@2024 Afarand., IRAN
ISSN: 2252-0805 The Horizon of Medical Sciences 2016;22(3):209-214
ISSN: 2252-0805 The Horizon of Medical Sciences 2016;22(3):209-214
Preventive Effects of Beta-Hydroxy-Beta-Methyl Butyrate On Cardiac Arrhythmias in Rats
ARTICLE INFO
Article Type
Original ResearchAuthors
Ravanbakhsh N. (1)Torabi N. (2)
Foadoddini M. (*)
(*) Atherosclerosis & Coronary Research Center, Birjand University of Medical Sciences, Birjand, Iran
(1) Medical Faculty, Birjand University of Medical Sciences, Birjand, Iran
(2) Physiology Department, Medical Faculty, Birjand University of Medical Sciences, Birjand, Iran
Correspondence
Address: Atherosclerosis & Coronary Research Center, Birjand University of Medical Sciences, Ghaffari Street, Birjand, Iran. Postal Code: 97178 53577Phone: +985632440488
Fax: +985632440488
foadmohsen@yahoo.com
Article History
Received: October 16, 2015Accepted: May 10, 2016
ePublished: June 30, 2016
ABSTRACT
Aims
One of the major factors in sudden cardiac arrest is the initiation and continuation of deadly arrhythmias during ischemia. It is known that beta-hydroxy-beta-methylbutyrate (HMB) has useful effects such as anti-inflammatory and anti-apoptosis effects in the skeletal muscles. The aim of this study was to investigate the preventive effects of HMB on the ventricular arrhythmias due to the ischemia.
Materials & Methods In the experimental study, 30 Wistar male rats were randomly divided into three groups including control, HMB320, and HMB700. As control group received normal saline, HMB320 and HMB700 groups orally received 320 and 700 mg/Kg HMB as gavage for 2 weeks, respectively. The rats, having been anesthetized, underwent 30-minute ischemia. Then, the numbers of premature ventricular contractions (PVC), the appearance duration of ventricular tachycardia (VT), and the ventricular fibrillation (VF) were assessed. Data was analyzed by SPSS 16 software using Kruskal-Walis, one-way ANOVA, Tukey’s post-hoc, and Chi-square tests.
Findings There was a significant reduction in the mean PVC number in HMB320 and HMB700 groups than control group (p=0.001). In addition, there was such a significant difference between the groups received the doses (p=0.008). There was a reduction in the mean appearance duration of VT in HMB320 and HMB700 groups than control group (p=0.001). There was a significant reduction in the mean appearance duration of VF in HMB700 group compared to control group, only (p=0.003).
Conclusion Through arrhythmias reduction, 2-week preventive consumption of HMB might considerably reduce the severe side effects of ischemia.
Materials & Methods In the experimental study, 30 Wistar male rats were randomly divided into three groups including control, HMB320, and HMB700. As control group received normal saline, HMB320 and HMB700 groups orally received 320 and 700 mg/Kg HMB as gavage for 2 weeks, respectively. The rats, having been anesthetized, underwent 30-minute ischemia. Then, the numbers of premature ventricular contractions (PVC), the appearance duration of ventricular tachycardia (VT), and the ventricular fibrillation (VF) were assessed. Data was analyzed by SPSS 16 software using Kruskal-Walis, one-way ANOVA, Tukey’s post-hoc, and Chi-square tests.
Findings There was a significant reduction in the mean PVC number in HMB320 and HMB700 groups than control group (p=0.001). In addition, there was such a significant difference between the groups received the doses (p=0.008). There was a reduction in the mean appearance duration of VT in HMB320 and HMB700 groups than control group (p=0.001). There was a significant reduction in the mean appearance duration of VF in HMB700 group compared to control group, only (p=0.003).
Conclusion Through arrhythmias reduction, 2-week preventive consumption of HMB might considerably reduce the severe side effects of ischemia.
CITATION LINKS
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[2]Holleyman CR, Larson DF. Apoptosis in the ischemic reperfused myocardium. Perfus. 2001;16(6):491-502.
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[5] Cascio WE, Yang H, Muller-Borer BJ, Johnson TA. Ischemia-induced arrhythmia: the role of connexins, gap junctions, and attendant changes in impulse propagation. J Electrocardiol. 2005;38(Suppl 4):55-9.
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[7]Nissen SL, Abumrad NN. Nutritional role of the leucine metabolite β-hydroxy β-methylbutyrate (HMB). J Nutr Biochem. 1997;8(6):300-11.
