Marcus N.J.,University of Nebraska Medical Center |
Del Rio R.,University of Nebraska Medical Center |
Schultz E.P.,University of Nebraska - Lincoln |
Xia X.-H.,Hebei Academy of Medical science |
Schultz H.D.,University of Nebraska Medical Center
Journal of Physiology | Year: 2014
In congestive heart failure (CHF), carotid body (CB) chemoreceptor activity is enhanced and is associated with oscillatory (Cheyne-Stokes) breathing patterns, increased sympathetic nerve activity (SNA) and increased arrhythmia incidence. We hypothesized that denervation of the CB (CBD) chemoreceptors would reduce SNA, reduce apnoea and arrhythmia incidence and improve ventricular function in pacing-induced CHF rabbits. Resting breathing, renal SNA (RSNA) and arrhythmia incidence were measured in three groups of animals: (1) sham CHF/sham-CBD (sham-sham); (2) CHF/sham-CBD (CHF-sham); and (3) CHF/CBD (CHF-CBD). Chemoreflex sensitivity was measured as the RSNA and minute ventilatory (V̇E) responses to hypoxia and hypercapnia. Respiratory pattern was measured by plethysmography and quantified by an apnoea-hypopnoea index, respiratory rate variability index and the coefficient of variation of tidal volume. Sympatho-respiratory coupling (SRC) was assessed using power spectral analysis and the magnitude of the peak coherence function between tidal volume and RSNA frequency spectra. Arrhythmia incidence and low frequency/high frequency ratio of heart rate variability were assessed using ECG and blood pressure waveforms, respectively. RSNA and V̇E responses to hypoxia were augmented in CHF-sham and abolished in CHF-CBD animals. Resting RSNA was greater in CHF-sham compared to sham-sham animals (43 ± 5% max vs. 23 ± 2% max, P < 0.05), and this increase was not found in CHF-CBD animals (25 ± 1% max, P < 0.05 vs. CHF-sham). Low frequency/high frequency heart rate variability ratio was similarly increased in CHF and reduced by CBD (P < 0.05). Respiratory rate variability index, coefficient of variation of tidal volume and apnoea-hypopnoea index were increased in CHF-sham animals and reduced in CHF-CBD animals (P < 0.05). SRC (peak coherence) was increased in CHF-sham animals (sham-sham 0.49 ± 0.05; CHF-sham 0.79 ± 0.06), and was attenuated in CHF-CBD animals (0.59 ± 0.05) (P < 0.05 for all comparisons). Arrhythmia incidence was increased in CHF-sham and reduced in CHF-CBD animals (213 ± 58 events h-1 CHF, 108 ± 48 events h-1 CHF-CBD, P < 0.05). Furthermore, ventricular systolic (3.8 ± 0.7 vs. 6.3 ± 0.5 ml, P < 0.05) and diastolic (6.3 ± 1.0 vs. 9.1 ± 0.5 ml, P < 0.05) volumes were reduced, and ejection fraction preserved (41 ± 5% vs. 54 ± 2% reduction from pre-pace, P < 0.05) in CHF-CBD compared to CHF-sham rabbits. Similar patterns of changes were observed longitudinally within the CHF-CBD group before and after CBD. In conclusion, CBD is effective in reducing RSNA, SRC and arrhythmia incidence, while improving breathing stability and cardiac function in pacing-induced CHF rabbits. © 2013 The Physiological Society.
Liu F.,Hebei Academy of Medical science
Zhongguo ying yong sheng li xue za zhi = Zhongguo yingyong shenglixue zazhi = Chinese journal of applied physiology | Year: 2011
To investigate the effect of hydrogen sulfide (H2S) on mitochondrial function in acute myocardial ischemia in rats. Acute myocardial ischemia models were established by ligating the left anterior descending coronary artery (LADC) of rats. Fourty-eight male SD rats were randomly divided into 6 groups (n = 8): sham operation group, ischemia group, ischemia + sodium hydrosulfide (NaHS) low, middle and high dose groups and ischemia + DL-proparglycine(PPG) group. The ultrastructures of myocardial mitochondria were observed with electron microscope. The content of H2S in plasma and the activity of cystathionine-gamma-lyase (CSE) in myocardial tissue of rats were respectively detected. The swelling and activity of myocardial mitochondria were determined. The activities of ATPase, GSH-Px, SOD and the content of malondial-dehyde (MDA) in myocardial mitochondria of rats were also measured. Compared with those of the sham operation group, the content of H2S in plasma, the activity of CSE in myocardial tissue and the activity of myocardium mitochondria were significantly decreased. The activities of ATPase, SOD, GSH-Px in myocardial mitochondria were significantly decreased, The content of malondial dehyde(MDA) in myocardial mitochondria and the swelling of mitochondria were distinctly increased in the ischemia group (P < 0.01). Compared with those of the ischemia group, the content of H2S in plasma and the activity of CSE in myocardial tissue were increased, and the activities of mitochondria, ATPase, SOD, and GSH-Px in myocardial mitochondria were significantly increased in ischemia + NaHS low, middle and high-dose groups; the swelling of mitochondria and the content of MDA in myocardial mitochondria were significantly decreased in ischemia + NaHS middle and high-dose groups (P < 0.05 or P < 0.01). The administration of PPG could partially reduce the myocardial protection of hydrogen sulfide (P < 0.05 or P < 0.01). It could be concluded that the administration of hydrogen sulfide could enhance the activities of mitochondrial ATPase, SOD, GSH-Px, decrease the level of mitochondrial lipid peroxidation, and play a protective effect against acute myocardial ischemia.
