Distinct cardiovascular and respiratory responses to short-term sustained hypoxia in juvenile Sprague Dawley and Wistar Hannover rats

2021 ◽  
Vol 230 ◽  
pp. 102746 ◽  
Author(s):  
Darlan S. Bazilio ◽  
Karla L. Rodrigues ◽  
Davi J.A. Moraes ◽  
Benedito H. Machado
2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Catherine Crinigan ◽  
Matthew Calhoun ◽  
Karen L. Sweazea

Chronic high fat feeding is correlated with diabetes and kidney disease. However, the impact of short-term high fat diets (HFD) is not well-understood. Six weeks of HFD result in indices of metabolic syndrome (increased adiposity, hyperglycemia, hyperinsulinemia, hyperlipidemia, hyperleptinemia, and impaired endothelium-dependent vasodilation) compared to rats fed on standard chow. The hypothesis was that short-term HFD would induce early signs of renal disease. Young male Sprague-Dawley rats were fed either HFD (60% fat) or standard chow (5% fat) for six weeks. Morphology was determined by measuring changes in renal mass and microstructure. Kidney function was measured by analyzing urinary protein, creatinine, and hydrogen peroxide (H2O2) concentrations, as well as plasma cystatin C concentrations. Renal damage was measured through assessment of urinary oxDNA/RNA concentrations as well as renal lipid peroxidation, tumor necrosis factor alpha (TNFα), and interleukin 6 (IL-6). Despite HFD significantly increasing adiposity and renal mass, there was no evidence of early stage kidney disease as measured by changes in urinary and plasma biomarkers as well as histology. These findings suggest that moderate hyperglycemia and inflammation produced by short-term HFD are not sufficient to damage kidneys or that the ketogenic HFD may have protective effects within the kidneys.


2004 ◽  
Vol 286 (6) ◽  
pp. R1121-R1128 ◽  
Author(s):  
Thomas E. Dick ◽  
Y.-H. Hsieh ◽  
Shaun Morrison ◽  
Sharon K. Coles ◽  
Nanduri Prabhakar

Sympathetic and respiratory motor activities are entrained centrally. We hypothesize that this coupling may partially underlie changes in sympathetic activity evoked by hypoxia due to activity-dependent changes in the respiratory pattern. Specifically, we tested the hypothesis that sympathetic nerve activity (SNA) expresses a short-term potentiation in activity after hypoxia similar to that expressed in phrenic nerve activity (PNA). Adult male, Sprague-Dawley (Zivic Miller) rats ( n = 19) were anesthetized (Equithesin), vagotomized, paralyzed, ventilated, and pneumothoracotomized. We recorded PNA and splanchnic SNA (sSNA) and generated cycle-triggered averages (CTAs) of rectified and integrated sSNA before, during, and after exposures to hypoxia (8% O2 and 92% N2 for 45 s). Inspiration (I) and expiration (E) were divided in half, and the average and area of integrated sSNA were calculated and compared at the following time points: before hypoxia, at the peak breathing frequency during hypoxia, immediately before the end of hypoxia, immediately after hypoxia, and 60 s after hypoxia. In our animal model, sSNA bursts consistently followed the I-E phase transition. With hypoxia, sSNA increased in both halves of E, but preferentially in the second rather than the first half of E, and decreased in I. After hypoxia, sSNA decreased abruptly, but the coefficient of variation in respiratory modulation of sSNA was significantly less than that at baseline. The hypoxic-evoked changes in sympathetic activity and respiratory pattern resulted in sSNA in the first half of E being correlated negatively to that in the second half of E ( r = −0.65, P < 0.05) and positively to Te ( r = 0.40, P < 0.05). Short-term potentiation in sSNA appeared not as an increase in the magnitude of activity but as an increased consistency of its respiratory modulation. By 60 s after hypoxia, the variability in the entrainment pattern had returned to baseline. The preferential recruitment of late expiratory sSNA during hypoxia results from either activation by expiratory-modulated neurons or by non-modulated neurons whose excitatory drive is not gated during late E.