[8]Pimentel GD, Rosa JC, Lira FS, Zanchi NE, Ropelle ER, Oyama LM, et al. β-Hydroxy-β-methylbutyrate (HMβ) supplementation stimulates skeletal muscle hypertrophy in rats via the mTOR pathway. Nutr Metab. 2011;8:11.
[9]Gerlinger-Romero F, Guimarães-Ferreira L, Giannocco G, Nunes MT. Chronic supplementation of beta-hydroxy-beta methylbutyrate (HMβ) increases the activity of the GH/IGF-I axis and induces hyperinsulinemia in rats. Growth Horm IGF Res. 2011;21(2):57-62.
[10]Sack MN, Yellon DM. Insulin therapy as an adjunct toreperfusion after acute coronary ischemia: A proposed direct myocardial cell survival effect independent of metabolic modulation. J Am Coll Cardiol. 2003;41(8):1404-7.
[11]Buerke M, Murohara T, Skurk C, Nuss C, Tomaselli K, Lefer AM. Cardioprotective effect of insulin-like growth factor I in myocardial ischemia followed by reperfusion. Proc Natl Acad Sci. 1995;92(17):8031-5.
[12]Vulcan PR. Role of β-Hydroxy-β-methylbutyrate (HMB) on inflammation after eccentric exercise [Dissertation]. Iowa: Iowa State University; 2012.
[13]Hsieh L, Chien SL, Huang MS, Tseng HF, Chang CK. Anti-inflammatory and anticatabolic effects of short-term beta-hydroxy-beta-methylbutyrate supplementation on chronic obstructive pulmonary disease patients in intensive care unit. Asia Pac J Clin Nutr. 2006;15(4):544-50.
[14]Stancliffe RA, Zemel MB. Role of β-Hydroxy-β-methylbutyrate (HMB) in leucine stimulation of muscle mitochondrial biogenesis. Faseb J. 2012;26(Suppl 1):251-6.
[15]Kornasio R, Riederer I, Butler-Browne G, Mouly V, Uni Z, Halevy O. β-hydroxy-β-methylbutyrate (HMB) stimulates myogenic cell proliferation, differentiation and survival via the MAPK/ERK and PI3K/Akt pathways. Biochim Biophys Acta. 2009;1793(5):755-63.
[16]Hausenloy DJ, Yellon DM. New directions for protecting the heart against ischemia–reperfusion injury: targeting the Reperfusion Injury Salvage Kinase (RISK)-pathway. Cardiovasc Res. 2004;61(3):448-60.
[17]Nissen S, Sharp RL, Panton L, Vukovich M, Trappe S, Fuller JC. β-Hydroxy-β-methylbutyrate (HMB) supplementation in humans is safe and may decrease cardiovascular risk factors. J Nutr. 2000;130(8):1937-45.
[18]Walker MJ, Curtis MJ, Hearse DJ, Campbell RW, Janse MJ, Yellon DM, et al. The Lambeth Conventions: guidelines for the study of arrhythmias in ischemia, infarction, and reperfusion. Cardiovasc Res. 1988;22(7):447-55.
[19]Foadoddini M, Esmailidehaj M, Mehrani H, Sadraei SH, Golmanesh L, Wahhabaghai H, et al. Pretreatment with hyperoxia reduces in vivo infarct size and cell death by apoptosis with an early and delayed phase of protection. Eur J Cardiothorac Surg. 2011;39(2):233-40.
[20]Dwivedi VK, Chandra M, Misra PC, Misra A, Misra MK. Status of some free radical scavenging enzymes in the blood of myocardial infarction patients. J Enzyme Inhib Med Chem. 2006;21(1):43-6.
[21]Chaudhuri A, Janicke D, Wilson MF, Tripathy D, Garg R, Bandyopadhyay A, et al. Anti-inflammatory and profibrinolytic effect of insulin in acute ST-segment–elevation myocardial infarction. Circ. 2004;109(7):849-54.
[2]Holleyman CR, Larson DF. Apoptosis in the ischemic reperfused myocardium. Perfus. 2001;16(6):491-502.
[3] Fliss H, Gattinger D. Apoptosis in ischemic and reperfused rat myocardium. Circ Res. 1996;79(5):949-56.
[4]Buja LM. Myocardial ischemia and reperfusion injury. Cardiovasc Pathol. 2005;14(4):170-5.
