Biomedical Engineering Reference
In-Depth Information
Acute versus chronic heat stress
- Acute and
chronic thermal stress exhibit differing responses
on glucocorticoid concentrations and levels are
elevated in acute response but not in chronic
stress (Collier et al.
1982b
) . The initial rise in
plasma glucocorticoids is due to activation of the
adrenocorticotrophin release in the hypothalamus
in response to thermoceptors of the skin (Chowers
et al.
1966
); the subsequent decline to normal
even after continuing heat stimulus indicates
other response probably a negative glucocorticoid
feedback and a decrease in the glucocorticoid
binding transcortin (Lindner
1964
) . The gluco-
corticoids act as vasodilators to help heat loss and
have stimulatory effect on proteolysis and lipoly-
sis, hence providing energy to the animal to
help offset the reduction of intake (Cunningham
and Klein
2007
) .
Concentration of cortisol is altered by acute
and chronic heat exposure (Christison and
Johnson
1972
) and by changes in photoperiod
(Leining et al
.
1980
) . Acute heat exposure (33-43°C,
40-60 RH%) of young and old buffalo calves has
been observed to induce significant increases in
plasma cortisol concentration. The values were
408 and 213% in young and old calves, respec-
tively (Nessim
2004
). In Friesian calves, plasma
cortisol concentration also increased from 11 to
29 ng/ml due to direct solar exposure during heat
stress (Yousef et al.
1997
) and increased from 3.8
to 6.5 ng/ml when ambient temperature increased
from 24 to 38°C in climatic chamber when
exposed to heat (Habeeb et al.
2001
) .
Abilay et al. (
1975b
) observed that cortisol
levels decreased during prolonged heat exposure
after a temporary increase at the beginning of
heat stress. The decline in cortisol in the heat-
stressed lactating cows and buffaloes during hot
months may be responsible for decline in milk
components. The increase of plasma cortisol
level during acute heat stress is attributed to the
fact that glucocorticoid hormones have hypergly-
caemic action through the gluconeogenesis pro-
cess, thus enhancing glucose formation in
heat-stressed animals. The decline which occurs
in chronic heat stress is attributed to the fact that
cortisol is thermogenic in animals and, conse-
quently, the reduction of adrenocortical activity
under thermal stress is a thermoregulatory
protective mechanism preventing a rise in meta-
bolic heat production in hot environment. This
indicates that the role of the adrenal cortex
gland in acute and chronic adaptation is not
similar and under the adrenal-thyroid axis
response to stress (Alvarez and Johnson
1973
) .
The study by Alvarez and Johnson (
1973
)
reported that glucocorticoids increased by 38%
after 1 h and 62% after 2 h of exposure of cattle
to hot conditions, reaching a peak of 120% at 4 h,
then declined gradually to values not different
from normal at 48 h and remained at or below
this level for the rest of the exposure duration. In
hot conditions, cortisol hormone is considered a
thermoregulatory protective mechanism against
metabolic heat production under thermal stress
(Collier et al.
1982b
) . Therefore, cortisol plays a
role in adaptation to short- and long-term heat
stress (Norman and Litwack
1987
; Beraidinell
et al.
1992
). The likely response and contradic-
tion in results observed in the cortisol levels to
change in ambient temperature may be due to the
differences in animals, their heat tolerance, phy-
siological status, production level, type of pro-
duction, blood sampling time and duration of
exposure to heat stress.
Cortisol and immunity
- The studies on the
plasma cortisol in response to thermal stress in
dairy cows are inconclusive and conflicting. The
exposure of cows to high environmental tempe-
rature may result in increased glucocorticoid
concentrations in the plasma (Wise et al.
1988a
;
Silanikove
2000
) . Conversely, other studies
reported conflicting results indicating that dairy
cattle kept under conditions of high environ-
mental temperature show a reduction in the levels
of glucocorticoid secretion (Abilay et al.
1975b
;
Ronchi et al.
2001
). Differences in the experi-
mental conditions have presumably contributed
to the disparity in these results. Late pregnancy
and nonlactation may be a source of additional
stimuli that, in cows exposed to high environ-
mental temperature, activate the hypothalamic-
pituitary-adrenal axis causing an increased
secretion of cortisol. However, studies in rats
also suggested an inhibitory effect of pregnancy
on stress-induced immunosuppression and
