Estimation of Myocardial Interstitial Norepinephrine Release After Brain Death Using Cardiac Microdialysis

Mertès, P. M.; Carteaux, J. P.; Jaboin, Y.; Pinelli, G; Abassi, K. El; Dopff, C.; Atkinson, Judith M.; Jp, Villemot; Burlet, C.; Boulangé, M

doi:10.1097/00007890-199402150-00010

Cited by 129 publications

(55 citation statements)

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“…19 The functional and structural cardiac changes after explosive injury to the brain have been directly correlated with high catecholamine levels, particularly norepinephrine and neuropeptide Y. 20 These factors may produce localized coronary vasospasm with insufficient blood flow for adequate myocardial perfusion, resulting in necrosis of the subendocardium of the left ventricle, petechial hemorrhage, contraction bands, and coagulative myocytolysis with a mononuclear cell infiltrate. 4,8,21 Exhaustion of catecholamine stores after autonomic storm may be so profound that hypotension results.…”

Section: Discussionmentioning

confidence: 99%

Activation of the Heart by Donor Brain Death Accelerates Acute Rejection After Transplantation

et al. 2000

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Background-Donor brain death upregulates expression of inflammatory mediators in the heart. It is hypothesized that these nonspecific changes trigger and amplify acute rejection in unmodified recipients compared with hearts from normal living donors. We examined the inflammatory and immunological consequences of gradual-onset donor brain death on cardiac allografts after transplantation. Methods and Results-Functioning hearts were engrafted from normotensive donors after 6 hours of ventilatory support.Hearts from brain-dead rats (Fisher, F344) were rejected significantly earlier (meanϮSD, 9.3Ϯ0.6 days) by their (Lewis) recipients than hearts from living donor controls (11.6Ϯ0.7 days, Pϭ0.03). The inflammatory response of such organs was accelerated, with rapid expression of cytokines, chemokines, and adhesion molecules and brisk infiltration of associated leukocyte populations. Upregulation of major histocompatibility class II antigens increased organ immunogenicity. Acute rejection evolved in hearts from brain-dead donors more intensely and at a significantly faster rate than in controls. Conclusions-Donor brain death is deleterious to transplanted hearts. The resultant upregulation of inflammatory factors provokes host immune mechanisms and accelerates the acute rejection process in unmodified hosts. (Circulation.

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Section: Discussionmentioning

confidence: 99%

Activation of the Heart by Donor Brain Death Accelerates Acute Rejection After Transplantation

et al. 2000

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“…Cremers et al [13] reported differences in basal NE concentration in the myocardium of the right and left ventricles due to different sympathetic innervation. However, others have not observed such differences [9] using anesthetized pigs. We found no quantitative map of myocardial NE release in the literature.…”

Section: Discussionmentioning

confidence: 90%

“…The use of microdialysis sampling to monitor NE in the myocardial interstitium has been previously reported [2,6,[8][9][10][11][12][13]. Most of these studies were performed in comparatively large experimental animals: cats, rabbits or pigs.…”

Section: Introductionmentioning

confidence: 99%

Determination of myocardial norepinephrine in freely moving rats using in vivo microdialysis sampling and liquid chromatography with dual-electrode amperometric detection

Gilinsky

Faibushevish

Lunte

2001

Journal of Pharmaceutical and Biomedical Analysis

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Myocardial norepinephrine (NE) is considered a meaningful parameter for estimation of cardiac function. Long lasting changes in myocardial NE appear to be not only a consequence of pathologic processes in the myocardium, but may be a factor responsible for some diseases (e.g. increased propensity for arrhythmias or negative effect on left ventricular contractility in congestive heart failure). In this respect monitoring of myocardial NE is of great importance. A microdialysis sampling technique coupled with liquid chromatography with electrochemical detection (LCEC) was developed to measure the in vivo NE concentration in the myocardial interstitium of conscious, freely moving rats. LCEC using a dual-electrode amperometric detection in the series configuration provided detection limits for NE of 10 pg/ml in 20 μl microdialysis samples. Microdialysis probes of the linear design were implanted in the myocardial tissue in the periphery of the left descending coronary artery. The basal steady-state concentration of NE in myocardial dialysate of awake, freely moving rats was found to be 0.17 ± 0.026 ng/ml. Delivery through the microdialysis probe of the NE reuptake inhibitor desipramine (DMI) at a concentration of 0.1 mM increased NE release to 153 ± 13% of control. If the concentration of DMI in the perfusate was increased to 1.0 mM, NE release increased to only 166 ± 21% of control.

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“…Direct release of toxic levels of catecholamines into the myocardium by the cardiac sympathetic nerve terminals is indicated as a more likely cause of neurocardiogenic injury than adrenal release of catecholamines into the systemic circulation in animal models. 13) No significant association was found between serum levels of either norepinephrine or epinephrine and cardiac troponin I release that indicate myocardial necrosis in patients with SAH. 18) However, a case of takotsubo cardiomyopathy resulting from dobutamine infusion was reproducible in the catheterization laboratory, suggesting that catecholamine-induced microvascular dysfunction may be the predominant etiological factor in takotsubo cardiomyopathy.…”

Section: Discussionmentioning

confidence: 95%

Takotsubo Cardiomyopathy Induced by Dobutamine Infusion During Hypertensive Therapy for Symptomatic Vasospasm After Subarachnoid Hemorrhage -Case Report-

Saito

Takahashi

Noshita

et al. 2010

Neurol. Med. Chir.(Tokyo)

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A 65-year-old female with subarachnoid hemorrhage (SAH) developed takotsubo cardiomyopathy induced by dobutamine infusion for vasospasm 9 days after onset of SAH. She underwent neck clipping of the ruptured cerebral aneurysm on day 1. Course after surgery was uneventful, but she developed motor aphasia on day 9. Hypertensive therapy was carried out under the diagnosis of symptomatic vasospasm. Half an hour after initiation of dobutamine infusion at 6 mg/kg/min, sudden symptoms of takotsubo cardiomyopathy developed. Fortunately, her symptoms recovered in a few days with supportive therapy without any consequences. Takotsubo cardiomyopathy is one pattern of cardiac dysfunction occasionally encountered after SAH. Possible mechanisms of this disorder include epicardial catecholamine cardiotoxicity. Therefore, generally, cardiac function is worst at the early stage of SAH, when sympathetic activity is highest, and recovers thereafter. Dobutamine infusion seems to have triggered the takotsubo cardiomyopathy in the present patient even 9 days after onset of SAH. Inotropic agents including dobutamine are often used during the course of SAH, and since takotsubo cardiomyopathy can occur in patients with SAH, this complication must be considered.

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Estimation of Myocardial Interstitial Norepinephrine Release After Brain Death Using Cardiac Microdialysis

Cited by 129 publications

References 0 publications

Activation of the Heart by Donor Brain Death Accelerates Acute Rejection After Transplantation

Activation of the Heart by Donor Brain Death Accelerates Acute Rejection After Transplantation

Determination of myocardial norepinephrine in freely moving rats using in vivo microdialysis sampling and liquid chromatography with dual-electrode amperometric detection

Takotsubo Cardiomyopathy Induced by Dobutamine Infusion During Hypertensive Therapy for Symptomatic Vasospasm After Subarachnoid Hemorrhage -Case Report-

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