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|Title:||Heat Stress Induced Fetal Dwarfing and Uterine Blood Flow in Sheep|
|Author(s):||Brown, David Ervin|
|Department / Program:||Animal Science|
|Degree Granting Institution:||University of Illinois at Urbana-Champaign|
|Subject(s):||Agriculture, Animal Culture and Nutrition|
|Abstract:||The present study defined and characterized heat stress induced fetal dwarfism in sheep and explored control mechanisms of uterine blood flow during heat stress in the gravid ewe. Initially, pregnant ewes were given a heat challenge for the last 23 or 56 days of gestation while ewes kept at thermoneutrality were either fed ad libitum or pair fed to the intake of heated ewes. After lamb sex and litter size adjustment, birth weight was reduced (P < .05), while thermal challenge and restricted fed ewes had normal birthweight lambs. The heat induced small lambs had normal bone lengths and muscle weights but relatively large livers (P < .05) and enlarged kidneys (P < .05). The small lambs had 30 and 56 day weights similar to the thermoneutral ewe treatment groups.
Two trials were conducted to determine if restricted feed intake would alleviate heat induced dwarfing. Birthweight adjusted for sex and litter size was reduced 1.8 kg in trial 1 (P < .05) and 1.9 kg in trials 1 and 2 combined (P < .06) with maternal heat stress. Lamb sex, litter size, lamb condition and gestation length were all correlated (P < .05). Restriction of feed to 70 percent or 85 percent of ad libitum intake during heat stress had no effect on lamb birthweight.
Pregnant ewes instrumented to monitor uterine blood flow (UBF) were used to determine the mechanisms controlling UBF during acute heat stress. Hexamethonium (H) or physiological saline (S) was infused while UBF was depressed during thermal challenge. At the start of infusions, rectal temperature (Tr), respiratory rate (R) and blood pH were elevated (P < .05) while PCO(,2), blood pressure (BP) and UBF were depressed (P < .05) in both treatments. Blood pressure and HR were depressed subsequent to H but not S treatment while UBF remained depressed during both H and S treatments. Uterine vascular resistance (UVR) subsequent to H and S remained at the thermoneutral level despite a 40-50 percent reduction in UBF and a 15 percent decrease in BP with H infusion. These data suggest depressed UBF during thermal challenge may result from uterine vascular bed autoregulation.
Phenoxybenzamine (PB) and propranolol (PR) were administered while UBF was depressed during heat stress to determine if circulating catecholamines may constrict the uterine vasculature. UBF was suppressed at the start of PB and PR treatments (P < .05). Neither treatment resulted in increased UBF, suggesting (alpha) and (beta) adrenergic mechanisms do not regulate UBF during heat stress.
The effect of 3-(N-morpholino)propane sulfonic acid buffer (MOPS) or saline (S) during thermal suppression of UBF was tested in nine ewes. UBF and PCO(,2) were decreased (P < .05) while Tr, HR, RR and arterial pH were elevated (P < .05) at the start of MOPS and S infusions. UBF increased from 305 ml/min at the start of MOPS to 390 ml/min at the end of a 45 min infusion (P = .14). The UBF of S treated ewes was 251 ml/min and 260 ml/min at the start and end of infusion, respectively. Increased UVR (P < .05) at the start of MOPS was reversed with MOPS infusion. These data suggest the uterine vascular bed has pH receptors for autoregulation of UBF during thermally induced respiratory alkalosis.
Thesis (Ph.D.)--University of Illinois at Urbana-Champaign, 1980.
|Date Available in IDEALS:||2014-12-13|