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Objective To develop a new type of stretcher to meet the needs of medical evacuation in high altitude region. Methods The stretcher was composed of a bearing plate, a protective shield, a control unit and external accessories. An enclosed space was formed by the shield and plate,and there were an air inlet and outlet in the shield to regulate the pressure and oxygen content in the space. An electric blanket was put on the plate, which was combined with the control unit to execute dynamic monitoring and control of the temperature and oxygen content in the shield.Results The stretcher enhanced the casualty safety during transport so that the effect of high altitude on casualty conditions could be decreased effectively. Conclusion The stretcher can be used for casualty transport in high-altitude conditions while reduce the casualty riks.
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AIM:To investigate the effects of hypoxia exposure on the structure and function of erythrocytes in rats at different time.METHODS:Male SD rats(n=40)were randomly divided into 5 groups,normal control group,1-week hypoxia group ,2-week hypoxia group ,3-week hypoxia group and 4-week hypoxia group ,with 8 rats per group.The rats in hypoxia groups were placed in the simulated 5800 m of high altitude in a hypobaric chamber for different time.The values of detected blood ,erythrocyte deformation index ,erythrocyte osmotic fragility ,erythrocyte oxygen dissociation ,e-rythrocyte apoptosis and bone marrow biopsy were determined.RESULTS:Compared with normal control group ,the red blood cell count ,hemoglobin content ,mean corpuscular volume and mean corpuscular hemoglobin significantly increased(P<0.01).Eversion rate of phosphatidylserine of erythrocytes increased.Oxygen half-saturation of hemoglobin increased(P<0.05).Bone marrow erythroid proliferation increased.The erythrocyte deformation index and erythrocyte osmotic fra-gility decreased significantly(P<0.01).In addition,oxygen dissociation curves shifted to the right.CONCLUSION:In the early stage of hypoxia ,compared with normal control group ,the changes of erythrocyte structure and function increase the oxygen supply to the tissue and are conducive to adapting to the plateau.However ,with the extension of hypoxia ,ex-cessive erythrocytosis results in thrombosis ,microcirculation disturbance and aggravating tissue hypoxia.
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<p><b>BACKGROUND</b>Oxygen inhalation therapy is essential for the treatment of patients with chronic mountain sickness (CMS), but the efficacy of oxygen inhalation for populations at high risk of CMS remains unknown. This research investigated whether oxygen inhalation therapy benefits populations at high risk of CMS.</p><p><b>METHODS</b>A total of 296 local residents living at an altitude of 3658 m were included; of which these were 25 diagnosed cases of CMS, 8 cases dropped out of the study, and 263 cases were included in the analysis. The subjects were divided into high-risk (180 ≤ hemoglobin (Hb) <210 g/L, n = 161) and low-risk (Hb <180 g/L, n = 102) groups, and the cases in each group were divided into severe symptom (CMS score ≥6) and mild symptom (CMS score 0-5) subgroups. Severe symptomatic population of either high- or low-risk CMS was randomly assigned to no oxygen intake group (A group) or oxygen intake 7 times/week group (D group); mild symptomatic population of either high- or low-risk CMS was randomly assigned to no oxygen intake group (A group), oxygen intake 2 times/week group (B group), and 4 times/week group (C group). The courses for oxygen intake were all 30 days. The CMS symptoms, sleep quality, physiological biomarkers, biochemical markers, etc., were recorded on the day before oxygen intake, on the 15th and 30th days of oxygen intake, and on the 15th day after terminating oxygen intake therapy.