Neuroendocrine activation after acute myocardial infarction.

McAlpine, Howard M.; Morton, J. J.; Leckie, Brenda J.; Rumley, Ann; Gillen, G.; Dargie, Henry J.

doi:10.1136/hrt.60.2.117

Cited by 183 publications

(68 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…33,34 In addition, angiotensin II and -or -adrenergic agonists activate myocardial MAPKs in the in-vivo rat heart. 35 Therefore, the activation of MAPKs in the noninfarcted LV and RV may be partially mediated by neurohumoral factors.…”

Section: Discussionmentioning

confidence: 99%

Activation of Mitogen-Activated Protein Kinases in the Non-Ischemic Myocardium of an Acute Myocardial Infarction in Rats.

Yoshida¹,

Yoshiyama²,

Omura³

et al. 2001

Jpn Circ J

View full text Add to dashboard Cite

fter myocardial infarction (MI), contractile impairment in the ischemic myocardium (IM) occurs suddenly and the non-ischemic myocardium adapts to the increased workload. Thereafter, the myocardial properties and morphology begin to change as the ventricular remodeling during the clinical course. The ventricular remodeling is accompanied by progressive chamber dilatation and subsequently an increased incidence of sudden death and congestive heart failure. [1][2][3][4][5] In the IM, the structural rearrangement is characterized by myocardial cell damage, inflammatory change and expression of extracellular matrix components. Furthermore, ventricular dilatation and myocardial hypertrophy can occur in the non-ischemic regions. 6 The process of ventricular remodeling after an acute myocardial infarction (AMI) involves topographical alternations in the ischemic and non-ischemic regions, 1,2 so an understanding of the myocardial response to AMI is important for appropriate therapeutic management.We previously reported that mitogen-activated protein kinases (MAPKs) are rapidly activated in the IM, followed by activation of transcriptional factors of activator protein 1 (AP-1) and mRNA expression of transforming growth factor -1, collagen types I and III, -myosin heavy chain, -skeletal actin and atrial natriuretic peptide. 7,8 MAPKs are a ubiquitous group of protein serine/threonine kinases and are important mediators of the signal transduction pathways responsible for cell growth, proliferation and apoptosis. [9][10][11][12] Therefore, this signal transduction system may be a key regulatory mechanism allowing cells to respond and eventually adapt to changes in myocardial ischemia. Although enhanced expression of the mRNAs was also observed in the non-ischemic region of the acutely infarcted heart, 7,8,13 the corresponding activities of MAPKs in that region are still unknown. The present study investigated whether the signal-transduction pathway of the non-ischemic myocardium shifted to ventricular remodeling after AMI by examining the myocardial activities of extracellular signal-regulated kinases (ERKs), c-Jun NH2 terminal kinases (JNKs) and p38MAPK, plus the AP-1 DNA binding activities in both the ischemic and non-ischemic regions of an infarcted rat heart. Furthermore, to clarify the possible cause of MAPKs activation, we measured the geometrical changes of the infarcted heart using echocardiography and then estimated the stretch and workload of the infarcted heart. Methods Production of the AMIMale Wistar rats weighing 290-310g (Clea Japan, Osaka, Japan) were used in the experiments. Myocardial infarction was produced as described previously. 7,8,14 Briefly, the rats were anesthetized by intraperitoneal injection of pentobarbital sodium (35 mg/kg). After intratracheal intubation, a left thoracotomy was performed under volume-controlled Activation of Mitogen-Activated Protein Kinases in the Non-Ischemic Myocardium of an Acute Myocardial Infarction in RatsKen Yoshida, MD; Minoru Yoshiyama, MD; Takashi Omura, MD; Yasuh...

show abstract

Section: Discussionmentioning

confidence: 99%

Activation of Mitogen-Activated Protein Kinases in the Non-Ischemic Myocardium of an Acute Myocardial Infarction in Rats.

Yoshida¹,

Yoshiyama²,

Omura³

et al. 2001

Jpn Circ J

View full text Add to dashboard Cite

show abstract

“…There are several lines of evidence which indicate that neurohumoral factors, such as the renin-angiotensin system and catecholamines, are activated during AMI in humans and play an important role in cardiac remodeling and/or the prognosis after AMI. 14,15) In addition, angiotensin II and kappa-opioid receptor stimulation regulate myocardial NHE1 in the in vivo rat heart. 3, 16,17) Thus, the regulation of NHE1 in non-infarcted myocardium may be partially mediated by neurohumoral factors, such as the renin-angiotensin system.…”

Section: )mentioning

confidence: 99%

Decreased Expression of Na+/H+ Exchanger Isoform 1 (NHE1) in Non-infarcted Myocardium after Acute Myocardial Infarction.

