The effect of oxygen on the growth of Oncorhynchus mykiss embryos with and without a chorion

Goldberg

et al. 2007

SUMMARY We investigated the influence of oxygen demand (developmental stage) and supply (hypoxia, water flow rate, the chorion and body movements) on the oxygen concentration within the boundary layer next to the chorion of embryos or skin of larvae of rainbow trout (Oncorhynchus mykiss). Oxygen microelectrodes were used to measure dissolved oxygen (DO) within the boundary layer of trout embryos and larvae. As the embryos and larvae developed, the DO gradient and the thickness of the boundary layer increased. The DO concentration within the boundary layer next to the chorion or skin surface decreased as the DO concentration in the free-stream water decreased. A decrease in water flow rate increased the magnitude of the gradient and thickness of the boundary layer. In normoxia, the DO in the perivitelline fluid inside the chorion was 16±3.0% saturation at 31 days post fertilization, indicating that the chorion was a significant barrier to oxygen diffusion. The number of body movements did not change when embryos were exposed to hypoxia before hatching, but after hatching, hypoxia resulted in a decrease in body movements of the larvae. Taken together, our data indicate that the oxygen boundary layer around trout embryos and larvae depends on both the oxygen demand and supply. The factors that significantly impacted boundary layer oxygen were developmental stage, free-stream oxygen levels, water flow rate, and the presence of the chorion.

Section: Introductionmentioning

confidence: 93%

Parameters influencing the dissolved oxygen in the boundary layer of rainbow trout (Oncorhynchus mykiss) embryos and larvae

Ciuhandu

Goldberg

et al. 2007

“…Dissolved O 2 was monitored daily in the normoxic (98.7±0.4%) and hypoxic (29.7±0.5%) treatment tanks throughout the experiment (Hach LDO101 electrode connected to Hach HQ30d meter, Hach Company, Mississauga, ON, Canada). Because hypoxia exposure delays salmonid development (Shumway et al, 1964;Hamor and Garside, 1976;Ciuhandu et al, 2005;Miller et al, 2008), embryo sampling was stage-matched for the two treatment groups. Embryos were sampled at Vernier Stages 27 (prehatch; circulatory system is formed and functioning), 30 (hatch), 32 and 33 (in preliminary experiments a large increase in P 50 was observed between these stages), and 35 (near-complete yolk absorption; Fig.…”

Section: Experimental Protocol Treatment Conditionsmentioning

confidence: 99%

Hypoxia delays hematopoiesis: retention of embryonic hemoglobin and erythrocytes in larval rainbow trout,Oncorhynchus mykiss, during chronic hypoxia exposure

Bianchini

2013

SUMMARYIn rainbow trout development, a switch occurs from high-affinity embryonic hemoglobin (Hb) and round, embryonic erythrocytes to lower-affinity adult Hb and oval, adult erythrocytes. Our study investigated the early ontogeny of rainbow trout blood properties and the hypoxia response. We hypothesized that hypoxia exposure would delay the ontogenetic turnover of Hb and erythrocytes because retention of high-affinity embryonic Hb would facilitate oxygen loading. To test this hypothesis we developed a method of efficiently extracting blood from individual embryos and larvae and optimized several techniques for measuring hematological parameters on microliter (0.5-2.0 μl) blood samples. In chronic hypoxia (30% of oxygen saturation), stage-matched embryos and larvae possessed half the Hb concentration, erythrocyte counts and hematocrit observed in normoxia. Hypoxia-reared larvae also had threefold to sixfold higher mRNA expression of the embryonic Hb α-1, β-1 and β-2 subunits relative to stage-matched normoxia-reared larvae. Furthermore, in hypoxia, the round embryonic erythrocytic shape persisted into later developmental stages. Despite these differences, Hb-oxygen affinity (P 50 ), cooperativity and the Root effect were unaltered in hypoxia-reared O. mykiss. The data support our hypothesis that chronic hypoxia delays the ontogenetic turnover of Hb and erythrocytes, but without the predicted functional consequences (i.e. higher than expected P 50 ). These results also suggest that the Hb-oxygen affinity is protected during development in chronic hypoxia to favor oxygen unloading at the tissues. We conclude that in early trout development, the blood-oxygen transport system responds very differently to chronic hypoxia relative to adults, possibly because respiration depends relatively more on oxygen diffusion than convection.

“…In addition, the encapsulated, non-motile embryos may remain under these conditions for up to 5 months prior to emergence (Youngson et al, 2004). Previous work has demonstrated that embryonic development of teleost fish is extremely sensitive to environmental conditions (Ørnsrud et al, 2004) and that chronic hypoxia exposure delays development in fish (Shumway et al, 1964;Hamor and Garside, 1976;Ciuhandu et al, 2005;Spicer and Burggren, 2003;Bagatto, 2005;Miller et al, 2008). The reduction in developmental rate represents an adaptive response to reduce O 2 demand (Miller et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

The ontogeny of regulatory control of the rainbow trout (Oncorhynchus mykiss) heart and how this is influenced by chronic hypoxia exposure

Miller

Gillis

2011

SUMMARYSalmonid embryos develop in cool waters over relatively long periods of time. Interestingly, hypoxic conditions have been found to be relatively common in some nesting sites (redds). The goals of this study were to determine the ontogeny of cardiac regulation in rainbow trout early life stages and how this is influenced by chronic hypoxia. The heart rate response to cholinergic and adrenergic receptor stimulation or inhibition was measured in individuals reared in normoxic (100% O 2 saturation) or hypoxic (30% O 2 saturation) conditions from fertilization to embryonic stages 22, 26 and 29, and larval stages 30 and 32. In normoxia, heart rate increased in response to -adrenergic receptor stimulation (isoproterenol) as early as embryonic stage 22, and decreased with the antagonist propranolol after this stage. Cholinergic stimulation (acetylcholine) was ineffective at all stages, but atropine (acetylcholine antagonist) increased heart rate at larval stage 32. This demonstrates that cardiac -adrenergic receptors are functional at early life stages, while cholinergic receptors are not responsive until after hatching. Collectively, embryos had cardioacceleration control mechanisms in place just after the heartbeat stage, while cardio-inhibitory control was not functional until after hatching. Chronic hypoxia exposure triggered bradycardia, increased the response to adrenergic stimulation in embryos and larvae, and delayed the onset of cholinergic control in larvae. In non-motile stages, therefore, survival in chronic low oxygen may depend on the ability to alter the cardiac ontogenic program to meet the physiological requirements of the developing fish.