</p><p><b>RESULTS</b>A total of 263 residents were finally included in the analysis. Among these high-altitude residents, CMS symptom scores decreased for oxygen inhalation methods B, C, and D at 15 and 30 days after oxygen intake and 15 days after termination, including dyspnea, palpitation, and headache index, compared to those before oxygen intake (B group: Z = 5.604, 5.092, 5.741; C group: Z = 4.155, 4.068, 4.809; D group: Z = 6.021, 6.196, 5.331, at the 3 time points respectively; all P < 0.05/3 vs. before intake). However, dyspnea/palpitation (A group: Z = 5.003, 5.428, 5.493, both P < 0.05/3 vs. before intake) and headache (A group: Z = 4.263, 3.890, 4.040, both P < 0.05/3 vs. before intake) index decreased significantly also for oxygen inhalation method A at all the 3 time points. Cyanosis index decreased significantly 30 days after oxygen intake only in the group of participants administered the D method (Z = 2.701, P = 0.007). Tinnitus index decreased significantly in group A and D at 15 days (A group: Z = 3.377, P = 0.001, D group: Z = 3.150, P = 0.002), 30 days after oxygen intake (A group: Z = 2.836, P = 0.005, D group: Z = 5.963, P < 0.0001) and 15 days after termination (A group: Z = 2.734, P = 0.006, D group: Z = 4.049, P = 0.0001), and decreased significantly in the group B and C at 15 days after termination (B group: Z = 2.611, P = 0.009; C group: Z = 3.302, P = 0.001). In the population at high risk of CMS with severe symptoms, oxygen intake 7 times/week significantly improved total symptom scores of severe symptoms at 15 days (4 [2, 5] vs. 5.5 [4, 7], Z = 2.890, P = 0.005) and 30 days (3 [1, 5] vs. 5.5 [2, 7], Z = 3.270, P = 0.001) after oxygen intake compared to no oxygen intake. In the population at high risk of CMS with mild symptoms, compared to no oxygen intake, oxygen intake 2 or 4 times/week did not improve the total symptom scores at 15 days (2 [1, 3], 3 [1, 4] vs. 3 [1.5, 5]; χ2 = 2.490, P = 0.288), and at 30 days (2 [0, 4], 2 [1, 4.5] vs. 3 [2, 5]; χ2 = 3.730, P = 0.155) after oxygen intake. In the population at low risk of CMS, oxygen intake did not significantly change the white cell count and red cell count compared to no oxygen intake, neither in the severe symptomatic population nor in the mild symptomatic population.</p><p><b>CONCLUSIONS</b>Intermittent oxygen inhalation with proper frequency might alleviate symptoms in residents at high altitude by improving their overall health conditions. Administration of oxygen inhalation therapy 2-4 times/week might not benefit populations at high risk of CMS with mild CMS symptoms while administration of therapy 7 times/week might benefit those with severe symptoms. Oxygen inhalation therapy is not recommended for low-risk CMS populations.</p>
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Adolescente , Adulto , Anciano , Femenino , Humanos , Masculino , Persona de Mediana Edad , Adulto Joven , Mal de Altura , Quimioterapia , Enfermedad Crónica , Quimioterapia , Hipoxia , Quimioterapia , Oxígeno , Usos Terapéuticos , Terapia por Inhalación de Oxígeno , MétodosRESUMEN
As human beings ascend to high altitude, a number of reactions may occur against hypoxic injuries. These hypoxic responses are related to intake, transportation and utility of the oxygen. As a crucial subcellular organelle of oxygen utility, mitochondrion is a central link of high altitude acclimatization, adaptation and mountain sicknesses. In this review, we discussed the recent advances in researches on hypoxic mitochondrial responses at high altitude.
