Sympathetic nerve regulation of cochlear blood flow during increases in blood pressure in humans

Abstract

The purpose of this work was to show that regulation of the blood flow to the cochlea by the sympathetic nervous system occurs in humans at the level of the cochlear microcirculation during increases in blood pressure and that its involvement depends on the pressure level. Eight anaesthetized patients undergoing tympanoplasty for hearing disease took part in a pharmacological protocol of stimulation and inhibition of the autonomic nervous system (ANS) to provide variations in systolic blood pressure (BPS) and cochlear blood flow (CBF). The CBF was measured by laser-Doppler flowmetry. Changes in autonomic nerve activity were brought about by changes in baroreceptor activity (BR) initiated by the injection of an alpha adrenergic agent before and after sympathetic and parasympathetic blockade. The CBF variations (delta CBF) were plotted against BPS increases at each stage of the ANS inhibition. The BR diminished significantly after alpha blockade, after alpha and beta blockade, and after alpha and beta blockade and atropine, by 50% (P < 0.01), 29% (P < 0.05), and 95% (P < 0.001) respectively. The BPS increased significantly (P < 0.01) by 36 (SD 9)%, 47 (SD 1)%, and 67 (SD 16)% respectively. The CBF response to an increase in BPS exhibited two opposing variations in the patients: CBF decreased significantly in one group, and increased significantly in the other group. In both groups, delta CBF decrease and delta CBF increase, respectively, were significant after ANS blockade; even so the decrease and increase, respectively, levelled off at BPS around 160 mmHg before ANS blockade. For BPS below 160 mmHg, correlations between delta CBF and BPS were significant before inhibition and after inhibition of ANS. For BPS below 160 mmHg, BPS and delta CBF were not correlated before inhibition of ANS, and were significantly correlated after inhibition of ANS. For BPS below 160 mmHg, CBF response to the BPS increase was the same before and after ANS blockade, i.e. ANS control did not predominate: even so, for BPS above 160 mmHg, the CBF response to BPS increase was different before and after ANS blockade: CBF varied significantly after ANS blockade as it varied for BPS below 160 mmHg, while it remained constant before ANS blockade that elicited ANS control of CBF. In conclusion, sympathetic nerve regulation via its vasomotor tone at the level of cochlear microcirculation occurred markedly when the blood pressure was above 160 mmHg; the autonomic nervous system would appear to control the cochlear blood flow against large variations in blood flow in response to hypertensive phenomena.

Management of Idiopathic Sudden Sensorineural Hearing Loss

“…These findings, the presence of low initial values of perilymphatic oxygenation in sudden deafness [20] and the association of sudden deafness with vascular and hematological disease, including macroglobulinemia, sickle cell disease or polycythemia, suggest a vascular cause for some cases of SHL, such as thrombosis, embolism, vascular spasm or hyperviscosity. Experimental and clinical studies have reported a variation of cochlear blood flow in relation to a variation of arterial pressure, or to sympathetic nerve stimulation, and SHL as a consequence to slow blood flow in the vertebrobasilar system and in the common carotid artery or associated with arterial hypotension [21][22][23][24][25]. Moreover, we have evidenced that an acute hypertension could induce a rapid and reversible decrease in the endochochlear potential in rats, similar to the decreased endocochlear potential observed in anoxic conditions (unpubl.…”

Remifentanil and controlled hypotension; comparison with nitroprusside or esmolol during tympanoplasty

“…In earlier studies that we performed on skin blood flow, we observed the same phenomenon, i.e., skin blood flow varied before blood pressure and heart rate. [25][26][27] In the present study, a target pressure of 80 mmHg was chosen to define hypotension in order to preserve "protective" autoregulatory mechanisms of cochlear blood flow that exist above this value; 28,29 below this level, the blood flow correlates with the arterial blood pressure. 28 The hypotensive effect of nitroprusside, esmolol and remifentanil on middle ear blood flow was a balanced result between their direct cardiac effect and/or vasomotor effect and the vasomotor drives originating from the counter-regulatory responses.…”

NADPH-diaphorase histochemistry reveals an autonomic-like innervation in the postnatal hamster cochlea

“…Electrophysiological tests report that cochlear vessels respond rapidly to sympathetic stimulation (Ren et al, 1993;Degoute et al, 1997). Autoregulation by the sympathetic system may protect the cochlea against these sudden blood pressure changes by constricting the vasculature when necessary (Brechtelsbauer et al, 1995;Laurikainen et al, 1997).…”