Effect of ischaemia on the adrenergic neurons of the rat heart: a fluorescence histochemical and biochemical study

Holmgren, Susanne; Abrahamsson, Tommy; Almgren, Olle; Bm, Eriksson

doi:10.1093/cvr/15.12.680

Cited by 59 publications

(28 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It has also previously been demonstrated that myocardial ischaemia causes a marked increase in noradrenaline over¯ow (Wennmalm, 1977;SchroÈ r et al, 1981a), probably due to a redistribution of noradrenaline from its storage sites in adrenergic nerve terminals into the extraneuronal space (Holmgren et al, 1981;SchroÈ r et al, 1981a;Muntz et al, 1984) which is initiated by enhanced exocytosis at short-term ischaemia (SchoÈ mig et al, 1984). This process is enhanced by nicotine (SchoÈ mig et al, 1987;KruÈ ger et al, 1995).…”

Section: Discussionmentioning

confidence: 93%

“…This catecholamine over¯ow during longer periods of ischaemia (i.e. 410 min) results in a redistribution of catecholamines in the ischaemic area of the ventricle (Holmgren et al, 1981;SchroÈ r et al, 1981a;Muntz et al, 1984) and is initiated by intraneuronal release of catecholamines from their storage vesicles (SchoÈ mig, 1990). Thus, nicotine-induced catecholamine release might stimulate the ischaemia-related catecholamine over¯ow and increase the severity of myocardial ischaemia.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Augmented myocardial ischaemia by nicotine – Mechanisms and their possible significance

Schrör

Zimmermann

Tannhäuser

1998

British J Pharmacology

View full text Add to dashboard Cite

1 To study the e ect of nicotine on the severity of experimental myocardial ischaemia, Langendor hearts of rabbits (n=7 ± 12 per group) were subjected to 2 h of low-¯ow ischaemia followed by 1 h of reperfusion. 2 Infusion of nicotine (100 ng ml 71 ) caused only minor changes in non-ischaemic conditions but a signi®cant (P50.05) increase in end-diastolic pressure (LVEDP), loss of creatine kinase (CK) and troponin (TnT) as well as increase in noradrenaline (NA) over¯ow in reperfused ischaemic hearts. 3 RT ± PCR was done on total RNA for mRNA expression of the constitutive (COX-1) and inducible cyclooxygenase (COX-2). There was no COX-2 in non-ischaemic hearts but a signi®cant expression in ischaemia (n=5) which was further increased by nicotine. These data were con®rmed at the protein level by Western blotting and additionally shown that COX-1 remained unchanged. 4 There was a marked increase in prostacyclin (PGI 2 ) and a 2 fold increase in NA over¯ow which were both stimulated by nicotine. 5 The aggravating e ects of nicotine on myocardial ischaemia (CK release) as well as the expression of COX-2 mRNA were prevented by pretreatment with the b-blocker pindolol (1 mM). 6 The data demonstrate marked deleterious actions of nicotine in reperfused ischaemic hearts. These actions are probably related to the increase in catecholamine over¯ow, are b-receptor-mediated and involve enhanced gene expression of COX-2.

show abstract

Section: Discussionmentioning

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Augmented myocardial ischaemia by nicotine – Mechanisms and their possible significance

Schrör

Zimmermann

Tannhäuser

1998

British J Pharmacology

View full text Add to dashboard Cite

show abstract

“…In skeletal muscle, morphologic evidence of ischemic damage can be seen in sympathetic nerves after 2 h of ischemia, while ischemic changes in myocytes are not evident until at least 3 h (16). In rabbit heart, partial depletion of myocardial catecholamine stores becomes evident after only 30 min of ischemia, and progresses to near total depletion after 2.5-5 h (17).…”

Section: Methodsmentioning

confidence: 98%

Reduction of sympathetic inotropic response after ischemia in dogs. Contributor to stunned myocardium.

