Why the study?
The role of the Kölliker-Fuse complex in baroreflex and chemoreflex responses has not been established.
Does bilateral microinjection of cobalt chloride into the Kölliker-Fuse nucleus alter cardiovascular responses to hypoxia and baroreceptor activation in anesthetized rats?
Does bilateral microinjection of cobalt chloride into the Kölliker-Fuse nucleus alter cardiovascular responses to hypoxia and baroreceptor activation in anesthetized rats?
The Kölliker-Fuse nucleus plays an essential role in generating the tachycardic component of the cardiovascular chemoreflex but does not participate in the baroreflex in anesthetized rats.
Does not support clinical translation in humans; leaves open Kölliker-Fuse nucleus as a chemoreflex target for future animal studies.
Introduction: Parabrachial Kölliker-Fuse (KF) complex, located in dorsolateral part of the pons, is involved in the respiratory control, however, its role in the baroreflex and chemoreflex responses has not been established yet. This study was performed to test the contribution of the KF to chemoreflex and baroreflex and the effect of microinjection of a reversible synaptic blocker (Cocl2) into the KF in urethane anesthetized rats. Methods: Activation of chemoreflex was induced by systemic hypoxia caused by N2 breathing for 30 seconds "hypoxic- hypoxia methods" and baroreflex was evoked by intravenous injection (i.v.) of phenylephrine (Phe, 20 µg /kg/0.05–0.1 mL). N2 induced generalized vasodilatation followed by tachycardia reflex and Phe evoked vasoconstriction followed by bradycardia. Results: Microinjection of Cocl2 (5 mM/100 nL/side) produced no significant changes in the Phe-induced hypertension and bradycardia, whereas the cardiovascular effect of N2 was significantly attenuated by the injection of CoCl2 to the KF. Conclusion: The KF played no significant role in the baroreflex, but could account for cardiovascular chemoreflex in urethane anesthetized rats.
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Mirzaei-Damabi et al. (2019) studied this question.
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