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Animales , Humanos , Adaptación Fisiológica , Altitud , Mal de Altura , Hipoxia , Mitocondrias , Patología , Oxígeno , FisiologíaRESUMEN
<p><b>OBJECTIVE</b>To evaluate the effects of hypobaric hypoxia on the expressions of death receptor 5 (DR5) and cellular FLICE-like inhibitory protein (c-FLIP) and the distribution of c-FLIP in the rat testis.</p><p><b>METHODS</b>Forty adult male SD rats were randomly divided into four groups of equal number: normoxia control, 3 d hypoxia, 15 d hypoxia and 30 d hypoxia. The control rats were raised at 300 m above the sea level, while the latter three groups of rats in a hypobaric chamber at a simulated altitude of 4000 m for 5, 15 and 30 days, respectively. Then the expressions of DR5 and c-FLIP were detected by immunoblotting and the distribution of c-FLIP in the testis observed by immunofluorescence.</p><p><b>RESULTS</b>The expressions of DR5 were 2.04 +/- 0.11, 1.97 +/- 0.12 and 2.34 +/- 0.11 in the 3 d, 15 d and 30 d hypoxia groups, respectively, significantly higher than 1.78 +/- 0.09 in the normoxia group (P < 0.05). The expressions of c-FLIP were 0.87 +/- 0.03 and 0.74 +/- 0.07 in the 15 d and 30 d hypoxia groups, respectively, significantly lower than 1.03 +/- 0.02 in the normoxia group (P < 0.05).</p><p><b>CONCLUSION</b>Simulated hypobaric hypoxia at 4000 m above the sea level increased the expression of DR5 and inhibited that of c-FLIP in the rat testis.</p>
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Animales , Masculino , Ratas , Proteína Reguladora de Apoptosis Similar a CASP8 y FADD , Metabolismo , Hipoxia , Metabolismo , Ratas Sprague-Dawley , Receptores del Ligando Inductor de Apoptosis Relacionado con TNF , Metabolismo , Testículo , MetabolismoRESUMEN
<p><b>OBJECTIVE</b>To investigate the effect of apelin on vasodilatation of isolated pulmonary arterial rings in rats and its relationship to the nitric oxide (NO) pathway, and to observe the difference of vasodilatation between hypoxic rats and normoxic rats.</p><p><b>METHODS</b>Thirty-six male Sprague-Dawley (SD) rats were randomly divided into hypoxic group and normoxic group. The effects of accumulated apelin on pulmonary arterial rings preconstricted with norepinephrine (NE) were observed by using tissue organ bath system. After pulmonary arterial rings were pretreated with three methods: removing the endothelium, pretreating with nitric oxide synthase inhibitor L-NAME or soluble guanylatecyclase inhibitor ODQ, the different effect of apelin was observed. In addition, the difference of vasodilatation between hypoxic rats and normal rats were observed.</p><p><b>RESULTS</b>(1) Exposure of intact endothelium pulmonary arterial rings preconstricted by NE to apelin at concentration (0.01 - 100 nmol/L) induced a significant concentration dependent relaxation. The maximal vasorelaxant effect of apelin was 10.62% +/- 2.60%, which was inhibited by removal of the endothelium (P < 0.01), pretreatment with L-NAME (P < 0.01) or ODQ (P < 0.01). (2) Response of pulmonary arterial rings from hypoxic pulmonary hypertension rats was decreased (P < 0.05). Compared to normal rats, at a concentration of 100 nmol/L, the response to apelin on arteries from hypoxic rats decreased 60.45% (P < 0.01). But the values of EC50 were not significantly different (P > 0.05).</p><p><b>CONCLUSION</b>These results indicate that apelin relaxes the pulmonary arterial rings of rats in an endothelium dependent manner, which may have a relationship to NO signaling pathway. The response of vasodilatation is decreased in the pulmonary arterial rings from the hypoxic rats.</p>
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Animales , Masculino , Ratas , Apelina , Hipoxia , Técnicas In Vitro , Péptidos y Proteínas de Señalización Intercelular , Farmacología , Óxido Nítrico , Metabolismo , Arteria Pulmonar , Distribución Aleatoria , Ratas Sprague-Dawley , Transducción de Señal , VasodilataciónRESUMEN
