Transmission of Information by the Arterial Blood Stream with Particular Reference to Carbon Dioxide

Abstract

An estimate of the amount of information transmitted by way of the arterial blood stream in animals is made. Many assumptions are necessary to pose the problem in analyzable form. Taking carbon dioxide as a representative substance, a distribution of maximum entropy is developed. Three points emerge: (1) that homeostatic stability can be related to chemoreceptor sensitivity if both are given statistical interpretations consistent with concepts of information transmission, (2) that the heart acts as a filter which has considerable smoothing effect which depends in a specific fashion upon the cardiac residual volumes, and (3) a numerical estimate of channel capacity is made. The estimate is undoubtedly high. Assuming values typical of man, the calculated channel capacity for CO(2) is 3.5 to 4.7 bits per second. Since some sixty substances of communication importance occupy the blood stream simultaneously, the blood stream has a total capacity near 250 bits per second if every chemical modality has the same properties as CO(2).

Mechanism of augmented exercise hyperpnea in chronic heart failure and dead space loading

“…We show that Q1–Q5 can be satisfactorily and consistently explained within this new unifying framework. Our results provide strong evidence indicating that the chemosensing mechanism at the controller is endowed with cognition and perception capabilities that may be responsive to putative drive signals mediated by within-breath Pa CO 2 oscillations, a form of dynamic chemoreceptor signaling which has been suggested to play an important role in the control of V̇ E independent of breath-to-breath fluctuations in the mean Pa CO 2 level (Band et al, 1980; Collier et al, 2008; Cross et al, 1982; Cunningham et al, 1973; Saunders, 1980; Yamamoto, 1960; Yamamoto, 1962). Preliminary findings of this work have been presented in abstract form (Poon, 2013a, b).…”

“…However, it is possible that the controller may confuse rebreathed CO 2 with inhaled CO 2 and treat them alike, since both of them are introduced via the airways. Such an “identity mix-up” is possible provided the respiratory chemosensing mechanism at the controller is responsive to dynamic chemoreceptor signaling mediated by within-breath Pa CO 2 oscillations rather than (or in addition to) breath-to-breath fluctuations of the mean Pa CO 2 level, as suggested previously by Yamamoto and others (Band et al, 1980; Collier et al, 2008; Cross et al, 1982; Cunningham et al, 1973; Saunders, 1980; Yamamoto, 1960; Yamamoto, 1962). In other words, the controller is likely “tricked” by the rebreathed CO 2 and may mistake it for inhaled CO 2 if the controller is “short-sighted” and reacts instinctively to the onrush of rebreathed CO 2 during each inspiration rather than “take a long view” to see that such rebreathed CO 2 does not really clog the CO 2 elimination mechanism on a breath-to-breath basis as inhaled CO 2 does.…”

Stride frequency and ventilation at constant carbon dioxide output.

“…After almost a century of debate, there is still no clear concensus as to which mechanism is responsible for exercise hypernoea. Filley and Heineken (1976), Wasserman et al (1974) and Yamamoto (1962) have all suggested mechanisms for a humourally mediated control of ventilation. Kao et al (1955Kao et al ( , 1963, with their cross circulation studies suggested afferent feedback from the working muscle as a control mechanism, while Eldridge (1977) has advocated the contribution of central neural control.…”

Control of ventilation during submaximal exercise: A brief review

“…In fact, literature on the topic suggests that mean PaCO 2 and pH are similar to resting values during short-term moderate exercise (Wasserman et al, 1981). Yamamoto and Edwards (1960) and Yamamoto (1962) were the first to suggest a control mechanism linked to PaCO 2 and {H + } a but which controlled ventilation independent of mean PaCO 2 /{H + } a . This hypothesis proposes that ventilation may be stimulated via breath by breath PaCO 2 and pH oscillations without a significant alteration in mean PaCO 2 or pH.…”