Time domains of the hypoxic ventilatory response in ectothermic vertebrates

Over a decade has passed since Powell et al. (Respir Physiol 112:123–134, 1998) described and defined the time domains of the hypoxic ventilatory response (HVR) in adult mammals. These time domains, however, have yet to receive much attention in other vertebrate groups. The initial, acute HVR of fish, amphibians and reptiles serves to minimize the imbalance between oxygen supply and demand. If the hypoxia is sustained, a suite of secondary adjustments occur giving rise to a more long-term balance (acclimatization) that allows the behaviors of normal life. These secondary responses can change over time as a function of the nature of the stimulus (the pattern and intensity of the hypoxic exposure). To add to the complexity of this process, hypoxia can also lead to metabolic suppression (the hypoxic metabolic response) and the magnitude of this is also time dependent. Unlike the original review of Powell et al. (Respir Physiol 112:123–134, 1998) that only considered the HVR in adult animals, we also consider relevant developmental time points where information is available. Finally, in amphibians and reptiles with incompletely divided hearts the magnitude of the ventilatory response will be modulated by hypoxia-induced changes in intra-cardiac shunting that also improve the match between O2 supply and demand, and these too change in a time-dependent fashion. While the current literature on this topic is reviewed here, it is noted that this area has received little attention. We attempt to redefine time domains in a more ‘holistic’ fashion that better accommodates research on ectotherms. If we are to distinguish between the genetic, developmental and environmental influences underlying the various ventilatory responses to hypoxia, however, we must design future experiments with time domains in mind

Shanghaied into the future: the Asianization of the future Metropolis in post-Blade Runner cinema

The clichéd 1930–1950 Western cinematic images of Shanghai as a fascinating den of iniquity, and, in contrast, as a beacon of modernity, were merged in Fritz Lang’s Metropolis. As a result, a new standard emerged in science ction lms for the representation of future urban conglomerates: the Asianized metropolis. e standard set by this lm, of a dark dystopian city, populated by creatures of all races and genetic codes, will be adopted in most of the representations of future cities in non-Asian cinema. is article traces the representation of Shanghai in Western cinema from its earliest days (1932– Shanghai Express) through Blade Runner (1982) to the present (2013– Her). Shanghai, already in the early 1930s, sported extremely daring examples of modern architecture and, at the same time, in non-Asian cinema, was represented as a city of sin and depravity. is dualistic representation became the standard image of the future Asianized city, where its debauchery was o en complemented by modernity; therefore, it is all the more seedy. Moreover, it is Asianized, the “Yellow Peril” incarnated in a new, much more subtle, much more dangerous way. As such, it is deserving of destruction, like Sodom and Gomorrah

Treatment with the selective serotonin reuptake inhibitor, fluoxetine, attenuates the fish hypoxia response

The selective serotonin reuptake inhibitor (SSRI) fluoxetine (FLX), the active ingredient of the antidepressant drug Prozac, inhibits reuptake of the neurotransmitter, serotonin (5-HT; 5-hydroxytryptamine), into cells by the 5-HT transporter (SERT). Given the role of 5-HT in oxygen detection and the cardiovascular and ventilatory responses of fish to hypoxia, we hypothesized that treatment of the Gulf toadfish, Opsanus beta, with FLX would interfere with their response to hypoxia. Toadfish treated intra-arterially with 3.4 μg.g(−1) FLX under normoxic conditions displayed a transient tachycardia and a biphasic caudal arterial blood pressure (P(CA)) response that are in direct conflict with the typical hypoxia response. Fish injected intraperitoneally with FLX under normoxia had resting cardiovascular and ventilatory parameters similar to controls. Upon exposure to hypoxia, control toadfish exhibit a significant bradycardia, reduction in P(CA) and an increase in ventilatory amplitude (V(AMP)) without any changes in ventilatory frequency (fV). Fish treated IP with 10 μg.g(−1) FLX showed an interference in the cardiovascular and ventilatory response to hypoxia. Interestingly, when treated with 25 μg.g(−1) FLX, the bradycardia and V(AMP) response to hypoxia were similar to control fish while the P(CA) response to hypoxia was further inhibited. These results suggest that SERT inhibition by FLX may hinder survival in hypoxia