2021 ◽  
Author(s):  
Peter R. Corridon

AbstractThe aim of the present study was to determine whether decellularized rat kidney microvascular and extracellular matrix (ECM) integrity could be preserved under in vivo conditions directly after transplantation. Whole kidneys were harvested from the Sprague Dawley rat and were decellularized by perfusion with 0.5% sodium dodecyl sulfate (SDS) for 24 hours, followed by phosphate-buffered saline (PBS) for an additional 24 hours. Decellularized kidneys were then transplanted into recipients and vascular high-molecular-weight (150-kDa) FITC dextrans were infused via the jugular vein. Blood was then allowed to flow through the decellularized transplant. Intravital multiphoton microscopy confirmed the suitable confinement of the dextrans within vascular tracks and preservation of the decellularized architecture that was monitored in the shortterm post transplantation.New and NoteworthyThe study confirmed in vivo microvascular and ECM preservation in the short-term post transplantation.


2001 ◽  
Vol 91 (5) ◽  
pp. 2205-2212 ◽  
Author(s):  
Haydar A. Demirel ◽  
Scott K. Powers ◽  
Murat A. Zergeroglu ◽  
R. Andrew Shanely ◽  
Karyn Hamilton ◽  
...  

These experiments examined the independent effects of short-term exercise and heat stress on myocardial responses during in vivo ischemia-reperfusion (I/R). Female Sprague-Dawley rats (4 mo old) were randomly assigned to one of four experimental groups: 1) control, 2) 3 consecutive days of treadmill exercise [60 min/day at 60–70% maximal O2 uptake (V˙o 2 max)], 3) 5 consecutive days of treadmill exercise (60 min/day at 60–70%V˙o 2 max), and 4) whole body heat stress (15 min at 42°C). Twenty-four hours after heat stress or exercise, animals were anesthetized and mechanically ventilated, and the chest was opened by thoracotomy. Coronary occlusion was maintained for 30-min followed by a 30-min period of reperfusion. Compared with control, both heat-stressed animals and exercised animals (3 and 5 days) maintained higher ( P < 0.05) left ventricular developed pressure (LVDP), maximum rate of left venticular pressure development (+dP/d t), and maximum rate of left ventricular pressure decline (−dP/d t) at all measurement periods during both ischemia and reperfusion. No differences existed between heat-stressed and exercise groups in LVDP, +dP/d t, and −dP/d t at any time during ischemia or reperfusion. Both heat stress and exercise resulted in an increase ( P < 0.05) in the relative levels of left ventricular heat shock protein 72 (HSP72). Furthermore, exercise (3 and 5 days) increased ( P < 0.05) myocardial glutathione levels and manganese superoxide dismutase activity. These data indicate that 3–5 consecutive days of exercise improves myocardial contractile performance during in vivo I/R and that this exercise-induced myocardial protection is associated with an increase in both myocardial HSP72 and cardiac antioxidant defenses.


2010 ◽  
Vol 26 (1) ◽  
pp. 75-82 ◽  
Author(s):  
Seung-Jun Kwack ◽  
Eun-Young Han ◽  
Jae-Seok Park ◽  
Jung-Yun Bae ◽  
Il-Young Ahn ◽  
...  
Keyword(s):  

2020 ◽  
Vol Volume 13 ◽  
pp. 111-124
Author(s):  
Dragana Komnenov ◽  
Peter E Levanovich ◽  
Natalia Perecki ◽  
Charles S Chung ◽  
Noreen F Rossi

2008 ◽  
Vol 35 (6) ◽  
pp. 448 ◽  
Author(s):  
Lai Fern Ow ◽  
David Whitehead ◽  
Adrian S. Walcroft ◽  
Matthew H. Turnbull

Pinus radiata L. were grown in climate-controlled cabinets under three night/day temperature treatments, and transferred between treatments to mimic changes in growth temperature. The objective was to determine the extent to which dark respiration and photosynthesis in pre-existing and new needles acclimate to changes in growth temperatures. We also assessed whether needle nitrogen influenced the potential for photosynthetic and respiratory acclimation, and further assessed if short-term (instantaneous, measured over a few hours) respiratory responses are accurate predictors of long-term (acclimated, achieved in days–weeks) responses of respiration to changing temperature. Results show that respiration displayed considerable potential for acclimation. Cold and warm transfers resulted in some acclimation of respiration in pre-existing needles, but full acclimation was displayed only in new needles formed at the new growth temperature. Short-term respiratory responses were poor predictors of the long-term response of respiration due to acclimation. There was no evidence that photosynthesis in pre-existing or new needles acclimated to changes in growth temperature. N status of leaves had little impact on the extent of acclimation. Collectively, our results indicate that there is little likelihood that respiration would be significantly stimulated in this species as night temperatures increase over the range of 10–20°C, but that inclusion of temperature acclimation of respiration would in fact lead to a shift in the balance between photosynthesis and respiration in favour of carbon uptake.


