Developmental Pb2+-Exposure induces cardiovascular pathologies in adult male rats

Abstract

Background: Developmental lead (Pb2+) exposure has been historically shown to alter the pathological functions of the cardiovascular system at high blood lead levels (i.e.,>15 μg/dL). However, given the time that has elapsed in the field (i.e., some 30 years), there is a great need for less clinical and more basic research on the cardiopathology of low blood lead levels (lBLLs; i.e.,<10 μg/dL). Further, most of the prior literature had focused solely on males as they had been reported to be more vulnerable to Pb2+ induced cardiovascular pathology. Aims and Objectives: To generate a model system of Pb2+-induced cardiovascular pathology that would be consistent with past reports, the present study examined male Long–Evans Hooded rats that were perinatally Pb2+ exposed (i.e., via their food with 996 ppm lead acetate in the rat chow) up until weaning (i.e., postnatal day 22; blood lead levels [BLLs]: 10–15 μg/dL) and were then removed from Pb2+ exposure for nearly 1.5 months (i.e., BLLs >3.33 μg/dL). Materials and Methods: Rats were then subjected to cardiovascular measures of systolic and diastolic blood pressures (SBP and DBP) and heart rates. Rats were sacrificed and their hearts were weighed; their thoracic aortas were collected and examined for microstructural and morphological changes through a scanning electron micrograph. Results: The data showed that compared to age matched control rats, the Pb2+ exposed rats have increased SBP, DBP, and heart rate with no differences in heart weight. These data show that early developmental Pb2+ exposure comprising lBLLs can cause significant cardiovascular pathological changes in rats. Conclusion: The present model of developmental Pb2+-exposure occurring early in life caused Pb2+-induced cardiopathology later in life through increased hypertension and reduced elasticity of the aorta media. These cardiovascular pathologies could further increase the likelihood of accelerated fronto executive dysfunctions due to the direct action of Pb2+ on neurons through inhibition of calcium dependent processes and might also contribute to vascular dementias.