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OBSTETRIC ANESTHESIA

The Effect of Maternal Cocaine Exposure on Neonatal Rat Cardiac Function

Lena S. Sun, MD^*,, Shin Takuma, MD, Rui Lui, MD, and Shunichi Homma, MD

Departments of *Anesthesiology, Pediatrics, and Medicine, College of Physicians and Surgeons of Columbia University, New York, New York

Address correspondence and reprint requests to Lena S. Sun, MD, College of Physicians and Surgeons of Columbia University, Department of Anesthesiology, 630 W. 168th St., BH4-440 North, New York, NY 10032. Address e-mail to lss4{at}columbia.edu,

Fetal cocaine exposure has been associated with a variety of cardiovascular dysfunctions in humans. We treated pregnant rats with either saline or cocaine at 60 mg/kg by gastric lavage for the entire gestational period and for 14 days after parturition. We then performed high-frequency transthoracic echocardiography to determine whether cocaine exposure affected neonatal cardiac contractile function in vivo in 7- and 14-day-old neonatal rats. All studies were performed in the unsedated, conscious state. Heart rate (HR) and systolic function, expressed as fractional area of change at the midpapillary muscle level, were calculated from two-dimensional images. Resting HR was faster in the cocaine-exposed group at both ages, but baseline contractile function was not different between control (CTL) and cocaine-exposed (COC) neonatal rats. Dobutamine induced a significant increase in HR in all groups at only the largest dose tested (Day 7 CTL HR increased from 438 ± 3 bpm to 462 ± 10 bpm; Day 7 COC HR increased from 466 ± 3 bpm to 493 ± 7 bpm; Day 14 CTL HR increased from 443 ± 4 bpm to 487 ± 4 bpm; Day 14 COC HR increased from 477 ± 4 bpm to 501 ± 5 bpm). Dobutamine elicited a significant increase in contractile response at both Day 7 (from 76.6% ± 0.6% to 81.5% ± 0.7%) and Day 14 in CTL (from 78.2% ± 0.7% to 81.9% ± 0.7%), but not in COC, animals (from 76.7% ± 0.8% to 78.9% ± 0.8% at Day 7 and from 76.8% ± 1.1% to 79.3% ± 0.8% at Day 14). Epinephrine induced a significant increase in contractile response in CTL, but not in COC, rats at Day 7 and had no effect on fractional area of change at 14 days of age in either CTL or COC animals. Our results indicate that perinatal cocaine exposure does not modify resting contractile function but attenuates the contractile response to ß-adrenoceptor stimulation in the neonatal rat. These results suggest that perinatal cocaine exposure may lead to decreased responsiveness to inotropic drugs during the early neonatal period.

IMPLICATIONS: Perinatal cocaine exposure decreases the cardiac response to adrenaline-like drugs often used to improve contractile function but has no effect on the ability of these drugs to increase heart rate in the neonatal rat.

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				K. D. Meyer and L. Zhang Short- and long-term adverse effects of cocaine abuse during pregnancy on the heart development Therapeutic Advances in Cardiovascular Disease, February 1, 2009; 3(1): 7 - 16. [Abstract] [PDF]