Wang R.-T.,Chengde Medical College |
Shen X.-B.,Chengde Medical College |
Zhou J.,Chengde Medical College |
Guan L.-H.,Chengde Medical College |
Zhang J.-X.,Hebei Academy of Medical science
Chinese Journal of New Drugs | Year: 2010
Objective: To investigate the protective effect of total flavonoids from scutellarea baicalensis stem-leaf (SSTF) on memory deficits and neuronal damage induced by bilateral injection of Aβ25-35 into rat hippocampus, and explore the mechanism. Methods: Male Wistar rats (n=30) were randomly divided into 3 groups. Intragastric SSTF (50 mg·kg-1) or distilled water was administered qd for 20 d. On the 8th day, saline or Aβ was injected to bilateral hippocampus. Morris water maze test was used to evaluate the memory from the d 15 for 5 days. On the 20th day, blood was collected to detect the malondialdehyde (MDA). Nissl staining was used to observe the change in the hippocampus. Results: After Aβ injection, the latency to find the hidden platform was significantly prolonged(P<0.05). SSTF significantly reduced the prolonged latency (P<0.05). Aβ-induced pathological changes in CA1 region included neuron loss, nuclear disappearance, and increased glial cells in the region of neuron loss. SSTF reduced these damages. MDA significantly increased after Aβ injection(P<0.05), and SSTF significantly inhibited the increase of MDA(P<0.05). Conclusion: SSTF may be beneficial for improving the learning and memory, attenuating neuron damage induced by Aβ25-35. The mechanism of SSTF might be to decrease the production of lipid peroxide, and then attenuate the oxidative stress induced by Aβ as well as decrease increased glial cells.
Liu F.,Hebei Medical University |
Liu G.-J.,Hebei Medical University |
Liu N.,Peoples Hospital of Dingzhou |
Zhang G.,Peoples Hospital of Dingzhou |
And 2 more authors.
Experimental and Therapeutic Medicine | Year: 2015
Hydrogen sulfide (H2S) is believed to be involved in numerous physiological and pathophysiological processes, and now it is recognized as the third endogenous signaling gasotransmitter, following nitric oxide and carbon monoxide; however, the effects of H2S on inflammatory factors in acute myocardial ischemia injury in rats have not been clarified. In the present study, sodium hydrosulfide (NaHS) was used as the H2S donor. Thirty six male Sprague Dawley rats were randomly divided into five groups: Sham, ischemia, isch¬emia + low dose (0.78 mg/kg) NaHS, ischemia + medium dose (1.56 mg/kg) NaHS, ischemia + high dose (3.12 mg/kg) NaHS and ischemia + propargylglycine (PPG) (30 mg/kg). The rats in each group were sacrificed 6 h after the surgery for sample collection. Compared with the ischemia group, the cardiac damage in the rats in the ischemia + NaHS groups was significantly reduced, particularly in the high dose group; in the ischemia + PPG group, the myocardial injury was aggravated compared with that in the ischemia group. Compared with the ischemia group, the levels of interleukin (IL) 1β, IL 6 and tumor necrosis factor α (TNF α) in the serum of rats in the ischemia + medium and high dose NaHS groups were significantly reduced, and the expression of inter-cellular adhesion molecule 1 (ICAM 1) mRNA and nuclear factor κ light chain enhancer of activated B cells (NF κB) protein in the myocardial tissues of rats was significantly reduced. In the ischemia + PPG group, the TNF α, IL 1β and IL 6 levels in the serum were significantly increased, the expression of ICAM 1 mRNA was increased, although without a significant difference, and the expression of NF κB was increased. The findings of the present study provide novel evidence for the dual effects of H2S on acute myocardial isch¬emia injury via the modulation of inflammatory factors. © 2015, Spandidos Publications. All rights reserved.
Li G.-F.,Hebei Medical University |
Luo H.-K.,Hebei Medical University |
Li L.-F.,Hebei Academy of Medical science |
Zhang Q.-Z.,Hebei Academy of Medical science |
And 7 more authors.
Clinical and Experimental Pharmacology and Physiology | Year: 2012
Hydrogen sulphide (H2S), one of three signalling gasotransmitters, plays an important role in oxidative stress and apoptosis. However, the effects of H2S on oxidative stress-induced apoptosis in focal cerebral ischaemic injury in rats have not been clarified. In the present study, sodium hydrosulphide (NaHS) was used as the H2S donor. Eighty-four Sprague-Dawley rats were randomly divided into six groups: sham, sham + low-dose (2.8 mg/kg) NaHS, sham + high-dose (11.2 mg/kg) NaHS, infarct, infarct + low-dose NaHS and infarct + high-dose NaHS. The focal cerebral ischaemic model was created by cranially inserting a nylon thread with a rounded tip into an internal carotid artery. Rats were killed 21 h after administration of NaHS. In the infarct + low-dose NaHS compared with infarct group, infarct volume was significantly decreased and injury to the mitochondria in nerve cells was mitigated. Furthermore, significant increases were seen in mitochondrial superoxide dismutase and glutathione peroxidase activity and neuronal bcl-2 protein levels, whereas mitochondrial malondialdehyde content and neuronal bax and caspase 3 protein levels were significantly decreased, in the infarct + low-dose NaHS compared with infarct group. The effects seen in the infarct group were significantly aggravated in the infarct + high-dose NaHS group. The findings of the present study provide novel evidence for the dual effects of H2S on focal cerebral ischaemic injury via modulation of oxidative stress-induced apoptosis. © 2012 The Authors Clinical and Experimental Pharmacology and Physiology © 2012 Wiley Publishing Asia Pty Ltd.