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The Trigeminocardiac Reflex as Oxygen Conserving Reflex in Humans: Its Ischemic Tolerance Potential

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The trigemino-cardiac reflex (TCR) is defined as a sudden onset of parasympathetic dysrhythmia, sympathetic hypotension, apnea or gastric hypermotility during the stimulation of any of the sensory branches of the trigeminal nerve. The sensory nerve endings of the trigeminal nerve transmit neuronal signals via the Gasserian ganglion to the sensory nucleus of the trigeminal nerve, forming the afferent pathway of the reflex arc. Through this physiological response, adjustments of the systemic and cerebral circulations are initiated to change cerebral blood flow in a manner that is not yet understood. It appears that the cerebrovascular response to hypoxemia is, to a large extent, due to this reflex and generated by the activation of neurons of the rostral ventrolateral reticular nucleus. TCR is therefore an “oxygen-conserving-reflex” in human as it produces cross-tolerance to oxygen deprivation, thus reinforcing cerebral adaptation to oxygen demand/ supply mismatching via energy-sparing pathways. The existence of such endogenous neuroprotective strategies may extend beyond the actually known clinical appearance of the TCR and include the prevention of other potential brain injury states as well. Thus, we show that the beneficial effects of TCR extend beyond providing neuroprotection during the acute phase after ischemia. Induction of growth factor expression and neurogenesis by TCR might be a positive adaptation for an efficient repair and plasticity in the event of an ischemic insult.

Keywords: Cardiac reflex; ischemia; ischemia tolerance; oxygen-conserving reflex; post conditioning; rostral ventrolateral reticular nucleus of the medulla

Document Type: Research Article


Publication date: November 1, 2008

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  • Vascular Disease Prevention publishes reviews as well as original papers to update all those concerned with this topic at the clinical or scientific level. In addition to clinically relevant topics, we consider reviews and original papers dealing with the more scientific aspects of vascular disease prevention. This includes the evaluation of emerging vascular risk factors, research dealing with the pathogenesis of atherosclerosis and the investigation of new treatment options both at the clinical and scientific level (e.g. epidemiology, patient-based studies, experimental models, in vitro experiments or molecular research). Therefore, another function of Vascular Disease Prevention is to bridge the gap between clinical practice and ongoing laboratory-based research.

    In particular, we welcome critical reviews and comments on recent trials. This is a topic that requires regular updates because of the large number of trials published every year.

    Debates are encouraged in the correspondence section of this journal.
    The editorial structure of Vascular Disease Prevention is set up with the aim of dealing with the submitted material as rapidly as possible. Specialist editors will provide a more expert and rapid assessment unlike a more centralized editorial structure.

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