<p><b>OBJECTIVE</b>To study the role of apelin in the prevention of pulmonary hypertension induced by hypoxia in rats.</p><p><b>METHODS</b>The animal model of hypoxic pulmonary hypertension was established by exposing the rats to isobaric hypoxic chamber for 4 weeks (8 h/d, 6 d/ w). Forty male Sprague-Dawley rats were randomly divided into control group (NC), hypoxic group(HH), hypoxic with low-dose apelin (5 nmol/(kg x d) group(LA) and high-dose apelin (10 nmol/(kg x d) (HA). [pGlu]apelin-13 was administered into the rats of apelin groups by mini-osmotic pump subcutaneously. The mean pulmonary arterial pressure(mPAP) and the mean carotid arterial pressure (mCAP) were measured by either right or left cardiac catheterization, and the weight ratio of right ventricule/left ventricule plus septum (RV/(LV + S)) were calculated. The Masson's trichrome stained lung specimens were examined by light microscope to examine the vessel wall area/total area (WA/TA), vessel cavity area/total area (CA/TA) and media thickness of pulmonary arterioles (PAMT). Meanwhile, the lung homogenates were assayed for the activity of supeeroxide dismutase (SOD) and the content of malondialdehyde (MDA).</p><p><b>RESULTS</b>(1) mPAP and RV/(LV + S) of HH group were significantly higher than those of NC group. mPAP of LA and HA groups were lower than those of HH group. The RV/(LV + S) of HA group was significantly lower than that of HH group, but there was no significant difference between HH group and LA group. (2) Masson's trichrome staining revealed that WA/TA and PAMT of HH group were higher than those of NC group. Administration of apelin significantly eliminated WA/TA and PAMT in LA and HA groups. (3) CA/TA of HH group was lower than that of NC group. Administration of apelin significantly elevated CA/TA in LA and HA groups. (4) The activity of SOD and content of MDA in HH group was, respectively, lower and higher than those in NC group. Apelin treatment increased the activity of SOD in LA and HA groups while decreased the content of MDA.</p><p><b>CONCLUSIONS</b>Apelin could play an important role in treatment of hypoxic pulmonary hypertension of rats and the mechanisms of protection were associated with vasodilation of pulmonary artery and inhibition of oxidative stress.</p>
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Animales , Masculino , Ratas , Cardiotónicos , Farmacología , Usos Terapéuticos , Hipertensión Pulmonar , Hipoxia , Péptidos y Proteínas de Señalización Intercelular , Farmacología , Usos Terapéuticos , Estrés Oxidativo , Arteria Pulmonar , Ratas Sprague-Dawley , VasodilataciónRESUMEN
<p><b>OBJECTIVE</b>To explore the effects of hypobaric hypoxia on the apoptosis of germ cells in male rats.</p><p><b>METHODS</b>Adult male Wistar rats were randomly divided into four groups: a control group raised at sea level; a 5 d, a 15 d and a 30 d hypoxic group raised in a hypobaric chamber simulating 5000 m altitude for 5 days, 15 days and 30 days respectively. Flow cytometry and TUNEL were used to evaluate the apoptosis of germ cells in the testis. Bax and Bcl-2 in the testis were measured by Western blot.</p><p><b>RESULTS</b>Seminiferous tubules with apoptotic germ cells were significantly more in the hypoxic groups than in the control (P < 0.01). Most apoptotic germ cells were spermatogonia and spermatocytes. Compared with the control group, apoptotic germ cells detected by PI flow cytometry were significantly increased in the hypoxic 15 d and 30 d groups (P < 0.05); Bax was significantly higher (P < 0.05), and so was the ratio of Bax to Bcl-2 in the hypoxic 30 d group (P < 0.01).</p><p><b>CONCLUSION</b>Hypoxia promotes apoptosis of testicular germ cells in male rats. Chronic hypoxia increases Bax expression in the rat testis.</p>
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Animales , Masculino , Ratas , Apoptosis , Hipoxia , Metabolismo , Patología , Etiquetado Corte-Fin in Situ , Distribución Aleatoria , Ratas Wistar , Espermatozoides , Biología Celular , Testículo , Metabolismo , Patología , Proteína X Asociada a bcl-2RESUMEN
