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Oxygen Consumption of the Isolated Heart of Octopus: Effects of Power Output and Hypoxia
Author(s) -
D. F. Houlihan,
Claudio Agnisola,
Neil McLeod Hamilton,
I. Trara Genoino
Publication year - 1987
Publication title -
journal of experimental biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.367
H-Index - 185
eISSN - 1477-9145
pISSN - 0022-0949
DOI - 10.1242/jeb.131.1.137
Subject(s) - cardiac output , aortic pressure , cardiology , oxygen , medicine , blood pressure , hypoxia (environmental) , heart rate , chemistry , organic chemistry
A technique is described which allowed the measurement of the oxygen consumption of the isolated heart of Octopus vulgaris. Contraction of the heart resulted in an aortic output and a flow through the heart muscle into coronary veins (the coronary output). The flow and oxygen content of the aortic output and the coronary output were measured with variable input pressures and constant output back pressure (volume loaded), variable output back pressure and constant aortic output (pressure loaded), and during hypoxia. Volume loading of the heart resulted in an increase in aortic output, power output and total oxygen consumption. Pressure loading increased power output and total oxygen consumption of the heart. Exposure to hypoxia decreased the aortic output, power output and total cardiac oxygen consumption. In the response of the heart to reduced work, brought about either by a reduced input pressure or by hypoxic perfusate, the power output was linearly related to the total oxygen consumption of the heart. The oxygen extracted from the coronary output accounted for 80–100% of the total oxygen consumption of the heart. Coronary output amounted to 30% of the total cardiac output at maximum power output. In volume-loaded hearts the volume of the coronary output increased as aortic output increased; in pressure-loaded hearts coronary output increased as power output increased, but aortic output remained constant. In hypoxia, the coronary output increased as the aortic output fell. At a perfusate Po2 of around 50 Torr (1 Torr = 133 Pa), the aortic output ceased although the heart continued to beat and the coronary output continued, accounting for all of the oxygen consumption of the heart. The coronary output flow in vitro therefore has the capacity to be varied independently of the aortic output flow to maintain the oxygen supply to the perfused cardiac muscle.

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