Current research in physiology最新文献

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.

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.

Background

Chronic exposure to hypoxia during vertebrate development can produce abnormal cardiovascular morphology and function. The aim of this study was to examine cardiac mitochondria function in an avian model, the chicken, in response to embryonic development under hypoxic (15% O₂), normoxic (21% O₂), or hyperoxic (40% O₂) incubation conditions.

Methods

Chicken embryos were incubated in hypoxia, normoxia, or hyperoxia beginning on day 5 of incubation through hatching. Cardiac mitochondria oxygen flux and reactive oxygen species production were measured in permeabilized cardiac fibers from externally pipped and 1-day post hatchlings.

Results

Altering oxygen during development had a large effect on body and heart masses of externally pipped embryos and 1-day old hatchlings. Hypoxic animals had smaller body masses and absolute heart masses, but proportionally similar sized hearts compared to normoxic animals during external pipping. Hyperoxic animals were larger with larger hearts than normoxic animals during external pipping. Mitochondrial oxygen flux in permeabilized cardiac muscle fibers revealed limited effects of developing under altered oxygen conditions, with only oxygen flux through cytochrome oxidase being lower in hypoxic hearts compared with hyperoxic hearts. Oxygen flux in leak and oxidative phosphorylation states were not affected by developmental oxygen levels. Mitochondrial reactive oxygen species production under leak and oxidative phosphorylation states studied did not differ between any developmental oxygen treatment.

Conclusions

These results suggest that cardiac mitochondria function of the developing chicken is not altered by developing in ovo under different oxygen levels.

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.

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.

Multiple lines of evidence suggest that an inability of the ventricle to contract in coordination with the pacemaker during anoxia exposure may suppress cardiac pumping rate in anoxia-tolerant turtles. To determine under what extracellular conditions the ventricle could be the weak link that limits cardiac pumping, we compared, under various extracellular conditions, the intrinsic contractile properties of isometrically-contracting ventricular and atrial strips obtained from 21 °C- to 5 °C- acclimated turtles (Trachemys scripta) that had been exposed to either normoxia or anoxia (16 h at 21 °C; 12 days at 5 °C). We found that combined extracellular anoxia, acidosis, and hyperkalemia (AAK), severely disrupted ventricular, but not right or left atrial, excitability and contractibility of 5 °C anoxic turtles. However, combined hypercalcemia and heightened adrenergic stimulation counteracted the negative effects of AAK. We also report that the turtle heart is resilient to prolonged diastolic intervals, which would ensure that contractile force is maintained if arrhythmia were to occur during anoxia exposure. Finally, our findings reinforce that prior temperature and anoxia experiences are central to the intrinsic contractile response of the turtle myocardium to altered extracellular conditions. At 21 °C, prior anoxia exposure preconditioned the ventricle for anoxic and acidosis exposure. At 5 °C, prior anoxia exposure evoked heightened sensitivity of the ventricle to hyperkalemia, as well as all chambers to combined hypercalcemia and increased adrenergic stimulation. Overall, our findings show that the ventricle could limit cardiac pumping rate during prolonged anoxic submergence in cold-acclimated turtles if hypercalcemia and heightened adrenergic stimulation are insufficient to counteract the negative effects of combined extracellular anoxia, acidosis, and hyperkalemia.

