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- W2783576409 abstract "Ischaemia increases sympathetic activity via both reflex and direct effects involving the hypothalamus and brainstem structures that provide excitatory drive to sympathetic pre-ganglionic motoneurones. Using an arterially perfused working heart-brainstem preparation, we evaluated the sympatho-excitatory response recorded from the thoracic sympathetic chain (tSC) in response to systemic ischaemia (produced by arresting perfusion transiently) before and after transecting at both the ponto-medullary (p-m) and medullary-spinal (m-s) junctions consecutively. Ischaemia produced a striking increase in tSC activity that persisted after transecting at both the p-m and m-s levels (intact: 70±3%; p-m: 77±7 %; m-s: 61±6 %; n=9). Similar responses were seen in sinoaortic denervated rats (n=4). Following administration of a ganglionic blocker (hexamethonium, 25 mg/kg) the ischaemic-induced sympatho-excitatory response was reduced (12±6 %, n=4). In m-s transected preparations, intrathecal injection of N2-saturated saline increased tSC discharge (22±3 %, n=4), which was attenuated by hexamethonium (5±1 %). These data indicate that the ischaemia induced increase in tSC activity is preserved by the spinal cord. We propose that neural mechanisms within the cervical-thoracic segments make a substantial contribution to the sympatho-excitatory response during systemic ischaemia. Supported by FAPESP & CNPq (Brazil) & the British Heart Foundation (UK)." @default.
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- W2783576409 date "2006-03-01" @default.
- W2783576409 modified "2023-10-18" @default.
- W2783576409 title "Significant contribution from the thoracic spinal cord in mediating ischaemia induced sympatho‐excitation." @default.
- W2783576409 doi "https://doi.org/10.1096/fasebj.20.4.a775-c" @default.
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