Cardiac remodelling in rainbow troutOncorhynchus mykissWalbaum in response to phenylhydrazine-induced anaemia
Author(s) -
Danielle L. Simonot,
Anthony P. Farrell
Publication year - 2007
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.004028
Subject(s) - rainbow trout , acclimatization , medicine , fish <actinopterygii> , endocrinology , hematocrit , biology , phenylhydrazine , zoology , chemistry , fishery , ecology , medicinal chemistry
We examined the nature, extent and timing of cardiac ventricular remodelling in response to chronic, chemically induced anaemia in warm- and cold-acclimated rainbow trout Oncorhynchus mykiss. Chronic anaemia was induced by bi-weekly injections of phenylhydrazine hydrochloride (PHZ) and resulted in transient but large decreases in haematocrit (Hct) and haemoglobin concentration. After 2 weeks of anaemia, relative ventricular mass (rM(V)) in warm-acclimated rainbow trout had already increased significantly and, by the eighth week of anaemia, rM(V) was 58% greater than in the sham-injected control fish. Temperature modulated the anaemia-induced ventricular remodelling and erythropoietic responses, as indicated by cold-acclimation reducing the extent of the cardiac remodelling and slowing erythropoietic recovery. For example, in cold-acclimated fish, PHZ reduced Hct to 8.8+/-1.9% (ranging from 4-16%) and increased rM(V) by 15% over a 4-week period, whereas the same treatment in warm-acclimated fish reduced Hct to only 17.4+/-2.1% (ranging from 6-29%) and yet increased rM(V) by 28%. Cold-acclimated fish also recovered more slowly from anaemia. In addition, warm-acclimated fish maintained compact myocardium between 32% and 37% during anaemia, while cold-acclimated fish responded with an increase in compact myocardium (from 29% to 37%). Routine cardiac output (Q) was continuously monitored following a single PHZ injection to examine the initial cardiac response to anaemia. Contrary to expectations, acute anaemia did not produce an immediate, proportionate increase in routine Q. In fact, Q did not increase significantly until Hct had decreased to 10%, suggesting that rainbow trout may initially rely on venous oxygen stores to compensate for a reduced arterial oxygen-carrying capacity. Thus, we conclude that myocardial oxygenation, acclimation temperature and cardiac work load could all influence anaemia-induced cardiac remodelling in rainbow trout.
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