Elevated Circulating Levels of Basic Fibroblast Growth Factor and Vascular Endothelial Growth Factor in Patients With Acute Myocardial Infarction

Tamura, Ken; Nakajima, Hitoshi; Rakue, Hiroyuki; Sasame, Atsuko; Naito, Yuichi; Nagai, Yoshiko; Ibukiyama, Chiharu

doi:10.1253/jcj.63.357

Cited by 32 publications

(20 citation statements)

References 36 publications

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“…This angiogenic response is dependent on VEGF (35,74). It has been documented that after myocardial infarction the VEGF is increased in the surviving myocardium (29,39,64,66) as observed in the current study. Despite the increase of VEGF in HF rats, previous studies have shown that neovascularization in the surviving myocardium is not able to maintain the adequate tissue perfusion (32,33).…”

Section: Discussionsupporting

confidence: 80%

Increase in parasympathetic tone by pyridostigmine prevents ventricular dysfunction during the onset of heart failure

Lataro¹,

Silva²,

Fazan³

et al. 2013

American Journal of Physiology-Regulatory, Integrative and Comp

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Lataro RM, Silva CA, Fazan R Jr, Rossi MA, Prado CM, Godinho RO, Salgado HC. Increase in parasympathetic tone by pyridostigmine prevents ventricular dysfunction during the onset of heart failure. Am J Physiol Regul Integr Comp Physiol 305: R908 -R916, 2013. First published August 28, 2013 doi:10.1152/ajpregu.00102.2013.-Heart failure (HF) is characterized by elevated sympathetic activity and reduced parasympathetic control of the heart. Experimental evidence suggests that the increase in parasympathetic function can be a therapeutic alternative to slow HF evolution. The parasympathetic neurotransmission can be improved by acetylcholinesterase inhibition. We investigated the long-term (4 wk) effects of the acetylcholinesterase inhibitor pyridostigmine on sympathovagal balance, cardiac remodeling, and cardiac function in the onset of HF following myocardial infarction. Myocardial infarction was elicited in adult male Wistar rats. After 4 wk of pyridostigmine administration, per os, methylatropine and propranolol were used to evaluate the cardiac sympathovagal balance. The tachycardic response caused by methylatropine was considered to be the vagal tone, whereas the bradycardic response caused by propranolol was considered to be the sympathetic tone. In conscious HF rats, pyridostigmine reduced the basal heart rate, increased vagal, and reduced sympathetic control of heart rate. Pyridostigmine reduced the myocyte diameter and collagen density of the surviving left ventricle. Pyridostigmine also increased vascular endothelial growth factor protein in the left ventricle, suggesting myocardial angiogenesis. Cardiac function was assessed by means of the pressure-volume conductance catheter system. HF rats treated with pyridostigmine exhibited a higher stroke volume, ejection fraction, cardiac output, and contractility of the left ventricle. It was demonstrated that the long-term administration of pyridostigmine started right after coronary artery ligation augmented cardiac vagal and reduced sympathetic tone, attenuating cardiac remodeling and left ventricular dysfunction during the progression of HF in rats.

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Section: Discussionsupporting

confidence: 80%

Increase in parasympathetic tone by pyridostigmine prevents ventricular dysfunction during the onset of heart failure

Lataro¹,

Silva²,

Fazan³

et al. 2013

American Journal of Physiology-Regulatory, Integrative and Comp

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“…As previously noted, MI is associated with upregulation of VEGF, bFGF, hepatocyte growth factor, [25][26][27][28][29][30][31] and VEGF receptors Flt-1 and Flk-1 28 in the surviving myocardium. These growth factor responses promote some limited degree of angiogenesis in the infarcted heart.…”

Section: Angiogenic Growth Factors and Their Receptorsmentioning

confidence: 55%

Bradycardia Induces Angiogenesis, Increases Coronary Reserve, and Preserves Function of the Postinfarcted Heart

Zhou

Zheng

et al. 2004

Circulation

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Background-We tested the hypothesis that induction of chronic bradycardia would trigger an upregulation of key growth factors and receptors, which would then lead to angiogenesis and improve coronary reserve in the left ventricle after myocardial infarction. Methods and Results-Bradycardia was induced in rats by administering alinidine via osmotic pumps beginning 1 day after coronary artery ligation. Echocardiographic analysis was conducted before and after treatment. Morphometric analysis was used in perfusion-fixed hearts to document arteriolar and capillary growth. Western blots were used to evaluate growth factor and receptor changes. During the first week of treatment, vascular endothelial growth factor (VEGF), VEGF receptor 1 (Flt-1), and basic fibroblast growth factor proteins were higher in the treated group, whereas VEGF receptor 2 (Flk-1), angiopoietin-1, and angiopoietin-2 were not affected by treatment. After 3 weeks, VEGF protein remained elevated, and bradycardia was associated with a higher capillary length density in the border (40%) and remote (14%) regions and a higher arteriolar length density in the septum (62%), despite a greater increase in left ventricular mass. Although arteriolar length density increased in all size classes, the greatest increase occurred in the smallest (terminal) arterioles. This vascular growth was associated with a 23% greater coronary reserve. Echocardiography revealed a smaller increase in ventricular volume and a greater preservation of ejection fraction in rats treated with bradycardia. Conclusions-Pharmacologic induction of bradycardia enhances vascularity and coronary reserve, preserves function of surviving myocardium, and therefore, is a noninvasive, therapeutic avenue that provides an alternative to gene therapy.

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“…However, Kranz et al recently reported that the serum VEGF concentration was similar in samples taken from the CS, 32 which disagrees with our results. In their study only 6 patients' samples were taken simultaneously from the CS, and they did not report whether or not heparin, which can reduce VEGF concentration, 31 was used before cannulation; this impedes analysis of the differences in results between studies.…”

Section: Cardiac Secretion Of Hgf and Vegf In Amimentioning

confidence: 99%

Serum Hepatocyte Growth Factor Predicts Ventricular Remodeling Following Myocardial Infarction.

Soeki

Tamura

Shinohara

et al. 2002

Circ J

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Elevated Circulating Levels of Basic Fibroblast Growth Factor and Vascular Endothelial Growth Factor in Patients With Acute Myocardial Infarction

Cited by 32 publications

References 36 publications

Increase in parasympathetic tone by pyridostigmine prevents ventricular dysfunction during the onset of heart failure

Increase in parasympathetic tone by pyridostigmine prevents ventricular dysfunction during the onset of heart failure

Bradycardia Induces Angiogenesis, Increases Coronary Reserve, and Preserves Function of the Postinfarcted Heart

Serum Hepatocyte Growth Factor Predicts Ventricular Remodeling Following Myocardial Infarction.

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