Goldfish were exposed to three qualitatively distinct forms of respiratory stress: phenylhydrazine HCI-induced reduction in blood oxygen-carrying capacity; transient (3 h) hypoxia; and transient (I or 2 h) temperature-forced increases in oxygen demand. Response embodied three common features: ( I ) the relative number of immature red cells increased, and these were 'H-thymidine positive;(2) the abundance of apparently karyorrhectic or degenerating cells rose; (3) cells undergoing a form of division became prevalent. Neither of the latter two cell types evidenced thymidine uptake. These observations suggest that respiratory distress triggers the proliferation of new erythrocytes, and that this is accompanied by elimination of some portion of the preexisting red cell population. It is hypothesized that the latter process limits viscosity-related elevation of cardiac work costs. The significance of division by circulating erythrocytes is not clear.

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To further assess the hypothesis that differential hemoglobin isomorph formation may be involved in the respiratory response of rainbow trout (Salmo gairdneri), yearling animals were first rendered acutely anemic by immersion in phenylhydrazine HCl. Erythropoiesis was then induced by gradual warming under normoxic and hypoxic conditions. While no significant differences in hemoglobin content were observed, trout exposed to hypoxia displayed transient, but significant differences in hematocrit. Significant variations in both the occurrence and abundance of specific isomorphs were also observed.

Immersion of goldfish, Carassius auratus, in 1 mg∙L−1 phenylhydrazine hydrochloride at 5 °C for 48 h led to reductions of 90–95% in hemoglobin and hematocrit within 10–14 days. Under similar conditions, 96-h exposures prompted heavy mortality. Fewer mortalities occurred after 24-h exposure periods; however, only modest reductions in O2-carrying capacity were seen. All higher concentration (2, 5, 10, 50 mg∙L−1) and temperature (10, 15, 20 °C) combinations led to complete mortality within 12–96 h regardless of exposure period (24, 48, 96 h). Exposure to phenylhydrazine hydrochloride caused decreases in hemoglobin and hematocrit, changes in the abundances of specific hemoglobin isomorphs, and the transient appearance of novel hemoglobin mobilities as well as evidence of osmo- and iono-regulatory dysfunction. Slow warming to 20 °C prompted red cell proliferation and hemoglobin synthesis and restoration of typical hemoglobin isomorph abundances. Incidence of transfer stresses was monitored by reference to differential leucocyte counts. Transfer led to lymphopenia and thrombopenia with neutrophilia and eosinophilia. Warming was accompanied by increases in lymphocyte and thrombocyte counts and reductions in those of monocytes and all granulocytes.