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Lipopolysaccharide-Induced Ionized Hypocalcemia and Acute Kidney Injury in Carotid Chemo/Baro-Denervated Rats.

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dc.contributor.author Fernández, Ricardo
dc.contributor.author Cortés, Paula
dc.contributor.author Del Río, Rodrigo
dc.contributor.author Acuña-Castillo, Claudio
dc.contributor.author Reyes, Edison
dc.date.accessioned 2016-05-20T14:28:24Z
dc.date.available 2016-05-20T14:28:24Z
dc.date.issued 2015
dc.identifier.citation Advances in Experimental Medicine and Biology, 2015, vol. 860, p. 161-166 es_CL
dc.identifier.uri http://dx.doi.org/10.1007/978-3-319-18440-1_18 es_CL
dc.identifier.uri http://hdl.handle.net/11447/290
dc.description Centro de Fisiología Celular e Integrativa es_CL
dc.description.abstract The acute kidney injury (AKI) observed during sepsis is due to an uncontrolled release of inflammatory mediators. Septic patients develop electrolytic disturbances and one of the most important is ionized hypocalcemia. AKI adversely affects the function of other organs and hypocalcemia is associated with cardiovascular and respiratory dysfunctions. Since carotid body chemoreceptors modulate the systemic inflammatory response during sepsis syndromes, we used pentobarbitone-anesthetized male Sprague-Dawley rats in control condition (SHAM surgery) and after bilateral carotid neurotomy (carotid chemo/baro-denervated, BCN). We evaluate serum creatinine (CRE), serum neutrophil gelatinase-associated lipocaline (NGAL), ionized calcium (iCa) and cardiac Troponin I (cTnI) 90 min after the IP administration of 15 mg/kg lipopolysaccharide (LPS) or saline. In the SHAM group, LPS failed to induce significant changes CRE, NGAL, or iCa, and increased cTnI. Conversely, in the BCN group LPS increased CRE and NGAL, decreased iCa, and enhanced the increase of cTnI. Our results suggest that carotid chemo/baro-receptors might contribute to the regulation of both renal function and calcemia during sepsis. In addition, results imply that the carotid chemo-baroreceptors serve as an immunosensory organ. es_CL
dc.language.iso en_US es_CL
dc.publisher Springer International Publishing AG es_CL
dc.subject Carotid body es_CL
dc.subject Sepsis es_CL
dc.subject Acute kidney injury es_CL
dc.subject Ionized hypocalcemia es_CL
dc.subject Cardiac Troponin I es_CL
dc.title Lipopolysaccharide-Induced Ionized Hypocalcemia and Acute Kidney Injury in Carotid Chemo/Baro-Denervated Rats. es_CL


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