Mechanisms behind the postprandial increase in cardiac output: a clue obtained from transplanted hearts

Abstract

Consumption of a meal is followed by an increase in cardiac output (CO) which appears to be closely related to the concomitant increase in blood flow to the gastrointestinal organs. To gain information on the mechanism behind this increase in CO we have previously used Doppler ultrasound technique to record circulatory responses to a standardized meal in five patients with recently transplanted and thus denervated hearts. We obtained the surprising result that they reacted to the consumption of a meal with a greater increase in CO than did five matched normal controls. The patients also presented above-normal levels of heart rate (HR) and CO at rest. The same five patients have now been tested 18 months later to re-examine their remarkable cardiac response to ingestion of a meal. The hearts of two patients showed some signs of reinnervation, whereas the hearts of the other three were apparently still fully denervated. However, all five patients once again evolved a marked cardiac response to ingestion of a meal. Postprandial CO reached significantly higher levels in the patients than in the controls. The persistence of such a pronounced postprandial augmentation of CO in transplanted and largely denervated hearts strengthens the assumption that the heart is induced to increase its postprandial performance through the action of a humoral agent of some sort, possibly one of the hormones from the duodenal-pancreatic region.

Autonomic control of cardiorespiratory interactions in fish, amphibians and reptiles

“…The underlying regulatory mechanism remains elusive. Interestingly, however, patients with transplanted and fully denervated hearts exhibit a pronounced postprandial rise in cardiac output (56), suggesting that the cardiac stimulation is not reflex in nature, but, at least partially mediated by humoral factor(s).…”

Histamine induces postprandial tachycardia through a direct effect on cardiac H2-receptors in pythons

“…In addition to the autonomic nervous systems (8, 15), the postprandial cardiovascular response is probably governed by the direct action of hormones such as endocrine regulatory peptides released from the gastrointestinal organs (3, 7, 12). In fact, patients with transplanted and fully denervated hearts exhibit a pronounced postprandial rise in cardiac output (19,44,45), suggesting that the cardiac stimulation is not reflex in nature, but, at least partially, mediated by humoral factor(s).Humans and the common mammalian model species, such as mice and rats, are adapted to consuming small meals at frequent intervals. The magnitude of the digestive responses is, therefore, low, and the underlying regulatory processes may be difficult to identify.…”

“…In addition to the autonomic nervous systems (8, 15), the postprandial cardiovascular response is probably governed by the direct action of hormones such as endocrine regulatory peptides released from the gastrointestinal organs (3, 7, 12). In fact, patients with transplanted and fully denervated hearts exhibit a pronounced postprandial rise in cardiac output (19,44,45), suggesting that the cardiac stimulation is not reflex in nature, but, at least partially, mediated by humoral factor(s).…”

Impaired hemodynamic response to meal intake in insulin-resistant subjects: an impedance cardiography approach

“…A pivotal role in the regulation of the postprandial phase is played by insulin, which mediates metabolic and hemodymanic actions (2)(3)(4) and achieves the so-called hemodynamic-metabolic coupling. Food ingestion also contributes to modulate heart and blood vessel responses (5). In the insulin-resistant (IR) state, the metabolic and vascular milieus are altered (6,7), which thus determine the unfavorable proatherogenic state, which has been thoroughly documented (8,9).…”