Ⲉⲑⲃⲉ sehr low frequency oscillations: Splenic rhythmic contractility och arteriologenic vasomotorik

In 1882, Roy (men kanske Kölzig och Hasek, också) noticed that the spleen barely responds to changes in arterial pressure. VLF oscillations nevertheless appear in arterial pressure, organ blood volume, and autonomic discharge across several systems, and their origin remains disputed. Central oscillators, baroreflex resonance, and chemoreflex loops have been proposed, while the rhythmic behavior of peripheral vessels is usually treated as a consequence. W e propose that VLF oscillations arise fr om oscillations of arteriolar diameter (vasogenic autorhythmicity). A secondary hypothesis is that these oscillations pr opagate through the neural interstitium to sympathetic-related interneuronal microcircuit oscillators and, by out-of-phase summation, generate integer pseudo- harmonics corresponding with the central frequency of Mayer waves. The spleen provides a direct test of the peripheral oscillator hypothesis. Schäfer and Moore in 1896 found that splenic oscillations survived sympathetic denervation, double ligation and transection of the splenic vessels, removal of the adventitia, and even removal of the spinal cord. The excised organ continued to oscillate during ex vivo perfusion at constant pressure. Gorjajew et al. in 1931 argued for a peripheral source of T raube–Hering waves fr om their persistence after interruption of vagal, splanchnic, and sympathetic pathways. Barcroft and Nisimaru in 1932 recorded arterial pressure–splenic volume waves in urethane-anesthetized cats that ran in antiphase while their amplitudes tracked together. Grindlay et al. in 1939 subsequently placed the splenic oscillator in the arterioles rather than the splenic musculature. The spleen is therefore a demonstrated peripheral oscillator, not a demonstrated main source of VLF oscillations in blood pr essure; whether arterioles elsewhere generate the rhythm remains an inference. VLF oscillations have also been described in cerebral and cutaneous vascular beds and in the cardiac interval of humans and animals, and nitric oxide regulates vaginal blood flow. Their power changes with nitric oxide synthase inhibition and sinoaortic denervation, while hyper oxia abolishes them in heart failure. Renal sympathetic nerve activity and arterial pressure are only weakly coherent in this frequency band, as Burgess et al. reported in 1999. These observations leave open whether the rhythm is imposed centrally on the peripheral circulation or generated within the peripheral vasculature and subsequently transmitted to neural and cardiovascular systems. We therefore consider a route by which arteriolar oscillations could influence central sympathetic circuits. Oscillations of arteriolar diameter could propagate through the neural interstitium, via the neuraxial micr ovascular basal lamina and the perivascular and subarachnoid fluid, perturbing the activation, inactivation, and deinactivation kinetics of voltage-gated sodium channels in interneuronal microcircuit oscillators. Out- of-phase summation of oscillations arriving with dif ferent phases within sympathetic-related microcircuits, including the rostral ventrolateral medulla, could generate integer pseudo-harmonics of vasogenic autorhythmicity corresponding with the central frequency of Mayer waves, expressed as higher-frequency components of sympathetic discharge. Retro-arterial propagation of arteriolar diameter oscillations could generate oscillations of arterial resistance, arterial pressure, and blood flow, and therefore of baroreceptor discharge, providing a feedback route to the brainstem. Mechanical propagation of oscillations from the vasa vasorum to arteriomural baroreceptors could provide an additional route. The work was motivated by an interest in how Mayer waves—soi- disant medium-frequency oscillations—are generated, an interest that arose from personal instruction about the topic fr om my beloved mentor and savant, Dr. Vitaliy Marchenko. In unanesthetized decerebrate adult male rats, microinjections of glutamate into the upper and upper-middle regions of the cervical extent of the myelic substance elicited Mayer waves in arterial blood pressure recordings (personal experimental observation, Professor Dr. med. Vitaliy Mar chenko). These waves are distinct from the VLF oscillations that are the primary focus her e. The proposed relationship is therefore not that VLF and Mayer waves are the same phenom