Respiration rates are reported as variable in the literature (Oliver, 1997). Two physiological effects of the alkaloids may account for the variability. First, decreased respiratory rates may be explained by actions of the alkaloids on the central nervous system. Alternatively, direct effects of the alkaloids on receptors in lung tissue and blood platelets may cause hypoxemia, resulting in a subsequent reflex increase in respiration rates. Which mechanism dominates is likely influenced by the environment surrounding the afflicted animal. Heart rate usually is unaffected or reflexively decreased in response to peripheral vasoconstriction and increased impedance to tissue blood flow (Oliver, 1997). Recent research by Aiken et al. (2007) supports the reflexive decrease (within 28 h) with a gradual increase back to baseline by 172 h after initial feeding of E+ tall fescue. These data, however, are in contrast to those in an earlier report by Walls and Jacobson (1970), where exposure of Holstein heifers to alcoholic extracts of toxic tall fescue (i.e., presumed to contain ergot alkaloid) resulted in elevated heart rates. Their earlier work (Carr and Jacobson, 1969) showed variable heart rate responses in male Holstein calves exposed to a similar alcoholic extract of toxic tall fescue. The variation in heart rate responses appears to be related to differences in dosage, routes of exposure, and/or nutrient status of the animals. Given that the ergot alkaloid levels are not known for the investigations conducted by Walls and Jacobson (1970) and Carr and Jacobson (1969), it is difficult to discern the exact relationship of their work to that of Aiken et al. (2007). These reports indicate a need for additional research to determine and understand how the ergot alkaloids affect heart and respiration rates.

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