A wide variety of substances taken into the human body can affect the fetal outcome
adversely. Of considerable interest among these substances are caffeine, nicotine
and alcohol. Caffeine, in particular, seems to be the most commonly used since
it is present in a number of dietry sources for example lea, coffee, cocoa, beverages,
chocolate bars and soft drinks (FredhoIm et al., 1999). Caffeine has also received
recently more attention as a model drug of abuse (Hughes et al., 1998).
A survey of the literature clarified that caffeirie could altw fetal development
and induce hematomas in the yolk sac as well as dysmorphogenesis in forelimb and
Rindlimb buds (Iwase et al., 1994). Early exposure to caffeine during pregnancy can
also increase the brain excitability (Guillet and Dunhnm, 1995).
Most studies concerned with the effects of caffeine on the cardiovascular system
have concentrated mainly on the physiological effects and to a lesser extent on
the gross morphological changes with marked discrepancy and controverted results.
Few studies claimed that there was no association between caffeine consumption
and the cardiovascular congenital anomalies apart from few hernangiomas (Shai-
Linin et al., 1982). On the other hand, Matsuka et al. (1987) noticed that caffeine
was n potent inducer of ventricular septa1 defects. Moreover, Miller et al. (1994) and
Miller et ul. (1997) stated that there was an accelerated maternal and fetal heart rates
with increased fetal aortic peak velocity following caffcine intake.
Up to our knowledge, little data exist about the ultrastructural changes induced
by prenatal intake of caffeine. Reviewing the literature revealed that the etiology of
the action of caffeine was still obscure, and various theories had been hypothesized.