1990 ◽  
Vol 259 (6) ◽  
pp. L451-L458 ◽  
Author(s):  
L. S. He ◽  
S. W. Chang ◽  
P. Ortiz de Montellano ◽  
T. J. Burke ◽  
N. F. Voelkel

The Fischer rat is known for its susceptibility to develop liver necrosis when challenged with paraquat (Smith et al., J. Pharmacol. Exp. Ther. 235: 172-177, 1985). We postulated that other organs, specifically the lung, may also be more susceptible to injury and examined whether lungs from Fischer (F) rats were injured more easily when challenged with active oxygen species than Sprague-Dawley (SD) rat lungs. We aimed to investigate whether increased susceptibility to oxidant injury was related to differences in lung antioxidant defenses. Perfused lungs from both rat strains were challenged by addition of H2O2 to the perfusate or by short-term hyperoxic ventilation. To assess nonoxidant modes of lung injury, we examined lung responses after exposure to protamine sulfate or neutrophil elastase. Intravascular H2O2 or 3 h in vitro hyperoxia caused lung edema in F but not SD rats, and elastase injured F rat lungs more than the lungs from SD rats. Protamine, however, injured the lungs from both strains to a similar degree. Catalase, but not superoxide dismutase or allopurinol, protected F rat lungs against edema, resulting from 3 h in vitro hyperoxia. The lung homogenate levels for reduced glutathione or conjugated dienes and the activities of lung tissue catalase, glutathione peroxidase, and cytochrome P-450 were not different between the two strains. Lung tissue ATP levels, however, were lower in F than in SD rats. Although the F rat strain appears to have an altered oxidant-antioxidant defense balance, the exact cause of the greater susceptibility to oxidant stress of the F rat strain remains elusive.


2019 ◽  
Vol 121 (5) ◽  
pp. 1822-1830 ◽  
Author(s):  
Daniela Accorsi-Mendonça ◽  
Leni G. H. Bonagamba ◽  
Benedito H. Machado

Sustained hypoxia (SH) activates chemoreceptors to produce cardiovascular and respiratory responses to bring the arterial partial pressure of O2 back to the physiological range. We evaluated the effect of SH (fraction of inspired O2 = 0.10, 24 h) on glutamatergic synaptic transmission and the interaction neuron-astrocyte in neurons of the nucleus tractus solitarii (NTS). Tractus solitarius (TS) fiber stimulation induced glutamatergic currents in neurons and astrocytes. SH increased α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid/kainate (AMPA/kainate) [−183 ± 122 pA ( n = 10) vs. −353 ± 101 pA ( n = 10)] and N-methyl-d-aspartate (NMDA) current amplitude [61 ± 10 pA ( n = 7) vs. 102 ± 37 pA ( n = 10)]. To investigate the effects of SH, we used fluoroacetate (FAC), an astrocytic inhibitor, which revealed an excitatory modulation on AMPA/kainate current and an inhibitory modulation of NMDA current in control rats. SH blunted the astrocytic modulation of AMPA [artificial cerebrospinal fluid (aCSF): −353 ± 101 pA vs. aCSF + FAC: −369 ± 76 pA ( n = 10)] and NMDA currents [aCSF: 102 ± 37 pA vs. aCSF + FAC: 108 ± 32 pA ( n = 10)]. SH increased AMPA current density [control: −6 ± 3.5 pA/pF ( n = 6) vs. SH: −20 ± 12 pA/pF ( n = 7)], suggesting changes in density, conductance, or affinity of AMPA receptors. SH produced no effect on astrocytic resting membrane potential, input resistance, and AMPA/kainate current. We conclude that SH decreased the neuron-astrocyte interaction at the NTS level, facilitating the glutamatergic transmission, which may contribute to the enhancement of cardiovascular and respiratory responses to baro- and chemoreflexes activation in SH rats. NEW & NOTEWORTHY Using an electrophysiological approach, we have shown that in nucleus tractus solitarii (NTS) from control rats, astrocytes modulate the AMPA and NMDA currents in NTS neurons, changing their excitability. Sustained hypoxia (SH) increased both glutamatergic currents in NTS neurons due to 1) a reduction in the astrocytic modulation and 2) an increase in the density of AMPA receptors. These new findings show the importance of neuron-astrocyte modulation in the excitatory synaptic transmission in NTS of control and SH rats.


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