of serotonin in the development of myocardial injury during its ischemia/reperfusion injury are still controversial.…”

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Myocardial Serotonin during Ischemia under Conditions of Ischemic Preconditioning

2014

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We studied the dynamics of interstitial serotonin during local myocardial ischemia under conditions of ischemic preconditioning in Wistar rats. Ischemic preconditioning increased serotonin content in the dialysate (p=0.003). During 30-min ischemia, ischemic preconditioning delayed serotonin increase just before the 20th min of ischemia. Ischemic preconditioning promoted short-term increase in the serotonin level in the myocardial interstitium but followed by prolonged ischemia, it delayed the accumulation of serotonin in the myocardial interstitium.

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“…Several possible triggers for IPC have been postulated, including adenosine, NE, and bradykinin [11, 12]. Previous studies on the effect of IPC have focused primarily on infarct size limitation [13], but its effect on cardiac sympathetic nerve injury is not known. During myocardial ischemia, massive myocardial NE release into the interstitial space was observed, caused by a nonexocytotic mechanism reflecting sympathetic nerve injury.…”

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Desipramine Pretreatment Improves Sympathetic Remodeling and Ventricular Fibrillation Threshold after Myocardial Ischemia

Jiang

et al. 2012

Journal of Biomedicine and Biotechnology

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Abnormal increase in sympathetic nerve sprouting was responsible for the ventricular arrhythmogenesis after myocardial infarction. This study investigated whether the norepinephrine transporter inhibitor, desipramine, can modulate sympathetic remodeling and ventricular fibrillation threshold (VFT) after myocardial ischemia-reperfusion. Rats were administered desipramine (0.8 mg/kg, IV) before or after myocardial ischemia. VFT, infarct size, tyrosine hydroxylase (TH) and growth-associated protein 43 (GAP43)-positive nerve fibers were measured after one week. The VFT of preischemic treatment group was 11.0 ± 2.65 V and significantly higher than that of control ischemic group (7.2 ± 1.30 V, P < 0.05). Infarct size in the preischemic treatment group (23.3 ± 2.4%) was significantly lower than that in the control ischemic group (30.8 ± 1.3%, P < 0.05) and the delayed application group (27.1 ± 2.6%, P < 0.05). The density of TH and GAP43-positive nerve fibers in the control ischemic group was significantly higher than that in the other three groups (P < 0.05). The density of nerve fibers improved after desipramine treatment. Moreover, there was a negative correlation between the VFT and both TH and GAP43-positive nerve fiber density in the infarct border zone (P < 0.05). Desipramine treatment before acute myocardial ischemia can decrease infarct size, improve sympathetic remodeling, and increase VFT and electrical stability of ischemic hearts. Desipramine appears to cause myocardial ischemic preconditioning.

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Inhibition of Norepinephrine Reuptake and Size of Myocardial Infarction during Focal Ischemia and after Preconditioning

Abstract: Experiments on rats showed that blockade of norepinephrine reuptake in the early reperfusion period after focal myocardial ischemia aggravates myocardial injury and abolishes the protective effect of ischemic preconditioning.

Cited by 3 publications

References 4 publications

Attenuation of post-myocardial infarction depression in rats byn-3 fatty acids or probiotics starting after the onset of reperfusion

Attenuation of post-myocardial infarction depression in rats byn-3 fatty acids or probiotics starting after the onset of reperfusion

Myocardial Serotonin during Ischemia under Conditions of Ischemic Preconditioning

Desipramine Pretreatment Improves Sympathetic Remodeling and Ventricular Fibrillation Threshold after Myocardial Ischemia

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