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Respiration and Acid-Base Physiology of the Spotted Gar, A Bimodal Breather : I. Normal Values, and the Response to Severe Hypoxia
1 Departments of Zoology and Marine Studies, The University of Texas at Austin, Port Aransas Marine Laboratory, Port Aransas, Texas 78373, U.S.A.; University of Pennsylvania, School of Medicine, Department of Physiology Philadelphia, Penna. 19104, U.S.A.
2 Departments of Zoology and Marine Studies, The University of Texas at Austin, Port Aransas Marine Laboratory, Port Aransas, Texas 78373, U.S.A.
In normally aerated water, at 20 °C, gar accounted for 42 % of their MOO2 from their lungs, while in hypoxic water (POO2
12 torr) their entire MOO2 was from the lung, and O2 was lost through the gills. CO2 excretion in both normoxia and hypoxia was primarily via the gills.
Lung ventilation increased 1150%, accompanied by an elevation of pulmonary perfusion from 5.9 to 12.1 ml.kg-1.min-1 in hypoxia, which accounts for the enhanced pulmonary MOO2. Cardiac output increased from 31 to 40.5 ml.kg-1.min-1 and systemic perfusion was maintained in hypoxia.
The difference in acid-base status between pre- and post-branchial blood (PCOCO2, pH and total CO2), changed only slightly during hypoxia, but the oxygen difference reversed. Normal dorsal aortic (DA) POO2 was 23.8 torr, ventral aortic (VA) 20.3; during aquatic hypoxia the mean values were 21.9 and 22.6, respectively. Blood pressure rose in both the VA and DA in hypoxia but the branchial vascular resistance did not change. The oxygen transfer factor did not change significantly between normoxia and hypoxia.
Anatomical studies of the gill microvasculature revealed a reduced and channelized lamellar circulation. No respiratory shunt pathways were found around the lamellae.
The physiological and anatomical data indicated that the gar did not change lamellar perfusion or use shunt pathways to avoid hypoxic O2 loss.
Submitted on April 1, 1981
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