Submitted on May 31, 2008
Revised on December 3, 2008
Accepted on December 13, 2008
Histamine induces postprandial tachycardia through a direct effect on cardiac H2-receptors in pythons
Nini Skovgaard1*, Kate Møller1, Hans Gesser2, and Tobias Wang3
1 University of Aarhus
2 Univ of Aarhus
3 University
* To whom correspondence should be addressed. E-mail: nini.jensen{at}biology.au.dk.
The intrinsic heart rate of most vertebrates studied, including humans, is elevated during digestion, suggesting that a non-adrenergic-non-cholinergic factor contributes to the postprandial tachycardia. The regulating factor, however, remains elusive and difficult to identify. Pythons can ingest very large meals and digestion is associated with a marked rise in metabolism that is sustained for several days. The metabolic rise causes more than a doubling of heart rate and a four-fold rise in cardiac output. This makes the python an interesting model to investigate the postprandial tachycardia. We measured blood pressure and heart rate in fasting Python regius, and at 24 and 48h after ingestion of a meal amounting to 25% of body weight. Digestion caused heart rate to increase from 25 to 56 min-1 while blood pressure was unchanged. The postprandial rise in heart rate was partially due to a doubling of intrinsic heart rate. The H2-antagonist did not affect heart rate of fasting snakes, but decreased heart rate by 15-20 min-1 at 24h into digestion, while it had no effects at 48h. Thus, the histaminergic tone on the heart rose from none to 30% at 24h, but vanished after 48h. In anesthetised snakes histamine caused a systemic vasodilatation and a marked increase in heart rate and cardiac output mediated through a direct effect on H2-receptors. Our study strongly indicates that histamine regulates heart rate during the initial phase of digestion in pythons. This study describes a novel regulation of the vertebrate heart.
