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Journal of Experimental Biology, Vol 96, Issue 1 405-412, Copyright © 1982 by Company of Biologists
JOURNAL ARTICLES |
H Gesser and E Jorgensen
The influence of hypercapnic acidosis upon the heart was examined in four vertebrate species. The CO2 in the tissue bath was increased from 2.7 to 15% at 12 degrees C for flounder (Platichthys flesus) and cod (Gadus morhua) and from 3 to 13% at 22 degrees C for turtle (Pseudemys scripta) and rainbow trout (Salmo gairdneri). During hypercapnia, as previously described, there was a decline and recovery of contractility in heart strips of flounder and turtle, and a sustained decrease in cod and rainbow trout. At high CO2 the increase in contractile force following increases in the extracellular Ca-concentration were smaller for the cod myocardium than for the other myocardia. The intracellular pH (pHi), measured with the DMO method, in heart strips of turtle and trout was significantly lower at high than at low CO2. This acidifying effect expressed as the increase in the intracellular concentration of hydrogen ions was larger in the turtle than in the trout myocardium. Intracellular Ca-activity, measured by efflux of 45Ca from preloaded heart strips, was unaffected by high CO2 in trout, but was raised in the other three species. Thus the ability to counteract the negative inotropic effect of hypercapnia is apparently not due to cellular buffering or extrusion of hydrogen ions. More probably it involves (a) a release of intracellular Ca; (b) a positive inotropic effect of an increase in intracellular Ca-activity.
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