Similar to immune response, sexual dimorphism has also been reported with respect to cardiac functions (Fig. 6.1). Findings from previous studies have shown that cardiac output, stroke volume, +dP/dt, -dP/dt, and total peripheral resistance were markedly altered after trauma-hemorrhage in males (Wang et al., 1993; Remmers et al., 1997;Angele et al., 1998c; Remmers et al., 1998a; Yao et al., 1998; Mizushima et al., 2000; Ba et al., 2001; Ancey et al., 2002; Kuebler et al., 2002; Ba et al., 2003;Yang et al., 2004). However, in proestrus females, which have high circulating levels of estrogen, cardiac functions are maintained after trauma-hemorrhage and fluid resuscitation (Fig. 6.1) (Ba et al., 2003). In contrast, cardiac functions are suppressed in ovariectomized females (Yang et al., 2004). Administration of a single dose of 17P-estradiol in ovariectomized females prevented the depression in cardiac function after trauma-hemorrhage (Mizushima et al., 2000; Yang et al., 2004). Similar administration of 17P-estradiol in males also prevented cardiac dysfunction after trauma-hemorrhage (Chaudry et al., 2003; Yang et al., 2004). Additional findings suggest that decreasing androgen levels by performing castration 2 weeks prior to trauma-hemorrhage significantly improved/restored cardiac function under those conditions (Chaudry et al., 2003; Yang et al., 2004). On the other hand, administration of male sex hormones 5a-DHT in castrated males and in females resulted in suppressed cardiac function after trauma-hemorrhage (Chaudry et al., 2003; Yang et al., 2004). Thus, similar to immune function, male sex hormones are found to suppress cardiac function; female hormones on the other hand prevent the suppression of cardiac function after trauma-hemorrhage. However, the mechanism of the beneficial effects of female or harmful effect of male steroids after trauma-hemorrhage remains to be established. Previous studies have shown that 17P-estradiol may mediate its salutary effect on cardiac function via modulation of proinflammatory cytokines such as IL-6 and TNF-a (Levine et al., 1990; O'Neill et al., 1994;Yamauchi-Takihara et al., 1995; Kerger et al., 1999; Mizushima et al., 2000; Yang et al., 2004). In addition, administration of 17P-estradiol also prevented the decrease in nitric oxide synthase and increased leukocyte infiltration (Angele et al.,
1998c). Both diminished nitric oxide synthase activity and increased leukocyte infiltration potentially contribute to altered cardiac functions after trauma hemorrhage (Miyao et al., 1993; Hierholzer et al., 1998; Kerger et al., 1999). Thus, estradiol-mediated prevention of both the decrease in nitric oxide synthase and increase of leukocyte infiltration is likely another potential mechanism by which estrogen mediates its salutary action on cardiac function after trauma-hemorrhage. Altogether, one or more than one of the above mechanisms could be responsible for the protective effects of 17P-estradiol observed in the males after trauma-hemorrhage and resuscitation.
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