V.N. Yartsev – Ph.D. (Biol.), Senior Research Scientist, Pavlov Institute of Physiology RAS (St.-Petersburg) E-mail: yartsev@infran.ru  

Acidosis is a condition that is often confronted by both disease-free people (e.g. due to excessive physical exercise) and patients (e.g. patients suffering from diabetes, lung and kidney diseases, etc.) [1]. Therefore, the investigation of the acidosis effect on the tone of different blood vessels and correspondingly on the blood supply to different organs is of a great theoretical and practical importance. Internal carotid artery is known to play a key role in supplying blood to the brain [2], but we failed to find works dealing with the effect of acidosis on the artery contractility. Previously, we have shown the profound inhibitory effect of acidosis on the rat tail artery constriction evoked by noradrenaline or by the neurogenic stimulation of the perivascular nerves [3]. The primary concern of this research is to examine the effects of acidosis on the neurogenic tone of the rat internal carotid artery. The experiments were carried out on the isolated segments of the artery. Neurogenic contraction of the vessel segment was evoked by periodic electrical field stimulation of perivascular nerves before and after addition of noradrenaline in cumulative concentration (from 0.01 μM to 10 μM). pH value of the solution (7.4 or 6.6, as required) was established by varying the amount of CO2 bubbled through the solution, thus modeling respiratory acidosis. In our experiments, acidosis was shown not to modify the artery resting tone. Noradrenaline-induced constriction of the internal carotid artery was slightly increased by acidosis, as opposed to the tail artery constriction significantly decreased by acidosis (Fig. 1). Neurogenic constriction of the internal carotid artery both in the absence and in the presence of noradrenaline in concentration from 0.01 μM to 0.1 μM was not modified by acidosis, in contrast to the tail artery constriction, which was significantly decreased by acidosis under the same conditions (Fig. 2). Noradrenaline-induced potentiation of the neurogenic constriction shown in our experiments was not modified by acidosis in the presence of low concentrations of noradrenaline (0.01-0.1 μM) and was increased significantly in the presence of high concentrations of noradrenaline (0.5 and 10 μM) and high frequency of electrical field stimulation (40 Hz). The rat internal carotid artery in contrast to the tail artery was shown not to dilate in the presence of the respiratory acidosis via decrease in the spontaneous, noradrenaline-evoked or neurogenic tone of the artery. This might be related to the defense of the brain from the adverse effect of acidic blood and/or high levels of carbon dioxide in the blood.

1. Celotto A.C., Capellini V.K., Baldo C.F., Dalio M.B., Rodrigues A.J., Evora P.R. Effects of acid-base imbalance on vascular reactivity // Braz. J. Med. Biol. Res. 2008. V. 41. № 6. P. 439–445.
2. Sato K.1., Sadamoto T., Hirasawa A., Oue A., Subudhi A.W., Miyazawa T., Ogoh S. Differential blood flow responses to CO2 in human internal and external carotid and vertebral arteries // J. Physiol. 2012. V. 590. № 14. P. 3277–3290.
3. Yarcev V.N., Karachenceva O.V. Vosstanovlenie noradrenalinom nejrogennoj vazoreaktivnosti, snizhennoj acidozom, pri raznyh chastotah elektrostimulyacii // Rossijskij fiziologicheskij zhurnal im. I.M. Sechenova. 2015. T. 101. № 9. S. 1042–1052.