Novel monohydroxamate drugs attenuate myocardial reperfusion-induced arrhythmias

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Novel monohydroxamate drugs attenuate myocardial reperfusion-induced arrhythmias. / Collis, C S; Rice-Evans, C; Davies, Michael Jonathan.

In: International Journal of Biochemistry & Cell Biology, Vol. 28, No. 4, 04.1996, p. 405-13.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Collis, CS, Rice-Evans, C & Davies, MJ 1996, 'Novel monohydroxamate drugs attenuate myocardial reperfusion-induced arrhythmias', International Journal of Biochemistry & Cell Biology, vol. 28, no. 4, pp. 405-13.

APA

Collis, C. S., Rice-Evans, C., & Davies, M. J. (1996). Novel monohydroxamate drugs attenuate myocardial reperfusion-induced arrhythmias. International Journal of Biochemistry & Cell Biology, 28(4), 405-13.

Vancouver

Collis CS, Rice-Evans C, Davies MJ. Novel monohydroxamate drugs attenuate myocardial reperfusion-induced arrhythmias. International Journal of Biochemistry & Cell Biology. 1996 Apr;28(4):405-13.

Author

Collis, C S ; Rice-Evans, C ; Davies, Michael Jonathan. / Novel monohydroxamate drugs attenuate myocardial reperfusion-induced arrhythmias. In: International Journal of Biochemistry & Cell Biology. 1996 ; Vol. 28, No. 4. pp. 405-13.

Bibtex

@article{9e4f49ea42a8462eac34f83290e487c2,
title = "Novel monohydroxamate drugs attenuate myocardial reperfusion-induced arrhythmias",
abstract = "The novel monohydroxamates N-methyl hexanoylhydroxamic acid, N-methyl acetohydroxamic acid, and N-methyl butyrohydroxamic acid have antioxidant and iron chelating properties. They attenuated reperfusion-induced contractile dysfunction following long periods of ischaemia (50 min) in the isolated rat heart. Here we compare their effects and that of the trihydroxamate desferrioxamine on reperfusion-induced arrhythmias following short duration ischaemia (10 min). Isolated rat hearts were perfused by the Langendorff method, subjected to regional ischaemia and reperfusion. Arrhythmias induced during the first 5 min of reperfusion were quantified. Drugs (all at 150 microM) were introduced during the last 2 min of ischaemia and remained throughout reperfusion. Although the monohydroxamate- and desferrioxamine-treated hearts showed a reduction in the incidence of ventricular tachycardia and fibrillation, only the reduction in the incidence of sustained fibrillation ( > 3 min duration) in N-methyl acetohydroxamic acid--(27{\%}), N-methyl hexanoylhydroxamic acid--(27{\%}) and desferrioxamine-treated hearts (20{\%}) was statistically significant (p < 0.05 vs control 73{\%}; n = 15). There was a reduction in the severity of the arrhythmias, manifest as a significant increase in the duration of sinus rhythm in all the monohydroxamate-treated hearts, and a significant reduction (vs control 218 +/- 29 s; mean +/- SEM) in the duration of ventricular fibrillation in hearts treated with N-methyl acetohydroxamic acid (101 +/- 31 s) and desferrioxamine (112 +/- 30 s). This improvement was offset by an increase in the duration of ventricular tachycardia, in hearts treated with N-methyl acetohydroxamic acid, N-methyl butyrohydroxamic acid and desferrioxamine. These results suggest that these novel monohydroxamates, particularly N-methyl acetohydroxamic acid, attenuate reperfusion-induced arrhythmias in this model when introduced during the ischaemic period.",
keywords = "Animals, Anti-Arrhythmia Agents, Cardiotonic Agents, Electrocardiography, Hemodynamics, Hydroxamic Acids, In Vitro Techniques, Male, Molecular Structure, Myocardial Contraction, Myocardial Reperfusion Injury, Rats, Rats, Wistar, Ventricular Fibrillation",
author = "Collis, {C S} and C Rice-Evans and Davies, {Michael Jonathan}",
year = "1996",
month = "4",
language = "English",
volume = "28",
pages = "405--13",
journal = "International Journal of Biochemistry & Cell Biology",
issn = "1357-2725",
publisher = "Elsevier",
number = "4",

}

RIS

TY - JOUR

T1 - Novel monohydroxamate drugs attenuate myocardial reperfusion-induced arrhythmias