<p><b>AIM</b>To determine the effect of agmatine on the proliferation of PASMCs induced by serum.</p><p><b>METHODS</b>Primary culture of rat PASMCs was prepared from adult male Wistar rat pulmonary artery by the method of tissue block anchorage. PASMCs were divided into two groups: control group and agmatine administration group. The activity of LDH in the medium was measured by chromatometry. The 3H-TdR incorporation was measured by liquid scintillometry. The cell cycle was measured by flow cytometry. The PCNA content was measured by image analysis.</p><p><b>RESULTS</b>Agmatine did not exert significant effect on the activity of LDH in the medium. Agmatine significantly decreased the 3H-TdR incorporation and PCNA content of PASMCs. Agmatine significantly decreased the cell ratio of G2/M phase and increased the cell ratio of G0/G1 phase. With the increment of the concentration of agmatine, 3H-TdR incorporation was significantly decreased correspondingly.</p><p><b>CONCLUSION</b>Agmatine has no significant cytotoxic effect on PASMCs. Agmatine can dose-dependently inhibit the proliferation of rat PASMCs induced by serum.</p>
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Animales , Masculino , Ratas , Agmatina , Farmacología , Proliferación Celular , Células Cultivadas , Músculo Liso Vascular , Biología Celular , Miocitos del Músculo Liso , Biología Celular , Arteria Pulmonar , Biología Celular , Ratas Wistar , SueroRESUMEN
<p><b>AIM</b>To explore the differentially expressed proteins between hypobaric hypoxic delayed preconditioning (HHDP) and normal mouse hippocampus.</p><p><b>METHODS</b>After the animal model of HHDP was constructed, hippocampal proteins were obtained by a series of abstraction with lysis solution containing high concentration urea. As soon as isoelectric focusing and SDS-PAGE was performed. The resolved proteins in the 2-DE gels were visualized by Coomassie blue R-250. The gels were scanned, and the images were processed with PDQuest software. Differential proteins were exactly excised from the gels, destained and digested with trypsin. The peptides were isolated and sent for MALDI-TOF-MS testing. Database searching was performed using peptide masses obtained from MALDI-TOF-MS.</p><p><b>RESULTS</b>Averages of 481 +/- 38 and 477 +/- 21 protein spots were detected in control gels and preconditioning gels, respectively. 169 +/- 6 protein spots were matched between these two types of gels. Among the matched spots, while the quantities of 21 +/- 12 spots in control gels increased by above 2 times than that in preconditioning one, the quantities of 33 +/- 10 spots in preconditioning gels increased by the same times than that in control one. The correlation coefficient between these two patterns were 0.7748 +/- 0.0267. 12 spots in preconditioning gels significantly increased compared with the control (P < 0.05, n = 4). Among 12 spots excised from the gels, perfect peptide mass fingerprinting spectrums of 8 spots were acquired. The results showed that one protein was fructose biphosphate aldolase A. Three proteins matched nothing might be new proteins. The other four proteins just matched the partial sequences of the proteins of database were no coincidence to it's isoelectric point and molecular weight. So they might be homological proteins.</p><p><b>CONCLUSION</b>Many proteins, for example fructose biphosphate aldolase A, has been differentially expressed in hippocampus of mice during HHDP. This may be one of the molecule mechanisms of HHDP.</p>
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Animales , Masculino , Ratones , Adaptación Fisiológica , Electroforesis en Gel Bidimensional , Hipocampo , Metabolismo , Hipoxia , Metabolismo , Hipoxia Encefálica , Metabolismo , Ratones Endogámicos BALB C , Proteínas , ProteomaRESUMEN
