Biomedical Engineering Reference
In-Depth Information
involve adrenocorticotrophic hormone (ACTH).
Heat stress-induced cortisol secretion (Roman-
Ponce et al.
1981
; Wise et al.
1988a
; Elvinger
et al.
1992
) may block oestradiol-induced sexual
behaviour (Hein and Allrich
1992
) . Increased
corticosteroid secretion (Roman-Ponce et al.
1981
) can inhibit GnRH and thus LH secretion
(Gilad et al.
1993
). Heat stress inhibited the
secretion of gonadotrophins in cows with low
plasma concentrations of oestradiol compared to
those with high concentrations (Gilad et al.
1993
) .
However, the high concentrations of oestradiol
can counteract the effect of heat stress. Therefore,
the response of neuroendocrine mechanism con-
trolling gonadotrophin secretion is different and
more sensitive to heat stress when concentrations
of plasma oestradiol are low in cows. The heat
stress may also act directly on the ovary to
decrease its sensitivity to gonadotrophin stimula-
tion (Wolfenson et al.
1997
) . Also the somatic
cells within the follicles (theca and granulosa
cells) may also be damaged by heat stress. In
terms of steroid production, the thecal cells and
granulosa cells were observed to be susceptible
to heat stress (Roth et al.
2001
) . Any alteration in
the secretory activity of the follicle and the cor-
pus luteum induced by heat stress would be
important factors in summer infertility in vulner-
able cows particularly high producing.
stimulating hormone, all of which are released in
response to heat stress (Engler et al.
1989
) . In
terms of the response to heat stress, ACTH acts
on the adrenal cortex to stimulate the synthesis
and secretion of glucocorticoids like cortisol.
The higher concentrations of cortisol in heat
stressed cows influence LH release and cortisol
has been implicated to inhibit LH in the bovine
species (Gangwar et al.
1965
) . Various studies
have shown that administration of natural or syn-
thetic glucocorticoids can inhibit the secretion of
the gonadotrophins in sheep (Juniewicz et al.
1987
) and in dairy cattle (Thibier and Rolland
1976
). Nevertheless, increased secretion of glu-
cocorticoids is not always associated with
decreased secretion of the gonadotrophins, par-
ticularly in cases of acute stress. Suppression of
reproduction is more likely under conditions of
chronic stress and may involve action at the
hypothalamus or pituitary. Furthermore, there
may be species differences in the extent to which
glucocorticoids inhibit the secretion of LH and
FSH (Tilbrook et al.
2000
) . Under prolonged
heat stress conditions, secretion of the gonado-
trophins may be suppressed and reproduction
may also be inhibited.
9.5
Prostaglandin
Heat stress compromises uterine environment
with decreased blood flow to the uterus and
increased uterine temperature which may lead
to implantation failure and embryonic mortality.
These effects are associated with the produc-
tion of heat-shock proteins by the endometrium
during heat stress and reduced production of
interferon-tau by the conceptus. Moreover, heat
stress can affect endometrial prostaglandin
secretion and activate luteolysis leading to pre-
mature luteolysis and embryo loss. Heat shock
of 42 and 43°C have been observed to increase
output of prostaglandins by cultured endome-
trium collected at day 17 of the oestrus cycle
(Putney et al.
1988
; Malayer and Hansen
1990
) .
However, heat stress on day 17 of pregnancy
increases uterine production in response to oxy-
tocin (Wolfenson et al.
1993
) .
9.4
Gonadotrophins
and Corticosteroids
Heat stress affects the hypothalamic-pituitary-
adrenal axis and the sympathoadrenal system
(Tilbrook et al.
2000
) to initiate and modulate
most of the activities. Stimulation of the hypo-
thalamic-pituitary-adrenal axis is character-
ised by activation of corticotrophin-releasing
factor (CRF) and arginine vasopressin (AVP)
neurones in the paraventricular nucleus and
secretion of these neuropeptides into the hypo-
physeal portal system to stimulate the corti-
cotrophs of the anterior pituitary gland (Tilbrook
et al.
2000
) . The corticotrophs produce a variety
of peptides derived from pro-opiomelanocortin,
including ACTH, endorphin and melanocyte-