et al. 2002

View full text Add to dashboard Cite

SUMMARYAlthough cardiac NHE1 is activated during myocardial ischemia and reperfusion injury, little is known about changes in expression in non-infarcted myocardium after acute myocardial infarction (AMI). The purpose of this study was to examine left ventricular function and region dependent NHE1 expression after myocardial infarction. Therefore, we produced two AMI models in rats, a small infarction model which was continuously ligated at the branches of the left coronary artery, and an extensive infarction model continuously ligated at the root of the artery. We examined NHE1 mRNA expression using RNase protection assay and protein levels using Western blot analysis in noninfarcted myocardium during the 24 hour period after AMI. The level of NHE1 mRNA and protein expression in the whole heart including the infarcted myocardium did not change after a small infarction. On the other hand, in the case of an extensive infarction, the levels of NHE1 mRNA and protein expression decreased significantly by 21.5% (P<0.05) and by 22.0% (P<0.05), respectively, in non-infarcted myocardium. Left ventricular systolic pressure (LVSP) decreased significantly by 13% and 38% with the branch and root ligation, respectively. However, left ventricular end-diastolic pressure (LVEDP) only increased with the root ligation. These results indicate that NHE1 expression decreased in response to extensive myocardial infarction only in non-infarcted myocardium. The present study may be important in furthering the understanding of NHE1 in myocardial infarction and suggests that decreased expression of NHE1 in non-infarcted myocardium may decrease the extent of cardiac cell injury. (Jpn Heart J 2002; 43: 273-282)

show abstract

“…10,11 In this setting, vasopressin levels increase concomitantly with the activation of other neurohormones such as renin and norepinephrine. 12 However, vasopressin level does not correlate with serum osmolarity in myocardial infarction, suggesting that nonosmotic mechanisms are involved. In patients with myocardial infarction, hyponatremia may be aggravated further by the concomitant activation of the renin-angiotensin system and increased catecholamine production.…”

Section: Discussionmentioning

confidence: 99%

A Prospective Study of in Hospital Outco Me of Acute Phase of Ste Mi With Hyponatremia

Harsoor¹,

Kinagi²,

Afiya³

2014

jemds

View full text Add to dashboard Cite

BACKGROUND AND OBJECTIVE:In acute STEMI, due to activation of the Baro receptors, there is activation of the sympathetic nervous system. This leads to release of hormones like vasopressin and also activation of renin angiotensin system. Magnitude of this neurohormonal change is related to the severity of the myocardial damage. Hyponatremia is a reflection of these hormonal changes. So serum Na+ level may be an indicator of the severity of ST elevation MI (STEMI). The aim of this study is to evaluate in hospital prognosis of acute ST segment elevation myocardial infarction with Hyponatremia. MATERIAL AND METHODS: This prospective observational study was conducted in patients presenting with acute ST-elevation myocardial infarction admitted in ICCU, Basaveshwar Teaching and General Hospital, Gulbarga attached to Mahadevappa Rampure Medical College during the period of Jan 2013 to July 2014.Qualifying patients underwent detailed history and clinical examination. Plasma sodium concentrations were obtained on admission and at 24, 48 and 72 hours thereafter. Study population were grouped into two groups, 50 patients with hyponatraemia were included in Group-I and 50 patients with normal plasma sodium level were in Group-II. Hyponatremia defined as plasma sodium level less than 135 mmol/L. In hospital outcome of these two groups of patients were evaluated and compared. RESULTS: The hypo and normo natremic groups were comparable with respect to baseline characteristics and in-hospital management. There was no statistically significant difference between the two groups regarding the incidence of risk factors of IHD. Hyponatremics had higher rates of in-hospital mortality (24%vs 6%p<0.01) composite of death, heart failure (72% vs. 36%, p=0.05) and arrhythmias (30% vs 6% p<0.01) Anterior myocardial infarction was more frequent in patients with hyponatremia, who showed advanced Killip class. After adjustment for covariates, hyponatremia was independently correlated with in-hospital mortality. CONCLUSION: Hyponatremia on admission in patients with acute ST Elevation MI is a strong independent predictor of prognosis and sodium levels may serve as a simple marker to identify patient at high risk.

show abstract

Neuroendocrine activation after acute myocardial infarction.

Cited by 183 publications

References 40 publications

Activation of Mitogen-Activated Protein Kinases in the Non-Ischemic Myocardium of an Acute Myocardial Infarction in Rats.

Activation of Mitogen-Activated Protein Kinases in the Non-Ischemic Myocardium of an Acute Myocardial Infarction in Rats.

Decreased Expression of Na+/H+ Exchanger Isoform 1 (NHE1) in Non-infarcted Myocardium after Acute Myocardial Infarction.

A Prospective Study of in Hospital Outco Me of Acute Phase of Ste Mi With Hyponatremia

Contact Info

Product

Resources

About