Feedlot and carcass traits of nulliparous and primiparous females representing eight breed types, including Bos taurus and Bos indicus x Bos taurus crosses, were evaluated. Nulliparous females (heifers) were in the feedlot for 4 mo; primiparous females (heiferettes) were fed for 2 1/3 mo after their calves were weaned at 6 mo of age. Heifers averaged higher (P less than .01) in dressing percentage, percentage of kidney fat, carcass grade (P less than .10), and color of lean (P less than .05) compared with heiferettes. Heiferettes exceeded the nulliparous group in feedlot ADG (P less than .01), fat thickness (P less than .05), and percentage of steak, roast, and bone (P less than .01). Parity effects on carcass weight, longissimus area, marbling, pH, and shear force value were not statistically significant. Dam breed types differed in several traits, including marbling (P less than .05) and percentage of steak (P less than .10), roast (P less than .01), and bone (P less than .01). Dam breed x parity interactions were nonsignificant. Results show that beef derived from heiferettes is competitive with heifer beef.
Metabolizable energy for maintenance (MEm) was estimated using 123 mature cows of eight diverse breed groups. Cows in each breed group were allotted at random 1) to limit-feeding to approximate maintenance or 2) to ad libitum access to feed. The MEm values were calculated by regression of change in body energy on ME intake. The MEm values for mature Hereford, Red Poll, Hereford x Red Poll, Red Poll x Hereford, Angus x Hereford, Angus x Charolais, Brahman x Hereford, and Brahman x Angus breed types were as follows: 145, 169, 148, 149, 144, 152, 139, and 143 kcal.kg-.75.d-1, respectively. Bos indicus-cross cows ranked lowest for MEm/kg.75. Angus x Hereford cows averaged highest in terms of grams of calf weaned per mature female exposed divided by yearly MEm requirement. Hereford x Red Poll reciprocal crosses on average required 640 kcal less total daily MEm per animal than Hereford and Red Poll straightbreds.
Ca2+ oscillations are important in the regulation of many cerebral arterial functions ranging from vasoconstriction to gene transcription. Without these oscillatory waveforms, there are alterations in the signaling pathways regulated by Ca2+. Previous work has shown that long term hypoxia (LTH) due to high altitude exposure can cause cerebral vascular dysfunction including changes in reactivity and morphology in the fetus as well as adult. Studies performed in cerebral arterial preparations have illustrated that LTH in sheep fetus and adult cause whole cell Ca2+ signaling dysfunctions that compromise vascular reactivity and contribute to cerebral arterial pathologies. Based on the premise that Ca2+ oscillations, vasoconstriction, vessel morphology, and LTH mediated cerebral arterial function are interrelated we tested the hypothesis that LTH impairs Ca2+ oscillations. The impact of LTH and maturation on Ca2+ signals in cerebral arterial myocytes was examined using confocal imaging techniques of flou‐4 loaded myocytes of basilar arteries from low (700m) or high altitude (3,801m) near term fetal or adult sheep. LTH decreased the intracellular Ca2+ signals independent of age due to a faster decay in the Ca2+ signal, an effect that could impair vasoconstriction, alter tissue structure, and compromise the regulation of cerebral blood flow. Along with producing smaller Ca2+ events, the data show that LTH inhibits the cell's ability to respond with Ca2+ signals in response to 30 mM potassium‐induced depolarization in fetal as well as adult sheep. LTH and ontogeny may also play interconnected roles in Ca2+ signaling as LTH inhibits distant communication between myocytes in fetal sheep, whereas in adult sheep it stimulates local signaling. These observations illustrate that altitude and maturation each modify Ca2+ signaling behavior in ways that likely impact arterial reactivity and other mechanisms related to the regulation of cerebral blood flow.Support or Funding InformationThis work is supported by The National Institutes of Health, Eunice Kennedy Shriver National Institute of Child Health and Human Development grant number HD083132, by the National Science Foundation under Grant No. MRI 0923559, and the Loma Linda University School of Medicine.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Gestational long term hypoxia (LTH) is a common prenatal stress caused by maternal anemia, high altitude living, smoking, and other disorders. Such gestational LTH can lead to a variety of cerebrovascular disorders in the neonate that compromise brain blood flow. Local and whole‐cell Ca2+ signals are important to the regulation of cerebrovascular tone. Rapid and localized Ca2+ transients, often referred to as sparks, activate large‐conductance K+ channels (BK), which dilate vessels. Whole‐cell Ca2+ oscillations, in comparison, are important to arterial contraction. Previous work shows that LTH and post‐natal maturity influence BK channel function in basilar arteries, arterial wall Ca2+ signals, cerebrovascular tone, as well as brain blood flow. We hypothesize that LTH‐dependent changes in spontaneous and depolarization mediated Ca2+ sparks and whole‐cell oscillations are important to BK channel activity, arterial wall Ca2+ signals, and vascular reactivity changes our group has previously observed. To begin evaluating the role of individual myocyte Ca2+ signals to the observed changes in cerebrovascular function, we isolated basilar arteries from adult and near term fetal (~141 gestational days) normoxic and hypoxic sheep that were raised at 3,800 m. for 110+ days. Cytosolic Ca2+ signals were examined in individual myocytes of intact arterial preparations loaded with fluo‐4 using laser scanning confocal microscopy techniques. Ca2+ spark activity as well as whole‐cell oscillations were enhanced by depolarizing myocytes with 30 mM K+. Maturation increased Ca2+ spark activity and depolarization‐dependent oscillations. LTH decreased oscillatory activity in fetal and adult animals but only spark frequency in adult myocytes. LTH decreased the area under the curve for Ca2+ oscillations independent of age as well as suppressed the ability of adult myocytes to respond to membrane depolarization. Depolarization, maturation, and LTH also influenced the spatial and temporal relationships of the Ca2+ oscillations. Overall, these observations illustrate that maturation and gestation at high‐altitude modify local and whole‐cell Ca2+ signaling, which likely contribute to adjustments in BK channel function, arterial wall Ca2+ signals, vasoreactivity, and cerebral blood flow that our group has examined in the past.Support or Funding InformationThis material is based upon work supported by NIH grants P01HD083132 (LZ). Imaging was performed in the LLUSM Advanced Imaging and Microscopy Core with support of NSF Grant MRI‐DBI 0923559 and the Loma Linda University School of Medicine.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Ca2+ entry through L‐Type channels mediate contraction of basilar arterial myocytes and whole‐cell Ca2+ waveforms are thought to be integral to this process. Based on previous evidence, we hypothesize that modifications, due to both long term hypoxia (LTH) and ontogeny, will affect the influence of depolarization on intracellular Ca2+ waves. Specifically, fetal arteries will have reduced Ca2+ signals while LTH will further reduce depolarization induced Ca2+ responses. In order to test this hypothesis, we examined Ca2+ wave activity using confocal fluorescence imaging techniques on basilar arterial myocytes in an en face preparation of low and high altitude fetal (FN, FH) and adult (AN, AH) sheep, where sheep were placed at 3,801 m for >100 days. Ca2+ waves were evaluated with and without 30mM K (30K), which was used to depolarize the myocytes. LTH decreased the area under the curve (AUC) independent of animal age. These changes in AUC were due to a faster decay in the Ca2+ signal. Depolarization with 30K increased Ca2+ wave amplitude and duration in all groups except for AH. These observations illustrate that both altitude and ontogeny play important roles in affecting various aspects of the Ca2+ signals. This likely contributes to the changes in arterial contractility that were previously observed with ontogeny and LTH and potentially other mechanisms pertaining to cerebral blood flow.Support or Funding InformationSupport from NIH and NSF
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