RESUMEN
Anthropogenic climate change is altering temperature regimes for coastal marine fishes. However, given that temperature changes will not occur in isolation of other stressors, it is necessary to explore the potential consequences of stress on the thermal tolerances and preferences of tropical marine fish in order to understand the thresholds for survival, and predict the associated coastal ecological consequences. In this study, we used exogenous cortisol injections to investigate the effects of a thermal challenge on checkered puffers (Sphoeroides testudineus) as a secondary stressor. There were no significant differences between control and cortisol-treated fish 48h following cortisol treatment for swimming ability (using a chase to exhaustion protocol), blood glucose concentrations or standard metabolic rate. In the lab, control and cortisol-treated puffers were exposed to ambient (29.1±1.5°C), ambient +5°C (heat shock) and ambient -5°C (cold shock) for 4h and to evaluate the consequences of abrupt temperature change on puff performance and blood physiology. Following cold shock, control fish exhibited increases in cortisol levels and weak 'puff' performance. Conversely, fish dosed with cortisol exhibited consistently high cortisol levels independent of thermal treatment, although there was a trend for an attenuated cortisol response in the cortisol-treated fish to the cold shock treatment. A 20-day complementary field study conducted in the puffer's natural habitat, a tidal creek in Eleuthera, The Bahamas, revealed that cortisol-injected fish selected significantly cooler temperatures, measured using accumulated thermal units, when compared to controls. These results, and particularly the discrepancies between consequences documented in the laboratory and the ecological trends observed in the field, highlight the need to establish the link between laboratory and field data to successfully develop management policies and conservation initiatives with regards to anthropogenic climate change.
Asunto(s)
Respuesta al Choque por Frío/efectos de los fármacos , Respuesta al Choque Térmico/efectos de los fármacos , Hidrocortisona/farmacología , Tetraodontiformes/fisiología , Animales , Bahamas , Glucemia , Natación , Temperatura , Tetraodontiformes/metabolismoRESUMEN
The consequences of stress on the behaviour of wild creek chub Semotilus atromaculatus outside the reproductive period were studied using a single intra-coelomic injection of cortisol, suspended in coconut butter, to experimentally raise plasma cortisol levels. Behaviour between cortisol-treated, sham-treated (injected with coconut butter) and control S. atromaculatus was compared in a mesocosm system, using a passive integrated transponder array, and in a natural stream system (excluding shams), using surgically implanted radio transmitters. While laboratory time-course studies revealed that the cortisol injection provided a physiologically relevant challenge, causing prolonged (c. 3 days) elevations of plasma cortisol similar to that achieved with a standardized chasing protocol, no differences in fine-scale movements were observed between cortisol-treated, sham-treated and control S. atromaculatus nor in the large-scale movements of cortisol-treated and control S. atromaculatus. Moreover, no differences were observed in diel activity patterns among treatments. Differential mortality, however, occurred starting 10 days after treatment where cortisol-treated S. atromaculatus exhibited nearly twice as many mortalities as shams and controls. These results suggest that, although the experimental manipulation of cortisol titres was sufficient to cause mortality in some individuals, there were compensatory mechanisms that maintained behaviours (i.e. including activity and movement) prior to death. This study is one of the first to use experimental cortisol implants outside a laboratory environment and during the non-reproductive period and yields insight into how wild animals respond to additional challenges (in this case elevated cortisol) using ecologically meaningful endpoints.
Asunto(s)
Cyprinidae/fisiología , Hidrocortisona/farmacología , Actividad Motora/efectos de los fármacos , Estrés Fisiológico , Animales , Conducta Animal/efectos de los fármacos , Hidrocortisona/sangre , Ríos , TelemetríaRESUMEN
Despite providing symptomatic relief in patients with congestive heart failure (CHF), supplemental oxygen (O(2)) has been demonstrated to increase total peripheral resistance. The present study investigated the possibility that O(2) inhalation reduces nitric oxide (NO) bioavailability, using endothelium-dependent (acetylcholine) and -independent (phentolamine) vasodilators, and the antioxidant ascorbic acid. Ten patients (nine male and one female) with primary left ventricular failure participated in the study. Forearm venous occlusion plethysmography was used to study blood flow responses to acetylcholine and the alpha-adrenergic antagonist phentolamine during inhalation of either room air or 100% O(2), with and without the simultaneous infusion of ascorbic acid. Neither O(2) inhalation (3.9+/-0.4 compared with 3.8+/-0.3 ml.min(-1).100 ml(-1)) nor ascorbic acid infusion (5.2+/-0.4 compared with 5.5+/-0.4 ml.min(-1).100 ml(-1)) affected resting forearm blood flow. The percentage increase from basal blood flow after acetylcholine infusion was not altered by either O(2) inhalation or ascorbic acid infusion (room air, 140+/-55%; O(2), 118+/-46%; ascorbic acid, 147+/-39%; ascorbic acid+O(2), 109+/-31%). O(2) inhalation did, however, reduce the dilation induced by phentolamine (room air, 131+/-24%; O(2), 80+/-14%; P<0.05). These data indicate that oxygen inhalation does not increase forearm vascular resistance. Secondly, preservation of reactivity to acetylcholine during O(2) inhalation suggests that degradation of NO by O(2)-derived free radicals is not enhanced. Attenuation of phentolamine-induced vasodilation during O(2) inhalation, however, implies increased adrenergic activity, which may possibly exacerbate the detrimental effects of elevated sympathetic activity in CHF.
Asunto(s)
Acetilcolina/farmacología , Brazo/irrigación sanguínea , Ácido Ascórbico/farmacología , Insuficiencia Cardíaca/terapia , Terapia por Inhalación de Oxígeno , Disponibilidad Biológica , Femenino , Humanos , Masculino , Persona de Mediana Edad , Óxido Nítrico/farmacocinética , Fentolamina/farmacología , Pletismografía/efectos de los fármacos , Flujo Sanguíneo Regional/efectos de los fármacos , Resistencia Vascular/efectos de los fármacos , Vasodilatadores/farmacologíaRESUMEN
The acute action of insulin on neurogenic flare was investigated using iontophoresis. Twenty-five patients with insulin-dependent diabetes mellitus (IDDM) and 25 age- and gender-matched controls were studied. Axon reflex vasodilatation was evoked by transdermal iontophoresis of acetylcholine (ACh) before and after skin treatment by the iontophoresis of insulin and measured using laser Doppler velocimetry. Axon reflex responses were reduced in IDDM patients compared with controls (p< 0.001) but were restored after the iontophoresis of insulin. Insulin iontophoresis had no effect on the size of the axon reflex response in control subjects (p > 0.05). This study confirms the reduction of the ACh-induced flare in human patients with IDDM and has demonstrated relatively rapid effects of insulin on this cutaneous neurogenic response.