OBJECTIVETo explore the effect of hypoxia on the peripheral blood T lymphocyte subsets and co-stimulatory molecules in rats so as to provide the basis for studying the intervention measure.

METHODSBefore hypoxia and during hypoxia at 8 000 m for 8 h, 3 d, 6 d and 10 d the change of peripheral blood T lymphocyte subsets and co-stimulatory molecules in rats were detected by flowcytometer with three-color immunofluorescence label.

RESULTSRats were exposed to hypoxia at 8 000 m for 8 hours, and CD3+, CD8+, CD8+ CD28- lymphocyte percentages were significantly decreased (P < 0.01) compared with that before hypoxia. After 3 days of hypoxia, besides aforesaid change, CD4+ CD28+ lymphocyte percentage also prominently decreased (P < 0.01) and CD4+ CD28- prominently increased (P < 0.01). After 6 and 10 days of hypoxia, CD3+, CD4+ lymphocyte percentages were further decreased, while CD8+ CD28+ lymphocyte percentage significantly increased (P < 0.01).

CONCLUSIONAfter exposed to hypoxia at 8 000 m for 8 hours and 3 days, activation of CD8+ and CD4+ T lymphocyte was prominently decreased, while with the prolong of exposed time activation of CD8+ T lymphocyte was significantly increased.

Altitude ; Altitude Sickness ; physiopathology ; Animals ; CD4-Positive T-Lymphocytes ; physiology ; CD8-Positive T-Lymphocytes ; physiology ; Hypoxia ; immunology ; physiopathology ; Lymphocyte Activation ; physiology ; Male ; Rats ; Rats, Wistar ; T-Lymphocytes ; physiology

Aging ; physiology ; Animals ; Female ; Male ; Mitochondria, Heart ; enzymology ; Mitochondrial Membrane Transport Proteins ; physiology ; Rats ; Rats, Sprague-Dawley ; Superoxide Dismutase ; metabolism ; Ventricular Function, Left ; physiology

OBJECTIVETo investigate the distribution and mechanism of coronary arteriole (CA) cell resting membrane potential (RP) in guinea pigs.

METHODSCell RP was recorded by intracellular microelectrode in isolated guinea pig coronary arteriole (diameter < 100 microm).

RESULTS(1) Experiments were carried out in 112 cells with a mean RP of (-65 +/- 4.2)mV, the distribution of coronary arteriole cell RP fitted by Gaussian function was bimodal, one peak was -43 mV termed high RP, the other was -74 mV termed low RP. 10 mmol/L K+ and 3 micromol/ L acetylcholine(ACh) induced hyperpolarization in high-RP cells with (-7.4 +/- 0.87) mV (n = 13) and (-15 +/- 1.24) mV (n = 16) respectively, and induced depolarization in low-RP cells with (9.6 +/- 1.2) mV (n = 23) and (8.7 +/- 0.69) mV (n = 15) respectively. (2) The inward rectifier K+ channel (K(ir)) blocker Ba2+ caused concentration-dependent depolarization in low-RP cells with an EC50 of 120 micromol/L 100 micromol/L Ba2+ or higher could shift low-RP cells to high-RP state, the response of these cells to high K+ and ACh became a hyperpolarization.

CONCLUSIONThe distribution of coronary vascular cell RP is bimodal, high K+ and ACh induce different responses in low and high RP cells. The two RP states are exchangeable mainly due to all-or-none conductance changes of K(ir).

Acetylcholine ; metabolism ; Animals ; Arterioles ; cytology ; Coronary Vessels ; cytology ; physiology ; Female ; Guinea Pigs ; Male ; Membrane Potentials ; physiology ; Microelectrodes ; Myocardium ; metabolism ; Potassium Channels, Inwardly Rectifying ; physiology

OBJECTIVETo evaluate wave intensity (WI) on left ventricular (LV) performance in the different hypertensive remolding hearts.

METHODS105 hypertensive and 98 control subjects were underwent noninvasive evaluation of carotid arterial wave intensity, LV structure and function.

