Current research in physiology最新文献

The reduced availability of dissolved oxygen is a common stressor in aquatic habitats that affects the ability of the heart to ensure tissue oxygen supply. Among key signalling molecules activated during cardiac hypoxic stress, nitric oxide (NO) has emerged as a central player involved in the related adaptive responses. Here, we outline the role of the nitrergic control in modulating tolerance and adaptation of teleost heart to hypoxia, as well as major molecular players that participate in the complex NO network. The purpose is to provide a framework in which to depict how the heart deals with limitations in oxygen supply. In this perspective, defining the relational interplay between the multiple (sets of) proteins that, due to the gene duplication events that occurred during the teleost fish evolutive radiation, do operate in parallel with similar functions in the (different) heart (districts) and other body districts under low levels of oxygen supply, represents a next goal of the comparative research in teleost fish cardiac physiology.

Warm acclimation in fish is often characterized by an increase in heat tolerance and a reduction in physiological rates to improve the scope to respond to additional challenges including further warming. The speed of these responses can determine their effectiveness. However, acclimation rates vary across levels of biological organization and are poorly understood in part because most research is conducted after an acclimation period of >3 weeks, when acclimation is presumed to be complete. Here we show that when rainbow trout were transferred from 10 to 18 °C, over 50% of the total reduction of maximum heart rate (ƒ_Hmax) (i.e. the thermal compensation at moderate temperatures) occurred within 72 h, with further compensation occurring more gradually over the following 25 days. Also, the ability to increase ƒ_Hmax with acute warming improved within 24 h resulting in a 30% rise in peak ƒ_Hmax, but this ultimately declined again with prolonged (28 days) exposure to 18 °C. In contrast with some previous studies, upper critical temperatures for ƒ_Hmax did not increase. Nonetheless, we demonstrate that rapid cardiac plasticity is possible in rainbow trout and likely blunts the impacts of thermal variation over relatively short timescales, such as that associated with heat waves and migration between water bodies.

Background

Antenatal/early postnatal hypothyroidism weakens NO-mediated anticontractile influence of endothelium in coronary arteries of adult rats, but it remains unclear whether this occurs in other vascular regions. We hypothesized that developmental thyroid deficiency is followed by region-specific changes in the endothelial NO-pathway activity in systemic vasculature. To explore this, we estimated the effects of antenatal/early postnatal hypothyroidism on NO-pathway activity and its potential local control mechanisms in rat mesenteric and skeletal muscle (sural) arteries.

Methods

Dams were treated with 6-propyl-2-thiouracil (PTU) in drinking water (0.0007%) during pregnancy and 2 weeks postpartum; control (CON) females received PTU-free water. Adult offspring (10–12-weeks) arteries were studied by wire myography, qPCR, and Western blotting.

Results

Endothelium removal or inhibition of NO-synthase with L-NNA augmented contractile responses to α₁-adrenoceptor agonist methoxamine. In PTU compared to CON group, these effects were stronger in sural arteries, but did not differ in mesenteric arteries. The responses of both arteries to NO-donor DEA/NO were similar in CON and PTU rats. mRNA contents of deiodinase 2 and thyroid hormone receptor α were similar in mesenteric arteries of two groups but were elevated in sural arteries of PTU group compared to CON. The abundance of eNOS protein was higher in sural arteries of PTU compared to CON rats.

Conclusion

Antenatal/early postnatal hypothyroidism is followed by an increase in NO-mediated anticontractile influence in sural, but not in mesenteric arteries of adult animals. The diversity of hypothyroidism effects may be due to different alterations of local T3 synthesis/reception in different vascular beds.

Asthma involves an increase in airway resistance even in periods between attacks, which generates changes in thoracoabdominal kinematics. The aim of the present study was to detect these adaptations at rest and after physical effort. Evaluations were performed using optoelectronic plethysmography at rest and immediately after physical effort of moderate intensity. Thirty-two children and adolescents participated in the present study (16 asthma- AG and 16 health controls-CG). After exercise, the AG exhibited a less variability of respiratory variables. The kinematic behavior of thoracoabdominal motion was the inverse of that found in healthy controls. These findings suggest mechanical and physiological adaptations to minimize the possible turbulence of the airflow and reduce the impact of airway resistance during physical exertion. Moreover, these changes are found even at rest and in patients whose asthma is clinically controlled.