[5] Cascio WE, Yang H, Muller-Borer BJ, Johnson TA. Ischemia-induced arrhythmia: the role of connexins, gap junctions, and attendant changes in impulse propagation. J Electrocardiol. 2005;38(Suppl 4):55-9.
[6]Zweier JL. Measurement of superoxide-derived free radicals in the reperfused heart. Evidence for a free radical mechanism of reperfusion injury. J Biol Chem. 1988;263(3):1353-7.
[7]Nissen SL, Abumrad NN. Nutritional role of the leucine metabolite β-hydroxy β-methylbutyrate (HMB). J Nutr Biochem. 1997;8(6):300-11.
[8]Pimentel GD, Rosa JC, Lira FS, Zanchi NE, Ropelle ER, Oyama LM, et al. β-Hydroxy-β-methylbutyrate (HMβ) supplementation stimulates skeletal muscle hypertrophy in rats via the mTOR pathway. Nutr Metab. 2011;8:11.
[9]Gerlinger-Romero F, Guimarães-Ferreira L, Giannocco G, Nunes MT. Chronic supplementation of beta-hydroxy-beta methylbutyrate (HMβ) increases the activity of the GH/IGF-I axis and induces hyperinsulinemia in rats. Growth Horm IGF Res. 2011;21(2):57-62.
[10]Sack MN, Yellon DM. Insulin therapy as an adjunct toreperfusion after acute coronary ischemia: A proposed direct myocardial cell survival effect independent of metabolic modulation. J Am Coll Cardiol. 2003;41(8):1404-7.
[11]Buerke M, Murohara T, Skurk C, Nuss C, Tomaselli K, Lefer AM. Cardioprotective effect of insulin-like growth factor I in myocardial ischemia followed by reperfusion. Proc Natl Acad Sci. 1995;92(17):8031-5.
[12]Vulcan PR. Role of β-Hydroxy-β-methylbutyrate (HMB) on inflammation after eccentric exercise [Dissertation]. Iowa: Iowa State University; 2012.
[13]Hsieh L, Chien SL, Huang MS, Tseng HF, Chang CK. Anti-inflammatory and anticatabolic effects of short-term beta-hydroxy-beta-methylbutyrate supplementation on chronic obstructive pulmonary disease patients in intensive care unit. Asia Pac J Clin Nutr. 2006;15(4):544-50.
[14]Stancliffe RA, Zemel MB. Role of β-Hydroxy-β-methylbutyrate (HMB) in leucine stimulation of muscle mitochondrial biogenesis. Faseb J. 2012;26(Suppl 1):251-6.
[15]Kornasio R, Riederer I, Butler-Browne G, Mouly V, Uni Z, Halevy O. β-hydroxy-β-methylbutyrate (HMB) stimulates myogenic cell proliferation, differentiation and survival via the MAPK/ERK and PI3K/Akt pathways. Biochim Biophys Acta. 2009;1793(5):755-63.
[16]Hausenloy DJ, Yellon DM. New directions for protecting the heart against ischemia–reperfusion injury: targeting the Reperfusion Injury Salvage Kinase (RISK)-pathway. Cardiovasc Res. 2004;61(3):448-60.
[17]Nissen S, Sharp RL, Panton L, Vukovich M, Trappe S, Fuller JC. β-Hydroxy-β-methylbutyrate (HMB) supplementation in humans is safe and may decrease cardiovascular risk factors. J Nutr. 2000;130(8):1937-45.
[18]Walker MJ, Curtis MJ, Hearse DJ, Campbell RW, Janse MJ, Yellon DM, et al. The Lambeth Conventions: guidelines for the study of arrhythmias in ischemia, infarction, and reperfusion. Cardiovasc Res. 1988;22(7):447-55.
[19]Foadoddini M, Esmailidehaj M, Mehrani H, Sadraei SH, Golmanesh L, Wahhabaghai H, et al. Pretreatment with hyperoxia reduces in vivo infarct size and cell death by apoptosis with an early and delayed phase of protection. Eur J Cardiothorac Surg. 2011;39(2):233-40.
[20]Dwivedi VK, Chandra M, Misra PC, Misra A, Misra MK. Status of some free radical scavenging enzymes in the blood of myocardial infarction patients. J Enzyme Inhib Med Chem. 2006;21(1):43-6.
[21]Chaudhuri A, Janicke D, Wilson MF, Tripathy D, Garg R, Bandyopadhyay A, et al. Anti-inflammatory and profibrinolytic effect of insulin in acute ST-segment–elevation myocardial infarction. Circ. 2004;109(7):849-54.