The influence of systemic immune activation on whole-body Ca trafficking and gastrointestinal tract (GIT) physiology are not clear. Thus, study objectives were to characterize the effects of lipopolysaccharide (LPS) on Ca pools and GIT dynamics to increase understanding of immune-induced hypocalcemia, ileus and stomach hemorrhaging. Twelve crossbred pigs [44 ± 3 kg body weight (BW)] were randomly assigned to 1 of 2 intramuscular treatments: (1) control (CON; 2 mL saline; n=6) or (2) LPS (40 µg LPS/kg BW; n=6). Pigs were housed in metabolism stalls to collect total urine and feces for 6 h after treatment administration, at which point they were euthanized, and various tissues, organs, fluids, and digesta were weighed, and analyzed for Ca content. Data were analyzed with the MIXED procedure in SAS 9.4. Rectal temperature and respiration rate increased in LPS relative to CON pigs (1.4°C and 32%, respectively; P≤0.05). Inflammatory biomarkers such as circulating alkaline phosphatase, aspartate aminotransferase, and total bilirubin increased in LPS compared with CON pigs whereas albumin decreased (P≤0.02). Plasma glucose and urea nitrogen decreased and increased, respectively, after LPS (43 and 80%, respectively; P<0.01). Pigs administered LPS had reduced circulating ionized Ca (iCa) compared to CON (15%; P<0.01). Considering estimations of total blood volume, LPS caused an iCa deficit of 23 mg relative to CON (P<0.01). Adipose tissue and urine from LPS pigs had reduced Ca compared to CON (39 and 77%, respectively; P≤0.05). There did not appear to be increased Ca efflux into GIT contents and no detectable increases in other organ or tissue Ca concentrations were identified. Thus, while LPS caused hypocalcemia, we were unable to determine where circulating Ca was trafficked. LPS administration markedly altered GIT dynamics including stomach hemorrhaging, diarrhea (increased fecal output and moisture), and reduced small intestine and fecal pH (P ≤ 0.06). Taken together, changes in GIT physiology suggested dyshomeostasis and alimentary pathology. Future research is required to fully elucidate the etiology of immune activation-induced hypocalcemia and GIT pathophysiology.

中文翻译：

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猪急性脂多糖挑战后的钙运输和胃肠道生理学

全身免疫激活对全身钙运输和胃肠道（GIT）生理的影响尚不清楚。因此，研究目标是表征脂多糖 (LPS) 对钙池和胃肠道动态的影响，以增进对免疫诱导的低钙血症、肠梗阻和胃出血的了解。将 12 头杂交猪 [44 ± 3 kg 体重 (BW)] 随机分配至 2 种肌肉注射治疗中的 1 种：(1) 对照（CON；2 mL 盐水；n=6）或 (2) LPS（40 µg LPS/kg）带宽；n=6)。治疗后6小时将猪圈养在代谢栏内收集总尿液和粪便，此时将其安乐死，并对各种组织、器官、体液和消化物进行称重，并分析钙含量。使用 SAS 9.4 中的 MIXED 程序分析数据。相对于 CON 猪，LPS 组的直肠温度和呼吸频率增加（分别为 1.4°C 和 32%；P≤0.05）。与CON猪相比，LPS中的炎症生物标志物如循环碱性磷酸酶、天冬氨酸转氨酶和总胆红素增加，而白蛋白减少(P≤0.02)。LPS后血浆葡萄糖和尿素氮分别降低和增加(分别为43％和80％；P＜0.01)。与CON相比，给予LPS的猪循环离子化Ca(iCa)减少(15％；P＜0.01)。考虑到总血容量的估计，LPS相对于CON导致iCa缺乏23mg(P＜0.01)。与 CON 相比，LPS 猪的脂肪组织和尿液中 Ca 含量降低（分别为 39% 和 77%；P≤0.05）。胃肠道内容物中的 Ca 外流似乎没有增加，并且其他器官或组织的 Ca 浓度也没有发现可检测到的增加。因此，虽然 LPS 导致低钙血症，但我们无法确定循环钙被贩运到​​何处。LPS 给药显着改变了胃肠道动态，包括胃出血、腹泻（粪便排出量和水分增加）以及小肠和粪便 pH 值降低（P ≤ 0.06）。总而言之，胃肠道生理学的变化表明体内平衡失调和消化道病理学。未来的研究需要充分阐明免疫激活引起的低钙血症的病因和胃肠道病理生理学。