Lupine Publishers | Journal of Veterinary Science
Introduction
Physiological effects of heat stress
Numerous physiological changes occurs in the digestive system, acid-base chemistry, and blood hormones during heat stress that leads to reduced nutrient intake, but many changes occurs as a result of strain in the animals. The temperature sensitive neurons which are located throughout the animal’s body and send information to the hypothalamus, which invokes numerous physiological, anatomical or behavioral changes in the attempt to maintain heat balance. During heat stress cows exhibit reduces feed intake, decreased activity, seek, shade and wind, increase respiratory rate, and increase both peripheral blood flow and sweating. These responses have deleterious effect on both production and physiologic status of the animal. Cows that were fed ad libitum in a thermal comfort environment, fed ad libitum in a thermal stress environment, or feed restricted intake in a thermal comfort environment had similar milk yields for both restricted intake and thermal stress treatments, and mammary blood flow tended to be lower compared with ad libitum feed cows in thermal comfort, suggesting blood flow was responsive to level of dry matter intake (DMI). The negative effects of heat stress on milk production is due to decreased nutrient intake and decreased nutrient uptake by the portal drained viscera of the cow. Which leads to blood flow shifted to peripheral tissues for cooling purposes may alter nutrient metabolism and contribute to lower milk yield during heat weather.Metabolic effect
Heat stress causes reduced metabolism in cattle leads to reduced thyroid hormone secretion and gut motility, resulting in increased gut fill. Higher blood plasma content of epinephrine and norephinephrine with high ambient temperatures is an indicator of stress response and reduces rate of passage in the digestive tract. Slower passage rate can lead to greater gut fill and limited intake but improved digestibility because of greater residence time in the gut.Effect on electrolytes and minerals
With increased respiration during heat stress, the expiration of CO2 exceeds the rate of its formation in the body. The partial pressure of CO2 of blood declines, creating a deficit of blood carbonic acid and resulting in respiratory alkalosis. This leads to elevated blood and urine PH and net acid excretion rate. The cow compensates for high blood PH by excreting HCO3 ions into the urine. Alkalemia depresses the rate of renal secretion of hydrogen ions, but increases the excretion of filtered HCO3, which subsequently leads to reduction in blood HCO3 concentration. Metabolic acidosis may occur if available Na in these regions is reduced, possibly increasing chloride absorption, draining HCO3 and increasing Cl in the plasma. Metabolic alkalosis may result from a reciprocal process.During hot weather, declining DMI and high lactation demand requires increased dietary mineral concentration. However, alterations in mineral metabolism also effect the electrolyte status of the cow during hot weather. The primary cation in bovine sweat is potassium (K) and sharp increases in the secretion of K through sweat occur during hot climatic conditions. The absorption of macro-minerals, including Ca, P, and K, declined during hot temperatures and also the trace element requirements may increase with elevated environment temperature. Lactating cows subjected to hot climatic conditions and supplemented with K well above minimum NRC recommendations (NRC, 1989) responded with greater milk yields.
Effect on Reproductive system
Heat stress reduces the length and intensity of estrus through the involvement of hypothalamus-hypophyseal-gonodal axis. Heat stress can cause an increase cortisol secretion and block estradiol induced sexual behavior. There is an altered secrection of LH and FSH at the hypophyseal level and steroids (androstenedione, progesterone and estradiol) at ovarian level in heat stressed animals. However in certain experiments it has been observed that circulatory cortisol concentration were transitatory during heat stress animal. The major effect of heat stress are, decreases the expression of estrus behavior, because of the physical lethargy produced by heat stress.Reduced physical activity its probably an adaptive response that limits heat production. The uterine and oviductal tissues may be compromised during heat stress for several reasons first, heat stress lead to a redistribution of blood from viscera organs to peripheral this result decreased perfusion of nutrients and hormone could compromise endometrial functions. Recent experiments suggest that heat stress can cause increase peripheral concentration of estradiol-17β between 1 and 4 days of estrus cycle and 11-12 of the cycle.
There are variation of hormonal responses to heat stress probably reflects the fact that ovarian steroid concentrations are depended not only rate to secretion from ovarian tissue but also On rate of vascular perfusion of ovary or on metabolism in liver's other organ. During heat stress the action of steroid hormone on reproductive tract become reduced because of increased synthesis of heat shock protein. Heat shock can lead to increased synthesis of HSP70 and heat shock protein 90 in endometrium. These protein are part of the complex of protein associating with progesterone and estrogen receptor. Increased synthesis of heats and protein might alter assembly, transport or binding of steroid receptor.
Conclusion
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