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Pulmonary hypertension and ECG changes from monocrotaline pyrrole in the rat
Abstract:
Chemically synthesized monocrotaline pyrrole (MCTP) was administered to adult male rats at a dose of 5 mg/kg in the tail vein. Controls received an equivalent volume of dimethylformamide vehicle. Rats were killed at 3, 5, 7, 10, and 14 days after treatment. Bronchopulmonary lavage fluid lactate dehydrogenase activity and lung weight were significantly elevated at 4 and 7 days, respectively, after MCTP, indicating that pulmonary damage had occurred. White blood cell count was elevated 7 days after treatment. Mean pulmonary arterial pressure was also first elevated in treated (22 +/- 3 mmHg) compared with control (16 +/- 1 mmHg) animals 7 days after treatment. Right ventricle-to-left ventricle plus septum weight ratios were significantly increased in treated (0.429 +/- 0.015) vs. control (0.320 +/- 0.015) animals 14 days after treatment. Development of right heart enlargement correlated with a shift in the QRS complex mean electrical axis in the frontal plane of the electrocardiogram. These results indicate that MCTP produces effects similar to that caused by monocrotaline, that pulmonary arterial pressure increases from control levels between 5 and 7 days after treatment, and that measurement of mean electrical axis of the electrocardiogram may be a useful, noninvasive method to monitor MCTP-induced cardiac changes in vivo.
Insights
Chemically synthesized monocrotaline pyrrole (MCTP) causes pulmonary damage and right heart enlargement in rats. Electrocardiogram changes may noninvasively monitor these cardiac effects.
Area of Science:
- Toxicology
- Cardiovascular Physiology
- Pulmonary Medicine
Background:
- Monocrotaline is a known pulmonary toxin.
- The effects of chemically synthesized monocrotaline pyrrole (MCTP) on cardiovascular and pulmonary systems require further investigation.
Purpose of the Study:
- To investigate the toxicological effects of MCTP in adult male rats.
- To assess MCTP-induced pulmonary damage, cardiac alterations, and potential noninvasive monitoring methods.
Main Methods:
- Adult male rats were administered MCTP (5 mg/kg) or vehicle intravenously.
- Pulmonary damage was assessed via broncho-pulmonary lavage fluid lactate dehydrogenase activity and lung weight.
- Cardiac changes were evaluated by measuring mean pulmonary arterial pressure, right ventricle-to-left ventricle plus septum weight ratio, and electrocardiogram (ECG).
Main Results:
- MCTP significantly elevated lactate dehydrogenase activity and lung weight, indicating pulmonary damage.
- Mean pulmonary arterial pressure and right ventricle-to-left ventricle plus septum weight ratio increased in MCTP-treated rats.
- ECG QRS complex shifts correlated with right heart enlargement, suggesting MCTP-induced cardiac remodeling.
Conclusions:
- MCTP induces pulmonary hypertension and right heart enlargement in rats, similar to monocrotaline.
- Pulmonary arterial pressure elevation occurs between 5 and 7 days post-treatment.
- ECG mean electrical axis measurement offers a potential noninvasive method for monitoring MCTP-induced cardiac changes.