RESULTS(1) There were increasing trends in the levels of blood pressure, LV end-diastolic diameter and LV mass index in the control, normal geometry group, concentric remodeling group, concentric and eccentric hypertrophy group. LV ejection fraction increased in the concentric hypertrophy group and decreased in the eccentric hypertrophy group in which mid-wall fractional shortening showed a decreasing trend. LV diastolic filling pressure presented increased progression accompanied by LV remodeling (P < 0.05). (2) Transient acceleration wave intensity (W1) in hypertensive subjects were higher than that in the control (P < 0.05). Transient deceleration wave intensity (W2) was lower than that in the control (P < 0.05). (3) W1 in the concentric hypertrophy group was higher and lower in the eccentric hypertrophy, compared with that in the control group, normal geometry group and concentric remodeling group (P < 0.05). W2 was lower in concentric hypertrophy group and eccentric hypertrophy group than that in the control, normal geometry group and concentric remodeling group (P < 0.05).

CONCLUSIONWI is a noninvasively obtained, clinically useful parameter for evaluation of LV performance.

Aged ; Blood Flow Velocity ; physiology ; Carotid Artery, Common ; physiopathology ; Case-Control Studies ; Female ; Humans ; Hypertension ; physiopathology ; Male ; Middle Aged ; Pulsatile Flow ; physiology ; Ventricular Function, Left ; physiology ; Ventricular Remodeling

Adolescent ; Alleles ; Asian Continental Ancestry Group ; genetics ; Erythropoietin ; genetics ; Ethnic Groups ; genetics ; Female ; Genotype ; Humans ; Male ; Polymorphism, Single Nucleotide ; Young Adult

OBJECTIVETo assess the clinical significance of ankle-brachial index(ABI) in aged Chinese hypertensive men and to determine the association of ABI with clinical coronary heart disease, stroke.

METHODSAnkle-brachial index (ABI) was measured by means of peripheral vascular lab in aged hypertensive men from 301 Hospital and Anzhen Hospital while the clinical characteristics of the study population were investigated and collected. ABI < or = 0.9 was defined as peripheral arterial disease (PAD), 1.01 - 1.30 as borderline PAD.

RESULTSThere were 244 aged Chinese hypertensive men with antihypertensive treatment and with mean age 76.47 +/- 9.75 enrolled in this study, in whom 15 men with missing data except general information and ABI measurement. The mean ABI was 0.941 +/- 0.258 with the highest frequency 1.01 - 1.30. Eighty five men were diagnosed as PAD, 22 as borderline PAD, 135 normal ABI and 2 with ABI > 1.3. ABI and rate of hypertension control in PAD and borderline PAD men were significantly lower than those with normal ABI. In both PAD and borderline PAD patients, the hypertension duration (except in borderline PAD), creatinine level, neutrophil count (except in borderline PAD), percentage of alcohol drinking, prevalence of diabetes mellitus (except in borderline PAD), coronary artery disease, stroke and dyslipidemia (except in borderline PAD) were significantly higher than those with normal ABI patients. The prevalences of PAD, borderline PAD, coronary artery disease and stroke in this study population were 35.1%, 9.1%, 64.0%, 40.5%, respectively. The prevalences of PAD, borderline PAD, coronary artery disease and stroke increased significantly with increasing age. Logistic regression analysis showed that lower ABI was inversely associated with clinical coronary artery disease and stroke after adjustment for age, body mass index, hypertension duration, rate of hypertension control, systolic blood pressure, diastolic blood pressure, status of smoking, alcohol drinking, diabetes mellitus, dyslipidemia. The fully-adjusted odds ratios (ORs) for PAD and borderline PAD group compared with normal ABI group for the prevalence of coronary artery disease, and stroke demonstrated that these conditions were conversely related to ABI.

CONCLUSIONAged hypertensive men have high prevalence of PAD. Low ABI level was independently associated with coronary artery disease and stroke.

Aged ; Aged, 80 and over ; Ankle Brachial Index ; China ; epidemiology ; Coronary Disease ; epidemiology ; etiology ; physiopathology ; Humans ; Hypertension ; complications ; physiopathology ; Male ; Middle Aged ; Prevalence ; Stroke ; epidemiology ; etiology ; physiopathology

OBJECTIVETo explore the interrelationship among dorsal motor nucleus of the vagus (DMV), locus coeruleus (LC) and raphe magnus nucleus (NRM) in the mechanism of the descending regulation on gastric motility, which may constitute a parasympathetic local circuit, work as a neural center of gastric modulation in brainstem.

