Evaluation of the Cardioprotective Effect of Granulocyte Colony Stimulating Factor in Patients with Carbon Monoxide Poisoning

Author:

Pourtaji Atena1ORCID,Sahebkar Amirhossein2ORCID,Poorzand Hoorak3ORCID,Moshiri Mohammad4ORCID,Mohammadpour Amir Hooshang5ORCID,Mousavi Seyed Reza4ORCID

Affiliation:

1. Pharmaceutical Research Center, Department of Pharmacodynamics and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran

2. Biotechnology Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran

3. Atherosclerosis Prevention Research Center, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran

4. Medical Toxicology Research Center, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran

5. Pharmaceutical Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran

Abstract

Background: Carbon monoxide (CO), which is well known as silent killer, has many toxic effects on organs with high rate of metabolism such as heart and brain. CO-induced cardiotoxicity resulted in a wide range of disabilities including electrocardiogram (ECG) abnormalities, elevation in level of cardiac enzymes, arrhythmias, impairment of left ventricular and myocardial infarction (MI). Cardio-protective effects of Granulocyte colony-stimulating factor (G-CSF) on infarcted heart was proved previously in various reports. Objective: In this study, possible effect of G-CSF on cardiac function of patients with moderate to severe acute CO poisoning was investigated. Methods: Cardioprotective effects of G-CSF in CO-poisoned patients was evaluated through ECG, Holter monitoring, echocardiography, and biochemical studies. Continuous intravenous infusion of G-CSF (90 µg/kg) and normal saline were administered respectively to treatment and placebo groups. Results: The results demonstrated that in moderate to severe CO poisoning, myocardial injury is common. ECG changes (e.g., ST-segment and T-wave changes, QTC), cardiac arrhythmias (e.g., heart blocks and ventricular arrhythmias), serum level of Troponin I, left ventricular ejection fraction were determined after G-CSF administration. Frequencies of ST depression, inversion or flatting of T wave and QTC in ECG were significantly reduced after G-CSF treatment. In addition, incidence of cardiac arrhythmias due to CO poisoning were reduced after G-CSF treatment. However, G-CSF did not exert protective effects on TPI level and function of left ventricular in CO-poisoned patients. Conclusion: GCSF could probably reduce CO-induced cardiac ischemia in patients with acute CO poisoning.

Funder

Mashhad University of Medical Sciences

Publisher

Bentham Science Publishers Ltd.

Subject

Biochemistry,General Medicine,Structural Biology

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