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Potential deleterious effect of [Beta]-adrenergic stimulation during warm-blood cardioplegia in rabbit hearts Cook, Richard Chung-Sop
Abstract
We hypothesized that β-adrenergic stimulation with isoproterenol during continuous normothermic cardioplegic arrest would enhance the regenerative and regulatory function of the myocardium, resulting in improved cardiac function. We studied isolated rabbit hearts paced at ~200 beats/minute and cross-circulated by a support rabbit. We measured ventricular pressure over a range of ventricular volumes to determine maximal elastance at baseline and 20 and 45 minutes after discontinuation of cardioplegia. Myocardial oxygen consumption measurements were performed simultaneously and during cardioplegic arrest. Hearts were prospectively randomized to receive either isoproterenol 0.1M or control in blinded fashion for 10 minutes during a 1 hour continuous warm blood cardioplegic arrest. Compared to control hearts, isoproterenol-treated hearts had trends towards longer time to first spontaneous heart-beat (control 141 ± 43 vs isoproterenol 200 ± 74 seconds, p = 0.07), and longer time to capture of atrial pacing (control 214 ± 52 vs isoproterenol 288 ± 91 seconds, p = 0.06). There was no difference observed in the myocardial oxygen consumption between isoproterenol-treated and control groups of hearts. Myocardial oxygen consumption decreased during administration of cardioplegia (p<0.01) but there was no significant change in myocardial oxygen consumption during isoproterenol infusion during cardioplegic arrest. There was a significant reduction in maximal elastance compared to baseline 20 minutes after discontinuation of cardioplegic arrest in both groups (control 7.3 ± 1.7 mmHg/μL vs 9.0 ± 1.7 irimHg/μL, p = 0.02, isoproterenol-treated 6.8 ± 2.8 mmHg/μL vs 8.2 ± 2.6 mmHg/μL, p = 0.01, respectively) with recovery of maximal elastance by 45 minutes in control hearts only. We conclude that exposure of hearts to isoproterenol during warm cardioplegic arrest has a deleterious effect which may be mediated through mechanisms independent of increased myocardial oxygen consumption.
Item Metadata
| Title |
Potential deleterious effect of [Beta]-adrenergic stimulation during warm-blood cardioplegia in rabbit hearts
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| Creator | |
| Publisher |
University of British Columbia
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| Date Issued |
2002
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| Description |
We hypothesized that β-adrenergic stimulation with isoproterenol during continuous
normothermic cardioplegic arrest would enhance the regenerative and regulatory function
of the myocardium, resulting in improved cardiac function. We studied isolated rabbit
hearts paced at ~200 beats/minute and cross-circulated by a support rabbit. We measured
ventricular pressure over a range of ventricular volumes to determine maximal elastance at
baseline and 20 and 45 minutes after discontinuation of cardioplegia. Myocardial oxygen
consumption measurements were performed simultaneously and during cardioplegic
arrest. Hearts were prospectively randomized to receive either isoproterenol 0.1M or
control in blinded fashion for 10 minutes during a 1 hour continuous warm blood
cardioplegic arrest. Compared to control hearts, isoproterenol-treated hearts had trends
towards longer time to first spontaneous heart-beat (control 141 ± 43 vs isoproterenol 200
± 74 seconds, p = 0.07), and longer time to capture of atrial pacing (control 214 ± 52 vs
isoproterenol 288 ± 91 seconds, p = 0.06). There was no difference observed in the
myocardial oxygen consumption between isoproterenol-treated and control groups of
hearts. Myocardial oxygen consumption decreased during administration of cardioplegia
(p<0.01) but there was no significant change in myocardial oxygen consumption during
isoproterenol infusion during cardioplegic arrest. There was a significant reduction in
maximal elastance compared to baseline 20 minutes after discontinuation of cardioplegic
arrest in both groups (control 7.3 ± 1.7 mmHg/μL vs 9.0 ± 1.7 irimHg/μL, p = 0.02,
isoproterenol-treated 6.8 ± 2.8 mmHg/μL vs 8.2 ± 2.6 mmHg/μL, p = 0.01, respectively)
with recovery of maximal elastance by 45 minutes in control hearts only. We conclude
that exposure of hearts to isoproterenol during warm cardioplegic arrest has a deleterious
effect which may be mediated through mechanisms independent of increased myocardial
oxygen consumption.
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| Extent |
4848241 bytes
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| Genre | |
| Type | |
| File Format |
application/pdf
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| Language |
eng
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| Date Available |
2009-08-12
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| Provider |
Vancouver : University of British Columbia Library
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| Rights |
For non-commercial purposes only, such as research, private study and education. Additional conditions apply, see Terms of Use https://open.library.ubc.ca/terms_of_use.
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| DOI |
10.14288/1.0090195
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| URI | |
| Degree | |
| Program | |
| Affiliation | |
| Degree Grantor |
University of British Columbia
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| Graduation Date |
2002-05
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| Campus | |
| Scholarly Level |
Graduate
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| Aggregated Source Repository |
DSpace
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Rights
For non-commercial purposes only, such as research, private study and education. Additional conditions apply, see Terms of Use https://open.library.ubc.ca/terms_of_use.