Previous studies have shown that treatment with recombinant adropin, a circulating peptide secreted by the liver and brain, restores glucose utilization in the hearts of diet-induced obese mice. This restoration of fuel substrate flexibility, which is lost in obese and diabetic animals, has the potential to improve contractile function in the diabetic heart. Using an ex vivo approach, we examined whether short-term adropin treatment could enhance cardiac function in a mouse model of diet-induced obesity. Our study showed that acute adropin treatment reduces inhibitory phosphorylation of pyruvate dehydrogenase in primary neonatal cardiomyocytes, and leads to moderate improvements in ex vivo cardiac function in mice fed a low fat diet. Conversely, short-term exposure to adropin led to a small decrease in cardiac function in mice fed a long-term high fat diet. Insulin treatment did not significantly alter cardiac function in adropin treated hearts from either low or high fat diet mice, however acute adropin treatment did moderately restore some aspects of downstream insulin signaling in high fat diet fed mice. Overall, these data suggest that in an ex vivo setting, acute adropin treatment alone is not sufficient to promote improved cardiac function in obese animals.

Introduction

Thermal adaptation in fish is accompanied by morphological and electrophysiological changes in the myocardium. Little is known regarding seasonal changes of spatiotemporal organization of ventricular excitation and repolarization processes. We aimed to evaluate transmural and apicobasal heterogeneity of depolarization and repolarization characteristics in the rainbow trout in-situ ventricular myocardium in summer and winter conditions.

Methods

The experiments were done in summer-acclimatized (SA, 18°C, n = 8) and winter-acclimatized (WA, 3°C, n = 8) rainbow trout (Oncorhynchus mykiss). 24 unipolar electrograms were recorded with 3 plunge needle electrodes (eight lead terminals each) impaled into the ventricular wall. Activation time (AT), end of repolarization time (RT), and activation-repolarization interval (ARI, a surrogate for action potential duration) were determined as dV/dt min during QRS-complex, dV/dt max during T-wave, and RT-AT difference, respectively.

Results

The SA fish demonstrated relatively flat apicobasal and transmural AT and ARI profiles. In the WA animals, ATs and ARIs were longer as compared to SA animals (p≤0.001), ARIs were shorter in the compact layer than in the spongy layer (p≤0.050), and within the compact layer, the apical region had shorter ATs and longer ARIs as compared to the basal region (p≤0.050). In multiple linear regression analysis, ARI duration was associated with RR-interval and AT in SA and WA animals. The WA animals additionally demonstrated an independent association of ARIs with spatial localization across the ventricle.

Conclusion

Cold conditions led to the spatial redistribution of repolarization durations in the rainbow trout ventricle and the formation of repolarization gradients typically observed in mammalian myocardium.

In mammals a central circadian clock is located in the suprachiasmatic nuclei of the hypothalamus, which regulates the innate physiological rhythms to the ambient 24-h light-dark cycle. Melatonin is an essential component of circadian rhythm. The study aimed to evaluate the effects of melatonin administration on the respiratory rate (RR) and heart rate (HR) and their circadian rhythmicity in donkeys subjected to packing (load carrying) during the hot-dry season. Twenty healthy pack donkeys, aged 2–3 years with average weight of 93 ± 2.7 kg were divided into two groups randomly for the experiment. Group 1 donkeys (packing with melatonin) were administered melatonin for seven days during the study and subjected to packing, while group 2 were packed without melatonin administration. Both groups of donkeys were packed three times within the week, one day apart, covering a total distance of 20 km on each experimental day. Meteorological parameters were recorded during the study period. RR and HR were measured pre- and immediately (15 min) post-packing. Continuous measurement of the parameters started 16 h later, after the last packing procedures for a period of 27 h at intervals of 3 h. Temperature-humidity index (THI) pre-packing (73.67 ± 0.7) was lower (P < 0.05) than that obtained post-packing (80.33 ± 1.2). The THI recorded during the continuous measurement was at its peak at 15:00 h (86), indicating that the afternoon hours were thermally stressful to the donkeys. The THI was strongly correlated with HR recorded in packing (without melatonin) compared to packing (with melatonin) donkeys. The RR and HR values in both groups of donkeys were significantly (P < 0.05) higher immediately after packing. However, the post-packing values of the parameters were not different (P > 0.05) between the two groups of donkeys. The mesor (adjusted arithmetic mean) and amplitude of RR and HR in packing (without melatonin) donkeys were significantly (P < 0.05) higher than that recorded in packing (with melatonin) donkeys. In conclusion, melatonin reduced negative influence on the circadian rhythmicity (mesor and amplitude) of RR and HR in donkeys by exerting its anti-stress and antioxidant effects. The study has demonstrated the beneficial effect of melatonin and its administration may mitigate excessive respiratory and cardiac activities that may reduce the work output of donkeys during the hot-dry season.