<p><b>AIM</b>To assay ET and NO in venous blood of native Tibetan and to investigate the effects of hypoxia on ET and NO levels in cultured umbilical venous endothelial cells of native Tibetan.</p><p><b>METHODS</b>ET and NO in venous blood of native Tibetan, immigrant Han and lowland Han were assayed. Umbilical venous endothelial cells (UVECs) from native Tibetan and immigrant Han newborns were cultured and divided into 4 groups: (1) Native Tibetan control group (TC), (2) Native Tibetan hypoxic group (TH), (3) Immigrant Han control group (HC), (4) Immigrant Han hypoxic group (HH). Supernatant was collected and ET and NO were detected.</p><p><b>RESULTS</b>Venous blood NO was significantly higher in native Tibetan than in immigrant Han, while ET lower in native Tibetan than in immigrant Han. ET excretion from UVECs was elevated while NO decreased in both Tibetan and Han groups after exposed to hypoxia. On time-points 12 h and 24 h, ET was significantly lower in TH than in HH, while concentration of NO showed no difference in TH and HH.</p><p><b>CONCLUSION</b>ET released by UVECs was higher in Han than in Tibetan after 12 h and 24 h hypoxic exposure, which may be in favor of lower vascular resistance and better fetal blood supply in Tibetan, and thus plays a role in the mechanisms of less intrauterine growth restriction (IUGR) throughout pregnancy and heavier birth weight of Tibetan newborns.</p>
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Humanos , Recién Nacido , Altitud , Pueblo Asiatico , Hipoxia de la Célula , Endotelina-1 , Metabolismo , Células Endoteliales de la Vena Umbilical Humana , Metabolismo , Óxido Nítrico , Metabolismo , Oxígeno , MetabolismoRESUMEN
<p><b>AIM</b>To investigate the dynamic changes and functions of urotensin II (U lI) receptor (UT) in pulmonary arteries of rats chronically exposed to hypoxia-hypercapnia.</p><p><b>METHODS</b>In rats with hypoxia-hypercapnia at 1, 2 and 4 weeks U II receptor binding of pulmonary arteries sarcolemma was determined by radioligand assay. U II mRNA and UTmRNA in various grades of pulmonary arterioles were measured by in situ hybridization.</p><p><b>RESULTS</b>(1) Mean pulmonary pressure (mPAP) and weight ratio of right ventricle to left ventricle and septum (RV/LV + S) of 1-week group were higher than those of normal control (NC) group by 26.2% and 21.6% (P < 0.01), respectively, and 2-week group higher than 1-week group by 22.5% and 14.1% (respectively, P < 0.01). However, no significant changes were found between 4-week and 2-week group. (2) U Il receptor (Bmax) of 1-week group was higher than NC group by 38.8%, 2-week group higher than 1-week group by 23.2%, and 4-week group increased 7.3% compared with 2-week group (respectively, P < 0.01). The UT changes were time-dependent, while the affinity to U II (Kd) was no different among each group. (3) UII mRNA in each grade of pulmonary arterioles of 2-week group and 4-week group were higher than NC group (respectively, P < 0.01), and those of 2-week group were higher than 1-week group by 5.9% (P > 0.05), 16.4% and 9.1% (respectively, P < 0.01), while no differences existed between 2-week group and 4-week group. (4) UT mRNA in each grade of pulmonary arterioles of all hypoxia-hypercapnia groups was higher than NC group (respectively, P < 0.01), and those of two abaxial grade vessels in 1-week group were the highest. No differences existed between 2-week group and 4-week group. (5) The pulmonary vessels remodeling were time-dependently aggravated by hypoxia-hypercapnia.</p><p><b>CONCLUSION</b>The dynamic changes of UT in pulmonary arterioles might have important contribution to the development of pulmonary hypertension and pulmonary arteriole remodeling induced by chronic hypoxia-hypercapnia in rats.</p>
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Animales , Masculino , Ratas , Arteriolas , Metabolismo , Hipercapnia , Metabolismo , Hipertensión Pulmonar , Metabolismo , Hipoxia , Metabolismo , Arteria Pulmonar , Metabolismo , Ratas Sprague-Dawley , Receptores Acoplados a Proteínas G , MetabolismoRESUMEN