METHODSUsing nucleus location, electric stimulation and lesion, together with microinjection, and recording the inter-gastric pressure.

RESULTS(1) LC stimulation could inhibit the gastric motility significantly (P < 0.01), DMV lesion weaken this effect, while blocking the a receptor on DMV could reverse the effect. (2) NRM stimulation reduced the amplitude of gastric constriction (P < 0.01), DMV lesion could abolish the effect, but blocking the 5-HT2A receptor on DMV depressed the gastric motility heavily (P < 0.01) like NRM stimulation. While LC lesion could abolish the effect of NRM stimulation, and microinjection of ritanserin into LC could likewise abolish it.

CONCLUSION(1) LC inhibit the gastric motility via a receptor in DMV, and meanwhile may excite it through 5-HT2A receptor in DMV, these two ways work together to keeping the gastric motility amplitude normally. (2) NRM inhibit the gastric motility via 5-HT2A receptor in LC.

Animals ; Brain Stem ; physiology ; Female ; Gastrointestinal Motility ; physiology ; Locus Coeruleus ; physiology ; Male ; Motor Neurons ; physiology ; Raphe Nuclei ; physiology ; Rats ; Rats, Sprague-Dawley ; Vagus Nerve ; physiology

OBJECTIVETo investigate the effect of mitochondrial permeability transition pore inhibitor cyclosporine A (CsA) on lipopolysaccharide (LPS)-induced acute lung injury in mice.

METHODSAll male ICR mice were randomly divided into five groups (n = 24): control group, LPS group, dexamethasone group, cyclosporine A(CsA) group and CsA + atractyloside(Atr) group. Six hours after treatment with LPS, the activity of lactate dehydrogenlase (LDH) in bronchoalveolar lavage fluid (BALF) and level of tumor necrosis factor-alpha (TNF-alpha) in lung tissue were detected. The lung wet weight/dry weight ratio and the pulmonary capillary permeability index were also detected.

RESULTSIn contrast to LPS group, the mitochondrial permeability transition pore inhibitor CsA induced a decrease in LDH activity in the BALF and TNF-alpha level in lung tissue, lung wet weight/dry weight ratio and the pulmonary capillary permeability index were declined. Atractyloside, the activator of mitochondrial permeability transition pore, almost abolished the role of CsA on LPS-induced lung injury.

CONCLUSIONThese results suggested that CsA plays the protective effect on LPS-induced lung injury in mice, it is likely through inhibiting the opening of mitochondrial permeability transition pore.

Acute Lung Injury ; chemically induced ; physiopathology ; prevention & control ; Animals ; Cyclosporine ; pharmacology ; L-Lactate Dehydrogenase ; metabolism ; Lipopolysaccharides ; Male ; Mice ; Mice, Inbred ICR ; Mitochondrial Membrane Transport Proteins ; antagonists & inhibitors ; Protective Agents ; pharmacology ; Tumor Necrosis Factor-alpha ; metabolism

OBJECTIVETo observe the effect of the signal pathway of phosphoinositol-3-kinase (PI3K)/Akt-antypical protein kinase C(iotazeta) (aPKC(iotazeta))-Nuclear factor-E2 related factor (Nrf2) on gamma-glutamylcysteine synthetase (gamma-GCS) of the bronchial epithelial cells of rats after exposure to cigarette smoke extracts (CSE).

METHODSgamma-GCS, Nrf2, p-Akt and p-aPKC(iotazeta) proteins were semi-quantified by Western blot. gamma-GCS protein expression was assessed by immunocytochemistry. gamma-GCS mRNA expression was detected by reverse transcription-polymerase chain reaction (RT-PCR). Nrf2 protein was observed by immunofluorescence. The rate of the cells expressed p-Akt were analyzed by flow cytometry. GSH content and gamma-GCS activity were measured.

