Biomedical Engineering Reference
In-Depth Information
Cows categorised as low, medium and high
producers tend to have higher milk temperatures
with increasing production (Igono et al.
1988
)
and concentrations of milk somatotropin decline
significantly when THI exceeded 70. The decline
probably occurs to reduce metabolic heat produc-
tion. Reduced concentration of key metabolic
hormones observed during heat stress is probably
an attempt to reduce metabolic heat production.
Scott et al. (
1983
) reported a negative relation-
ship for plasma thyroxine concentration and
rectal temperature, but the initiation of night
cooling, at the time when rectal temperature was
highest, was most beneficial in maintaining ther-
moneutral plasma thyroxine concentration, sug-
gesting that strategically cooling the heat-stressed
cow could enhance the metabolic potential.
Heat stress is a major contributing factor to the
low fertility of dairy cows during summer
(Ingraham et al.
1974
; Ray et al.
1992
; Thompson
et al.
1996
; Al-Katanani et al.
1999
; Khodaei
et al.
2006
). Effects of heat stress on reproductive
hormones and other physiological functions are a
direct consequence of the increase in body tem-
perature due to heat stress or of the physiological
changes cows undergo to reduce the magnitude
of hyperthermia (De Rensis and Scaramuzzi
2003
; Khodaei
2003
) . High ambient temperature
adversely affects normal reproduction of cattle
(Plasse et al.
1970
), swine (Edwards et al.
1968
)
and sheep (Thwaites
1968
) , the syndrome being
short oestrus, abnormal oestrus cycle, increased
proportion of abnormal ova shed, decreased fer-
tilisation rate and increased embryonic and fetal
mortality early in gestation (Stott
1972
) . These
physiological manifestations as influenced by
environmental heat have been associated with
altered endocrine functions (Stott and Wiersma
1971
). Hormonal secretion in animals during
heat stress including short-term and long-term
temperature modification using environmental
chambers, seasonal comparisons of hormonal
profiles and the use of microclimatic modification
during periods of heat stress has been extensively
evaluated. Differences in experimental conditions
contribute to the disparity in results on hormonal
secretions during heat stress. Some of the varia-
tions in hormonal responses to heat stress reflect
that ovarian steroid concentrations are dependent
not only on rate of secretion from ovarian tissue
but also on rate of vascular perfusion of the ovary,
on possible adrenal release in case of progester-
one, on metabolism in the liver and other organs
and on the degree of haemodilution or haemo-
concentration (Wise et al.
1988a
) . The extent to
which heat stress affects other physiological
characteristics could lead to variable changes in
steroid hormone concentrations in peripheral
blood. Heat stress can also cause either dilution,
concentration or no effect on blood plasma
volume (Richards
1985
; McGuire et al.
1989
;
Johnson et al.
1991
; Elvinger et al.
1992
) , and the
nature of effect of heat stress on blood volume
affects steroid hormone concentrations in blood.
Hyperthermia has been shown to decrease ovar-
ian blood flow (Lublin and Wolfenson
1996
) and
to inhibit angiogenesis (Fajardo et al.
1988
) .
Blood flow and vascular density determine the
follicular perfusion rate, which directly influences
the rates of nutrient uptake and hormonal release
by the follicle.
2
Thyroxine (T
4
) and
Triiodothyronine (T
3
)
Thyroid hormones are important in an animal's
adaptation to a hot environment. The thyroid
gland secretes triiodothyronine (T
3
) and tet-
raiodothyronine/thyroxine (T
4
) which provide a
major mechanism important for acclimation
(Johnson and Van Jonack
1976
; Horowitz
2001
)
and are known indicators of heat stress (Pusta
et al.
2003
) . Both triiodothyronine (T
3
) and thy-
roxine (T
4
) are associated with metabolic homeo-
stasis and are susceptible to climatic changes
(Perera et al
.
1985
). Shade or cooling can, there-
fore, alter thyroid activity when cattle are exposed
to heat stress (Collier et al.
1982a
; Aggarwal
2004
; Aggarwal and Singh
2009
; Table
2
). It is
well known that heat acclimation decreases
endogenous levels of thyroid hormones and that
mammals that have adapted to warmer climates
follow this pattern (Johnson and Van Jonack
1976
; Horowitz
2001
) . These hormones are the
primary determinants of basal metabolic rate and
