|
| |
|
|
|
|
||||
| Home Help Feedback Subscriptions Archive Search Table of Contents | ||||
|
Fig. 4. Comparison of the ability of preconditioning (5 min ofhypoxic pre-exposure)
to protect (A) hypoxia-sensitive (Gamperl
et al., 2001) and (B) hypoxia-tolerant
(Gamperl et al., 2004) trout
hearts from the myocardial dysfunction that follows more prolonged exposure to
hypoxia. In A, 5 min of hypoxic pre-exposure completely eliminated the loss of
myocardial function that normally followed the `Hypoxia-high workload'
protocol. In B, preconditioning with 5 min of hypoxia either did not affect,
or increased, the amount of myocardial dysfunction following exposure to `30
min of hypoxia'. Top panels, maximum cardiac output; middle panels, maximum
stroke volume; bottom panels, heart rate. Note that the hypoxia-tolerant trout
hearts in B required twice the duration of hypoxia (15 vs 30 min),
and 6 times the workload, as compared with hypoxia-sensitive hearts (A) to
achieve a comparable (15–20%) decrease in post-hypoxic myocardial
function. Values were obtained by comparing maximum in situ cardiac
function before and after the treatment protocols. All values are means
± S.E.M. (N=7–9).
Dissimilar letters indicate a significant difference at P<0.05, as
determined by one-way ANOVA. Hypoxia in these experiments was defined as
perfusate PO2=5–10 mmHg. Control hearts
were only exposed to oxygenated saline.
|