<p><b>AIM</b>To observe the effects of acute hypoxia and adenosine on splenic T lymphocyte proliferation.</p><p><b>METHODS</b>Wistar rats were divided into control and hypoxic group, and the latter were exposed to hypoxia (5000 m simulated high altitude, 23 h/d). Three days later, spleen cells were collected and stimulated by 5.0 microg/ml and 2.5 microg/ml concanavalin A (ConA) to determine the splenocyte proliferation. The proliferation was also observed after addition of different amount of adenosine to culture medium.</p><p><b>RESULTS</b>Acute hypoxia and adenosine had marked inhibitory effect on mitogenic response to Con A in splenic T cells, and the inhibitory effect induced by adenosine displayed concentration-dependent.</p><p><b>CONCLUSION</b>Acute hypoxia may impair the T cell function and adenosine could be involved in this process.</p>
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Animales , Masculino , Ratas , Adenosina , Farmacología , Proliferación Celular , Concanavalina A , Farmacología , Medios de Cultivo , Química , Hipoxia , Ratas Wistar , Bazo , Biología Celular , Linfocitos T , Biología CelularRESUMEN
<p><b>AIM</b>To explore whether hypoxic response and breath holding at sea level could predict acute mountain sickness (AMS).</p><p><b>METHODS</b>113 men aged (19 +/- 1) years took part in this study. Blood oxygen saturation (SaO2), heart rate and blood pressure were measured during the course of breathing 10% O2 for 10 minutes and breath holding. Two days later after reaching Lasa (3 658 m altitude) by air, the symptomatic scores of AMS were evaluated. Then the relations between them were analyzed.</p><p><b>RESULTS</b>The SaO2 reduced progressively and the heart rate speeded up, while the blood pressure represented increase at first and then decrease within 10 min during the short-term hypoxia. The heart rate was lower during short-term hypoxia in subjects who developed AMS than in subjects doing well. But significant reverse correlation existed only between AMS scores and heart rate at 7th min after hypoxic breathing (r = -0.176).</p><p><b>CONCLUSION</b>Limited information can be gained on AMS score by assessing physiological responses to short-term hypoxia and breath holding at sea level.</p>
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Adolescente , Humanos , Masculino , Adulto Joven , Enfermedad Aguda , Mal de Altura , Diagnóstico , Contencion de la Respiración , Hipoxia , Diagnóstico , Inhalación , Intercambio Gaseoso PulmonarRESUMEN
<p><b>AIM</b>To observe the effects of hypoxia on DNA synthesis and the expression of collagen type I and III mRNA in cultured adult rat cardiac fibroblasts.</p><p><b>METHODS</b>Cardiac fibroblasts(CFs) were isolated from adult Wistar rat ventricule and cultured in vitro either in normoxic or hypoxic condition. Studies were conducted with the second passage of CFs. The changes of DNA synthesis was determined by measuring the incorporation of 3H-TdR into DNA and the changes of expression of pro-alpha1 (I) collagen, pro-alpha1(III) mRNA were measured by in situ hybridization respectively.</p><p><b>RESULTS</b>The 3H-TdR incorporation of CFs was increased by 34% (P < 0.05) and 36% (P < 0.01) after 6 h, 12 h hypoxia (2% O2) exposure respectively. The level of pro-alpha1(I) collagen mRNA expression was significantly elevated in the cells under hypoxia for 4 h, 8 h, and 12 h. The expression of pro-alpha1(III) mRNA increased when cells were cultured under hypoxia for 2 h.</p><p><b>CONCLUSION</b>These results suggest that hypoxia alone can upregulate DNA synthesis and expression of collagen type I and III mRNA in adult rat cardiac fibroblasts. It may be one of the important mechanisms by which hypoxic myocardial fibrosis occur.</p>
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Animales , Masculino , Ratas , Hipoxia de la Célula , Células Cultivadas , Colágeno Tipo I , Metabolismo , Colágeno Tipo III , Metabolismo , ADN , Fibroblastos , Metabolismo , Miocitos Cardíacos , Biología Celular , ARN Mensajero , Genética , Ratas WistarRESUMEN