The immune-suppressive role of sex steroids in mammals is well documented, but information on other vertebrates is limited. The present study was planned to analyze the effect of testosterone and progesterone in the modulation of immune functions of leucocytes in a reptile, Natrix piscator. Reptiles are unique organisms and this study is novel in that it provides an insight into immune-reproductive cross-talk in a reptile. Leucocytes were isolated from peripheral blood, cultured with different concentrations of testosterone and progesterone and different immune parameters like phagocytosis, superoxide production, and nitrite release were assessed. Lymphocytes were isolated and cell-mediated immunity was assessed through proliferation responses utilizing tetrazolium salt. Concentration-dependent suppressive effects of both the steroids on immune responses were observed. A differential suppressive effect of testosterone was also observed when a lymphocyte proliferation assay was studied. Using receptor antagonists such as cyproterone acetate and mifepristone restored the immune responses of cultured cells. It was summarized that gonadal steroids mediate a direct suppressive effect on innate and cell-mediated immune responses of blood immune cells. It was concluded that when gonadal steroids are high in reproductive seasons, the immune functions are suppressed to gain optimum reproductive success.

The prediction of running performance at different competitive distances is a challenge, since it can be influenced by several physiological, morphological and biomechanical factors. In experienced male runners heterogeneous for maximal oxygen uptake (VO₂max), endurance running performance can be well predicted by several key parameters of aerobic fitness such as VO₂max and its respective velocity (vVO₂max), running economy, blood lactate response to exercise, oxygen uptake kinetics and critical velocity. However, for a homogeneous group of well-trained endurance runners, the relationship between aerobic fitness parameters and endurance running performance seems to be influenced by the duration of the race (i.e., middle vs. long). Although middle-distance and ultramarathon runners present high aerobic fitness levels, there is no accumulating evidence showing that the aerobic key parameters influence both 800-m and ultramarathon performance in homogeneous group of well-trained runners. The vVO₂max seems to be the best predictor of performance for 1500 m. For 3000 m, both vVO₂max and blood lactate response to exercise are the main predictors of performance. Finally, for long distance events (5000 m, 10,000 m, marathon and ultramarathon), blood lactate response seems to be main predictor of performance. The different limiting/determinants factors and/or training-induced changes in aerobic parameters can help to explain this time- or distance-dependent pattern.

Nociception is a fundamental acute protective mechanism that prevents harm to an organism. Understanding the integral processes that control nociceptive processing are fundamental to our appreciation of which cellular and molecular features underlie this process. There is an extensive understanding of how sensory neurons interpret differing sensory modalities and intensities. However, it is widely appreciated that the sensory neurons do not act alone. These work in harmony with inflammatory and vascular systems to modulate pain perception. The spinal cord has an extensive interaction with the capillary network in the form of a blood spinal cord barrier to ensure homeostatic control of the spinal cord neuron milieu. However, there is an extensive appreciation that disturbances in the blood spinal cord barrier contribute to the onset of chronic pain. Enhanced vascular permeability and impaired blood perfusion have both been highlighted as contributors to chronic pain manifestation. Here, we discuss the evidence that demonstrates alterations in the blood spinal cord barrier influences nociceptive processing and perception of pain.