Ciuffo¹,

Ouyang²,

Becker³

et al. 1985

J. Clin. Invest.

View full text Add to dashboard Cite

Eight open chest dogs underwent 25 min of coronary occlusion to determine whether brief myocardial ischemia disrupts the normal myocardial inotropic response to sympathetic nervous stimulation. If so, this could represent a mechanism contributing to postischemic myocardial dysfunction.Myocardial segment shortening was measured using ultrasonic dimension crystals before and after coronary artery occlusion and reperfusion. Left ansa subclavia stimulation and systemic norepinephrine (NE) infusion were used to test the myocardial inotropic response to neural stimulation and direct exposure to the sympathetic mediator, respectively.Before coronary artery occlusion, base-line preischemic segment shortening (12.5±1.6%) (SEM) increased during both sympathetic stimulation (20.2±1.4%) and NE infusion (19.7±1.1%). The control segment responded similarly. After ischemia and reperfusion there was no significant change in heart rate, aortic or left ventricular pressures, nor changes in control segment shortening. In contrast, shortening in the postischemic segment was markedly reduced compared to baseline (4.1±2.4%), and no longer responded to sympathetic stimulation (2.4±2.8%), while responsiveness to systemic NE was maintained (12.9±2.0%), P < 0.001, which suggested injury to the sympathetic-neural axis during the period of ischemia. This reduced response to neural stimulation was persistent for up to 2 h after reperfusion.Left atrial or intracoronary infusion of bretylium tosylate, which releases norepinephrine from nerve terminals, resulted in an immediate inotropic response in the postischemic segment, which indicated that total depletion of NE from nerve terminals during the Ischemic period had not occurred. Disruption of sympathetic neural responsiveness is likely a component of the mechanism of postischemic myocardial dysfunction whenever there is appreciable sympathetic drive to the heart.

show abstract

“…Postmortem analyses of infarcted human myocardium show abnormal increases in numbers of sympathetic axons adjacent to the site of injury (Cao, et al, 2000a). Ischemic injury appears to be the cause of the remodeling, as coronary artery ligation induces hyperinnervation in dogs (Lai, et al, 2000;Zhou, et al, 2004) and rats (Ahonen, et al, 1975;Paessens and Borchard, 1980;Holmgren, et al, 1981;Vracko, et al, 1990;Kaye, et al, 2000;Li, et al, 2004). Through enhanced norepinephrine-mediated myocardial depolarization, abnormally increased sympathetic nerve density may be proarrhythmogenic and represent a significant factor in post-infarct sudden cardiac death.…”

Section: Introductionmentioning

confidence: 99%

Sympathetic hyperinnervation and inflammatory cell NGF synthesis following myocardial infarction in rats

et al. 2006

View full text Add to dashboard Cite

Sympathetic hyperinnervation occurs in human ventricular tissue after myocardial infarction and may contribute to arrhythmias. Aberrant sympathetic sprouting is associated with elevated nerve growth factor (NGF) in many contexts, including ventricular hyperinnervation. However, it is unclear whether cardiomyocytes or other cell types are responsible for increased NGF synthesis. In this study, left coronary arteries were ligated and ventricular tissue examined in rats 1-28 days post-infarction. Infarct and peri-infarct tissue was essentially devoid of sensory and parasympathetic nerves at all time points. However, areas of increased sympathetic nerve density were observed in the peri-infarct zone between post-ligation days 4-14. Hyperinnervation occurred in regions containing accumulations of macrophages and myofibroblasts. To assess whether these inflammatory cells synthesize NGF, sections were processed for NGF in situ hybridization and immunohistochemistry. Both macrophage1 antigen-positive macrophages and α-smooth muscle actin immunoreactive myofibroblasts expressed NGF in areas where they were closely proximate to sympathetic nerves. To investigate whether NGF produced by peri-infarct cells induces sympathetic outgrowth, we cocultured adult sympathetic ganglia with peri-infarct explants. Neurite outgrowth from sympathetic ganglia was significantly greater at post-ligation days 7-14 as compared to control tissue. Addition of an NGF function-blocking antibody prevented the increased neurite outgrowth induced by periinfarct tissue. These findings provide evidence that inflammatory cell NGF synthesis plays a causal role in sympathetic hyperinnervation following myocardial infarction.

show abstract

Effect of ischaemia on the adrenergic neurons of the rat heart: a fluorescence histochemical and biochemical study

Cited by 59 publications

References 0 publications

Augmented myocardial ischaemia by nicotine – Mechanisms and their possible significance

Augmented myocardial ischaemia by nicotine – Mechanisms and their possible significance

Reduction of sympathetic inotropic response after ischemia in dogs. Contributor to stunned myocardium.

Sympathetic hyperinnervation and inflammatory cell NGF synthesis following myocardial infarction in rats

Contact Info

Product

Resources

About