<p><b>AIM</b>To evaluate the hemodynamic effects of aminophylline and nifedipine in patients with HAPE.</p><p><b>METHODS</b>10 patients with HAPE undergone Swan-Ganz catheter. The parameters of hemodynamics and arterial blood gases in HAPE were measured before and after administration of nifedipine 20 mg sublingually and aminophylline 0.25 g intravenously respectively.</p><p><b>RESULTS</b>After administering 0.25 g aminophylline the mPAP and PVR significantly decreased, the cardiac output and the level of PaO2, SaO2 increased obviously, the mSAP, HR did not change so much. After using 20 mg nifedipine, the mPAP, PVR and mSAP also decreased, while the cardiac output, HR and the level of PaO2, SaO2 did not show any changes.</p><p><b>CONCLUSION</b>Both of aminophylline and nifedipine can attenuate pulmonary hypertension in patients with HAPE, but the effect of aminophylline was better than the effect of nifedipine.</p>
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Adulto , Humanos , Masculino , Altitud , Mal de Altura , Quimioterapia , Aminofilina , Usos Terapéuticos , Hipertensión Pulmonar , Quimioterapia , Nifedipino , Usos Terapéuticos , Resultado del TratamientoRESUMEN
<p><b>AIM</b>To study the effects of hypoxia alone or combined-exercise on blood viscosity and cardiac function of rats.</p><p><b>METHODS</b>22 wistar rats were divided into 3 groups: I normoxic control; II hypoxia and III hypoxia-combined exercise. Rats of II and III groups were subjected to hypobaric hypoxia for 5 weeks (23 h/day). They were first brought to simulated 4 000 m altitude, where rats of the III group were forced to swim for 1 h/day (6 days/week). Then the animals were ascent to 5 000 m. Cardiac function were detected by polygraph, the blood viscosity was assayed by E-viscosimeter, 99mTc radiolabelled frog red blood cell was used to measure the cardiac output.</p><p><b>RESULTS</b>Hypoxia alone caused an increase in blood hematocrit (Hct) and viscosity. Cardiac function of the left and right ventricles, especially +/- dp/dt(max) was also increased. Hypoxia-combined-exercise did not cause further increase in Hct, while the blood viscosity was decreased. Cardiac function increased further in both ventricles and the cardiac output was increased by 20% after hypoxia-combined-exercise.</p><p><b>CONCLUSION</b>During acclimatization to hypoxia, moderate exercise can decrease the blood viscosity and increase the cardiac function. These changes may be advantageous in delivering oxygen to tissues and may be favorable for promoting acclimation to high altitude.</p>
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Animales , Ratas , Altitud , Presión Sanguínea , Viscosidad Sanguínea , Gasto Cardíaco , Hematócrito , Hipoxia , Sangre , Ratas Wistar , Natación , Función Ventricular Izquierda , Función Ventricular DerechaRESUMEN
<p><b>AIM</b>To explore the effects of hypoxia on expression of inducible nitric oxide synthase (iNOS) mRNA in cultured rat astrocytes.</p><p><b>METHODS</b>Cultured rat astrocytes were randomly divided into 4 groups: glutamate group (G), hypoxic group (H), hypoxia + glutamate group (H + G) and the control (C). Cells of control group were exposed to normoxic (95% air, 5% CO2) condition, and cells of G and H + G were incubated with 100 micromol/L L-glutamate, cells of H and H + G exposed to hypoxic conditions (5% CO2, 95% N2) at 37 degrees C. Each group had five timepoints which included 0 h, 3 h, 6 h, 12 h, 24 h, respectively. Expression of mRNAs of iNOS were detected with reverse transcription polymerase chain reaction (RT-PCR).</p><p><b>RESULTS</b>Expression of iNOS mRNA was not detectable in G and C, while it increased dramatically and continuously from 6 h to 24 h in H and G + H. Expression of iNOS mRNA was significantly higher in H than both in G and C at 6 h, 12 h and 24 h, and expression of iNOS mRNA was the highest of all groups in G + H.</p><p><b>CONCLUSION</b>Hypoxia upregulates the expression of iNOS mRNA in cultured astrocytes. Glutamate does not induce the expression of iNOS mRNA but enhance the effect of hypoxia, which is maybe one of the adaptive mechanisms of hypoxia-induced cerebral dilation.</p>