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1.
本实验观察了80只家兔在急性缺氧6、12、24、48;60、71h后肺指数、血浆心钠素(ANP)、抗利尿激素(AVP)、醛固酮(ALD)及尿量的变化。结果表明:在缺氧24-72h,肺指数明显升高,尿量减少、缺氧16h,血浆ANP明显升高;而缺氧48和60h无ANP升高现象。缺氧72h,血浆ANF又明显高于缺氧前水平;血浆ACP只在缺氧24h明显升高;血浆ALD未见显著性变化。这些结果提示:在缺氧状  相似文献   

2.
目的:探讨使用外源性肺表面活性物质(PS)治疗能否减轻烟雾吸入所致肺组织细胞损害。方法:Wistar大鼠随机分为5组:Ⅰ组,正常对照;Ⅱ组,烟雾吸入;Ⅲ组,烟雾+PS+机械通气(MV);Ⅳ组,烟雾+盐水+MV;Ⅴ组,烟雾+MV,伤后5min经气管导管注入PS(100mg/kg)或等量盐水,MV4h,观察24h,检测动脉血气、肺水量、支气管肺泡灌洗液(BALF)中白细胞分类计数及乳酸脱氢酶(LDH)、血管紧张素转换酶(ACE)和碱性磷酸酶(AKP)活性、胎盘型碱性磷酸酶(PLAP)含量、肺泡壁纤维成分含量及病理检查等。结果:Ⅱ组伤后发生呼吸衰竭、肺水肿及肺部急性炎症反应,BALF中LDH、AKP、ACE和PLAP水平均明显升高,肺泡壁纤维成分含量显著减少。Ⅲ组血气较Ⅱ组明显改善,但BALF中各酶水平、肺泡壁纤维成分含量及肺部炎症、水肿等无显著减轻。Ⅳ、Ⅴ组治疗无效。结论:烟雾吸入伤早期外源性PS治疗能一定程度改善呼吸功能,但对肺组织细胞损害无明显保护作用,不能减轻继发性炎症反应和急性肺水肿  相似文献   

3.
Wang Y  Wang XM  Han JS 《生理学报》1998,50(2):217-221
我们采用反转录-聚合酶链反应(RT-PCR)方法,观察了δ阿片受体肽类激动剂「D-Pen^2.5」enkephalin(DPDPE)及非肽类激动剂BW373U86对δ受体mRNA表达的影响,并比较了两者作用的差异性。结果如下:(1)DPDPE作用24及48h可使δ受体mRNA表达水平显著降低,则BW373U86只在24h有显著抑制作用;(2)DPDPE在10^-6mol/L时即可使δ受体的mRNA  相似文献   

4.
目的:探讨使用外源性肺表面活性物质(PS)治疗能否减轻烟雾吸入所致肺组织损害。方法:Wistar大鼠随机分为5组:I组,正常对照;Ⅱ组,烟雾吸入;Ⅲ组,烟雾+PS+机械通气(MV);Ⅳ组,烟雾+盐水+MV;Ⅴ组,烟雾+MV,伤后5min经气管导管注入PS(100mg/kg)或等量盐水,MV4h,观察24h,检测动脉血气、肺水量、支气管肺泡灌洗液(BALF)中白细胞分类计数及乳酸脱氢酶(LDH)、血  相似文献   

5.
本文就植物血细胞凝集素(PHA)作用的不同时间对小鼠脾脏淋巴细胞γ-谷氨酰基转肽酶(γ-GT)活性的影响进行了观察。结果表明,脾脏淋巴细胞转化率随给予PHA时间的延长而上升,对照组<24h组<48h组<72h组;淋巴细胞γ-GT活性于24h明显强于对照组(P<0.001),随着PHA作用时间的延长其γ-GT活性逐渐下降,即48h组与对照组已无显著差异,而72h组却低于对照组(P<0.001)。可见PHA在小鼠体内对γ-GT活性有很大影响。  相似文献   

6.
脂多糖对离体培养大鼠血管平滑肌细胞增殖的影响   总被引:2,自引:0,他引:2  
Li J  Lin SX  Li Y  Zhao HL  Jia B 《生理学报》1999,51(1):14-18
本研究观察到10-7~10-5kg/L脂多糖(lipopolysacharide,LPS)可显著促进血管平滑肌细胞(VSMC)的增殖及DNA的合成(P<005)。5×10-4~10-3kg/LLPS却抑制VSMC的增殖及DNA的合成,降低其活力(P<001),并呈时间依赖效应。一氧化氮合酶抑制剂NNitroLArginine(LNNA)可拮抗LPS的抑制作用。大剂量LPS作用组VSMC上清液中一氧化氮(NO)代谢产物NO-3和NO-2的含量与对照组相比显著增加(P<001),48h组比24h组增加91%,72h组比48h组增加45%;同时,诱导性一氧化氮合酶(inductivenitricoxidesynthase,iNOS)免疫组化染色呈阳性。结果表明,低浓度LPS促进VSMC增殖和DNA合成,而高浓度LPS却明显抑制VSMC增殖和DNA合成,降低其活力。这种抑制作用可能与LPS诱导VSMC产生的NO有关。  相似文献   