High amplitude electroencephalogram (EEG) events, like unitary K-complex (KC), are used to partition sleep into stages and hence define the hypnogram, a key instrument of sleep medicine. Throughout sleep the heart rate (HR) changes, often as a steady HR increase leading to a peak, what is known as a heart rate surge (HRS). The hypnogram is often unavailable when most needed, when sleep is disturbed and the graphoelements lose their identity. The hypnogram is also difficult to define during normal sleep, particularly at the start of sleep and the periods that precede and follow rapid eye movement (REM) sleep. Here, we use objective quantitative criteria that group together periods that cannot be assigned to a conventional sleep stage into what we call REM0 periods, with the presence of a HRS one of their defining properties. Extended REM0 periods are characterized by highly regular sequences of HRS that generate an infra-low oscillation around 0.05 Hz. During these regular sequence of HRS, and just before each HRS event, we find avalanches of high amplitude events for each one of the mass electrophysiological signals, i.e. related to eye movement, the motor system and the general neural activity. The most prominent features of long REM0 periods are sequences of three to five KCs which we label multiple K-complexes (KCm). Regarding HRS, a clear dissociation is demonstrated between the presence or absence of high gamma band spectral power (55–95 Hz) of the two types of KCm events: KCm events with strong high frequencies (KCmWSHF) cluster just before the peak of HRS, while KCm between HRS show no increase in high gamma band (KCmNOHF). Tomographic estimates of activity from magnetoencephalography (MEG) in pre-KC periods (single and multiple) showed common increases in the cholinergic Nucleus Basalis of Meynert in the alpha band. The direct contrast of KCmWSHF with KCmNOHF showed increases in all subjects in the high sigma band in the base of the pons and in three subjects in both the delta and high gamma bands in the medial Pontine Reticular Formation (mPRF), the putative Long Lead Initial pulse (LLIP) for Ponto-Geniculo-Occipital (PGO) waves.

Background

Sympathetic stimulation of central arteries, such as coronary and carotid arteries, cause vasodilation in healthy subjects, but vasoconstriction in those with increased cardiovascular risk. This study compared vasoreactivity to sympathetic stimulation between abdominal aorta and carotid artery in healthy young individuals (young group, n = 20), in patients with abdominal aortic aneurysm (AAA group, n = 20) and in a healthy older group, age- and gender matched with AAA group (matched group, n = 18).

Method

All subjects underwent cold pressor test, while performing concomitantly duplex ultrasound of abdominal aorta and carotid artery vasoreactivity. Observer-independent software was used to analyze and calculate magnitude and timing of maximum vasodilation or vasoconstriction. Pearson's correlation coefficient was calculated to investigate vasoreactivity between arteries.

Results

Carotid artery reactivity [Interquartile range 25%, Interquartile range 75%] did not significantly differ between the young, matched and AAA group (3.5% [1.4, 4.7], 2.6% [2.0, 4.1] and 2.2% [-1.9, 3.7], respectively, p = 0.301). Abdominal aortic responsiveness demonstrated larger differences between young (4.9% [-0.2, 8.4]), matched (3.3% [-2.5, 4.4]) and individuals with AAA (0.5% [-3.9, 4.1], p = 0.059). Pooled analysis showed a significant correlation between carotid and abdominal aortic vasoreactivity (r = 0.444, p = 0.001). Subgroup analyses demonstrated significant correlation between both arteries in young (r = 0.636, p = 0.003), but not matched (r = −0.040, p = 0.866) or AAA group (r = 0.410, p = 0.129).

Conclusions

Sympathetic stimulation induces powerful vasodilation of the carotid artery and abdominal aorta, which is significantly correlated in healthy individuals. No such correlation is present in abdominal aortic aneurysm patients. This suggests the aneurysm alters local abdominal aorta vasoreactivity, but not the carotid artery.

Respirometry, based on oxygen uptake, is commonly employed for measuring metabolic rate. There is a growing need for metabolic rate measurements suitable for developmental studies, particularly in Danio rerio, where many important developmental stages occur at < 4 mm. However, respirometry becomes more challenging as the size of the organism reduces. Additionally, respirometry can be costly and require significant experience and technical knowledge which may prohibit uptake in non-specialist/non-physiology labs. Thus, using equipment routine in most developmental/molecular biology laboratories, we measured glucose uptake in 96-h post fertilisation (hpf) zebrafish larvae and compared it to stop-flow respirometry measures of oxygen uptake to test whether glucose uptake was a suitable alternative measure of metabolic rate. A Passing-Bablok regression revealed that within a 95% limit of agreement, the rate of glucose uptake and the rate of oxygen uptake were equivalent as measures of metabolic rate in 96 hpf Danio rerio larvae. Thus, the methodology we outline here may be a useful alternative or a complementary method for assessing metabolic rate in small organisms.