Abstract
Introduction: Cardiovascular stress, such as that due to the synthetic catecholamine, isoprenaline (iso), can induce myocardial infarction (MI). Ethanolamine (etn) is a biogenic amine, found in certain food types, that protects the isolated rat heart against ischaemia-reperfusion injury. The aim of this study was to investigate the cardioprotective effects of acute etn on iso-induced MI.
Methods: Male Wistar rats (250-350g) were divided into four groups: Control (saline injections only), iso + etn (iso 67mg/kg, s.c. and etn 10mg/kg i.p.), iso (67mg/kg, s.c. and a saline injection), and etn (saline injection and 10mg/kg i.p.). Rats were anaesthetised with sodium pentobarbitone (60mg/kg, i.p.) and mechanically ventilated with room air. Arterial blood pressure was measured from the right carotid artery and the electrocardiogram (ECG) was recorded from surface leads. Infarct size was measured using triphenyltetrazolium chloride (TTC) staining and the byproducts of lipid peroxidation were quantified.
Results: Iso administration significantly increased the infarct size (62.0 ± 3.9%, p<0.001) (mean ± SEM) compared to control rats that displayed a background TTC-negative artefact (23.7 ± 2.7%). The heart weight/body weight (HW/BW) ratio was also significantly raised in iso rats (4.6 ± 0.1, p<0.001) compared to control rats (3.4 ± 0.02). Iso + etn (5.0 ± 0.2 p<0.05) treated rats displayed significantly greater HW/BW ratio compared to iso-treated rats. However, there was no significant difference in infarct size between iso and iso + etn. Iso + etn treated rats had a lower death rate (1.9%) compared to iso-treated rats (11.3%). There was a significant increase in the amount of conjugated dienes (CD) in iso rats (59.56 ± 2.6μmol/L) compared to control rats (39.9 ± 4.0μmol/L, p<0.05). There was no significant difference in the generation of CDs between control and iso + etn treated rats.
Conclusion: In summary, etn seems to protect the rat from iso-induced MI; however the possibility of increased cardiac hypertrophy needs further investigation.
The
Methods: Male Wistar rats (250-350g) were divided into four groups: Control (saline injections only), iso + etn (iso 67mg/kg, s.c. and etn 10mg/kg i.p.), iso (67mg/kg, s.c. and a saline injection), and etn (saline injection and 10mg/kg i.p.). Rats were anaesthetised with sodium pentobarbitone (60mg/kg, i.p.) and mechanically ventilated with room air. Arterial blood pressure was measured from the right carotid artery and the electrocardiogram (ECG) was recorded from surface leads. Infarct size was measured using triphenyltetrazolium chloride (TTC) staining and the byproducts of lipid peroxidation were quantified.
Results: Iso administration significantly increased the infarct size (62.0 ± 3.9%, p<0.001) (mean ± SEM) compared to control rats that displayed a background TTC-negative artefact (23.7 ± 2.7%). The heart weight/body weight (HW/BW) ratio was also significantly raised in iso rats (4.6 ± 0.1, p<0.001) compared to control rats (3.4 ± 0.02). Iso + etn (5.0 ± 0.2 p<0.05) treated rats displayed significantly greater HW/BW ratio compared to iso-treated rats. However, there was no significant difference in infarct size between iso and iso + etn. Iso + etn treated rats had a lower death rate (1.9%) compared to iso-treated rats (11.3%). There was a significant increase in the amount of conjugated dienes (CD) in iso rats (59.56 ± 2.6μmol/L) compared to control rats (39.9 ± 4.0μmol/L, p<0.05). There was no significant difference in the generation of CDs between control and iso + etn treated rats.
Conclusion: In summary, etn seems to protect the rat from iso-induced MI; however the possibility of increased cardiac hypertrophy needs further investigation.
The
| Original language | English |
|---|---|
| Pages (from-to) | 174 |
| Journal | SA Heart Journal |
| Volume | 9 |
| Issue number | 3 |
| Publication status | Published - 2012 |
| Externally published | Yes |