RESULTSGSH content, Nrf2 protein of nucleus, p-aPKC(iotazeta) protein, p-Akt protein and positive cells, gamma-GCS protein and mRNA and activity were significantly increased after exposure to CSE for 3 hours. aPK(iotazeta) inhibitor RO813220 significantly reduced the expression of p-aPKC(iotazeta) protein, gamma-GCS protein and mRNA and activity, but enhanced Nrf2 protein of cytoplasm expression, had no effect on p-Akt. p-Akt inhibitor LY294002 and RO813220 + LY294002 decreased p-aPKC(iotazeta) protein, p-Akt protein and positive cells, gamma-GCS protein and mRNA and activity expression, increased Nrf2 protein of cytoplasm expression. The correlation analysises demonstrated that there were a positive correlation between Nrf2 and gamma-GCS, p-Akt, p-aPKC(iotazeta), between p-Akt and Nrf2, p-aPKC(iotazeta), gamma-GCS, between p-aPKC(iotazeta) and Nrf2, p-Akt, gamma-GCS.

CONCLUSIONCSE might upregulate gamma-GCS expression through PI3K/Akt-aPKC(iotazeta)-Nrf2 signaling pathway in the bronchial epithelial cells of rats.

Animals ; Bronchi ; cytology ; enzymology ; Environmental Exposure ; adverse effects ; Epithelial Cells ; enzymology ; GA-Binding Protein Transcription Factor ; metabolism ; Glutamate-Cysteine Ligase ; genetics ; metabolism ; Isoenzymes ; metabolism ; Male ; Oncogene Protein v-akt ; metabolism ; Phosphatidylinositol 3-Kinases ; metabolism ; Protein Kinase C ; metabolism ; RNA, Messenger ; genetics ; metabolism ; Rats ; Rats, Sprague-Dawley ; Signal Transduction ; Tobacco Smoke Pollution ; adverse effects

OBJECTIVETo explore the alterations in pulmonary arterial reactivity during pulmonary arterial hypertension at the early-stage of pulmonary fibrosis in rats.

METHODSSixty-six male Sprague-Dawley rats were randomly divided into 2 groups: bleomycin (BLM) group and sham group. The rats in BLM group were received single intratracheal instillation of BLM (5 mg/kg), and the rats in sham group received equal volume of 0.9% normal saline (NS). The alterations in pulmonary arterial reactivity were measured by vascular tension detected technique, the pathomorphological changes in the wall of pulmonary arteries were displayed with Hematoxylin-Eosin (HE) staining, the degree of fibrosis in lung was revealed with Masson staining, and the mean pulmonary arterial pressure was detected via a catheter in the pulmonary artery.

RESULTS(1) The contractile response to a- adrenoceptor agonist phenylephrine (PE), of pulmonary arteries both with remaining endothelium and with removing endothelium, from BLM-treated rats , was reduced significantly, compared with sham rats (P both < 0.05). (2) The relaxant response to the endothelially dependent vasodilator acetylcholine (Ach), of pulmonary arteries with remaining endothelium, from BLM-treated rats, was also reduced, compared with sham rats (P < 0.01). (3) In sham rats, the contractile response to (omega) -nitro-L-arginine methyl ester (L-NAME) plus PE, of pulmonary arteries with remaining endothelium, was enhanced, compared with that to PE alone (P < 0.01), while in BLM group, the contractile responses to L-NAME plus PE, of pulmonary arteries with remaining endothelium, was not different from that to PE alone (P > 0.05). (4) In BLM group, vascular endothelial cells lost. (5) In BLM group, the initial stage of fibrogenesis was observed in lungs, and the mean pulmonary arterial pressure increased, compared with that in sham group (P < 0.05).

CONCLUSIONThe abnormal responsibility of pulmonary arteries occurred during pulmonary arterial hypertension at the early-stage of pulmonary fibrosis in rats.

Animals ; Familial Primary Pulmonary Hypertension ; Hypertension, Pulmonary ; complications ; physiopathology ; Male ; Pulmonary Artery ; physiopathology ; Pulmonary Fibrosis ; complications ; physiopathology ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Vasomotor System ; physiology