AU - Collis, C S

AU - Rice-Evans, C

AU - Davies, Michael Jonathan

PY - 1996/4

Y1 - 1996/4

N2 - The novel monohydroxamates N-methyl hexanoylhydroxamic acid, N-methyl acetohydroxamic acid, and N-methyl butyrohydroxamic acid have antioxidant and iron chelating properties. They attenuated reperfusion-induced contractile dysfunction following long periods of ischaemia (50 min) in the isolated rat heart. Here we compare their effects and that of the trihydroxamate desferrioxamine on reperfusion-induced arrhythmias following short duration ischaemia (10 min). Isolated rat hearts were perfused by the Langendorff method, subjected to regional ischaemia and reperfusion. Arrhythmias induced during the first 5 min of reperfusion were quantified. Drugs (all at 150 microM) were introduced during the last 2 min of ischaemia and remained throughout reperfusion. Although the monohydroxamate- and desferrioxamine-treated hearts showed a reduction in the incidence of ventricular tachycardia and fibrillation, only the reduction in the incidence of sustained fibrillation ( > 3 min duration) in N-methyl acetohydroxamic acid--(27%), N-methyl hexanoylhydroxamic acid--(27%) and desferrioxamine-treated hearts (20%) was statistically significant (p < 0.05 vs control 73%; n = 15). There was a reduction in the severity of the arrhythmias, manifest as a significant increase in the duration of sinus rhythm in all the monohydroxamate-treated hearts, and a significant reduction (vs control 218 +/- 29 s; mean +/- SEM) in the duration of ventricular fibrillation in hearts treated with N-methyl acetohydroxamic acid (101 +/- 31 s) and desferrioxamine (112 +/- 30 s). This improvement was offset by an increase in the duration of ventricular tachycardia, in hearts treated with N-methyl acetohydroxamic acid, N-methyl butyrohydroxamic acid and desferrioxamine. These results suggest that these novel monohydroxamates, particularly N-methyl acetohydroxamic acid, attenuate reperfusion-induced arrhythmias in this model when introduced during the ischaemic period.

AB - The novel monohydroxamates N-methyl hexanoylhydroxamic acid, N-methyl acetohydroxamic acid, and N-methyl butyrohydroxamic acid have antioxidant and iron chelating properties. They attenuated reperfusion-induced contractile dysfunction following long periods of ischaemia (50 min) in the isolated rat heart. Here we compare their effects and that of the trihydroxamate desferrioxamine on reperfusion-induced arrhythmias following short duration ischaemia (10 min). Isolated rat hearts were perfused by the Langendorff method, subjected to regional ischaemia and reperfusion. Arrhythmias induced during the first 5 min of reperfusion were quantified. Drugs (all at 150 microM) were introduced during the last 2 min of ischaemia and remained throughout reperfusion. Although the monohydroxamate- and desferrioxamine-treated hearts showed a reduction in the incidence of ventricular tachycardia and fibrillation, only the reduction in the incidence of sustained fibrillation ( > 3 min duration) in N-methyl acetohydroxamic acid--(27%), N-methyl hexanoylhydroxamic acid--(27%) and desferrioxamine-treated hearts (20%) was statistically significant (p < 0.05 vs control 73%; n = 15). There was a reduction in the severity of the arrhythmias, manifest as a significant increase in the duration of sinus rhythm in all the monohydroxamate-treated hearts, and a significant reduction (vs control 218 +/- 29 s; mean +/- SEM) in the duration of ventricular fibrillation in hearts treated with N-methyl acetohydroxamic acid (101 +/- 31 s) and desferrioxamine (112 +/- 30 s). This improvement was offset by an increase in the duration of ventricular tachycardia, in hearts treated with N-methyl acetohydroxamic acid, N-methyl butyrohydroxamic acid and desferrioxamine. These results suggest that these novel monohydroxamates, particularly N-methyl acetohydroxamic acid, attenuate reperfusion-induced arrhythmias in this model when introduced during the ischaemic period.

KW - Animals

KW - Anti-Arrhythmia Agents

KW - Cardiotonic Agents

KW - Electrocardiography

KW - Hemodynamics

KW - Hydroxamic Acids

KW - In Vitro Techniques

KW - Male

KW - Molecular Structure

KW - Myocardial Contraction

KW - Myocardial Reperfusion Injury

KW - Rats

KW - Rats, Wistar

KW - Ventricular Fibrillation

M3 - Journal article

C2 - 9026351

VL - 28

SP - 405

EP - 413

JO - International Journal of Biochemistry & Cell Biology

JF - International Journal of Biochemistry & Cell Biology

SN - 1357-2725

IS - 4

ER -

ID: 138287655