7.
为探讨脑内心房钠尿肽(ANP)的作用,本工作采用SD大鼠,用放射免疫方法测定3/4肾大部切除与高盐摄食后脑内ANP的含量。结果表明,对照组大鼠脑内ANP分布广泛。3/4肾切除大鼠每日饮水量,尿量均比对照组高(P<0.05),尿钠浓度低于对照组时,脑内ANP含量尽管略有增加,但10个核团(下丘脑室周核、弓状核、室旁核、视前室周核、中缝背核、尾壳核、杏仁核、脑桥背侧部、蓝斑和大脑皮质)ANP含量和对照组无明显差别(P>0.05)。高盐摄食组每日饮水量和尿量均比对照组高,且尿钠浓度高于对照组,同时下丘脑室周核和弓状核ANP含量比对照组高(P<0.05)。上述结果提示,大脑第三脑室前腹侧区(AV3V区)的ANP可能在水盐调节上发挥重要作用。  相似文献   

8.
脑内血管紧张素Ⅱ系统在穹窿下器升压反应中的作用   总被引:7,自引:0,他引:7  
Chang YZ  Gu YH 《生理学报》1999,51(1):38-44
文献报道脑内存在血管紧张素Ⅱ系统。与此一致,本工作用氨基甲酸乙脂麻醉、箭毒制动、人工呼吸的大鼠观察到:(1)穹窿下器(SFO)、室旁核(NPV)或NPV的投射区:延髓头端腹外侧区(RVLM)、导水管周围灰质(PAG)、蓝斑(LC)内注入血管紧张素Ⅱ(AⅡ)均引起升压反应;(2)SFO升压反应可被双侧NPV或RVLM内预先注入[Sar1,Thr8]AⅡ(STAⅡ,AⅡ拮抗剂)明显衰减,NPV升压反应也可被RVLM内注入STAⅡ削弱;(3)双侧PAG用STAⅡ预处理后,AⅡ引起的NPV或SFO升压反应均明显减小;(4)NPV升压反应还可被双侧LC内预先注射STAⅡ衰减,但SFO升压反应不受影响。结合我们以往工作曾显示兴奋PAG或LC均可作用于RVLM引起升压反应,目前的结果表明:SFO内的AⅡ能神经元通过NPV内AⅡ能神经元,不仅可直接作用于RVLM引起升压反应,而且还可间接通过PAG作用于RVLM起升压作用,但LC不参与SFO升压反应。  相似文献   

9.
研究了氧化修饰极低密度脂蛋白(ox-VLDL)对小白鼠腹腔巨噬细胞内脂质堆积作用及其机制。经Cu~(2+)修饰后VLDL的电泳迁移率及脂质过氧化物含量均显著增加。ox-VLDL更易导致小鼠腹腔巨噬细胞内脂质堆积。以相同浓度(300μgTG/mL)或不同浓度(200─500μgTG/mL)的ox-VLDL及正常VLDL(n-VLDL)与巨噬细胞温育24h,前者使巨噬细胞内TG堆积均比后者显著(P<0.01)。同时,随ox-VLDL的脂质过氧化物含量(TBARS水平)增加,巨噬细胞内TG含量的百分率相应增加。以50μg蛋白/mL的n-LDL,ox-LDL,n-VLDL及ox-VLDL与巨噬细胞温育60h。细胞内CE堆积中氧化组均比正常组高(P<0.01)。巨噬细胞对~(125)I-n-VLDL与~(125)I-ox-VLDL的结合、降曲线均有饱和趋势。两结合曲线无明显差异,但细胞对后者降解的量比前者多。结合的竞争实验表明,n-VLDL能抑制大部分~(125)I-ox-VLDL与细胞结合,而Ac-LDL只能抑制小部分。结果表明ox-VLDL主要通过受体途径:大部分经过n-VLDL受体,小部分经过清道夫受体被巨噬细胞摄  相似文献   

10.
在麻醉大鼠观察了向延髓腹外侧区微量注射NO合成酶抑制剂N-硝基左旋精氨酸(LNNA)和硝普钢(SNP)对血压、心率和肾交感神经活动的影响,旨在探讨中枢左旋精氨酸-NO通路在动脉血压调节中的作用及其机制。实验结果如下:(1)向延髓腹外侧头端区(RVLM)注射L-NNA后,平均动脉压(MAP)升高,肾交感神经活动(RSNA)增强;心率(HR)减慢,但无统计学意义。MAP和RSNA的变化持续30min以上;此效应可被预先静注左旋精氨酸所逆转。(2)向RVLM微量注射SNP,MAP降低,RSNA减弱;但HR的变化无统计学意义。(3)向延髓腹外侧尾端区(CVLM)注射L-NNA,MAP降低,HR减慢,RSNA减弱。(4)向CVLM微量注射SNP,MAP升高,RSNA增强,而心率无明显变化。以上结果表明,中枢左旋精氨酸-NO通路对延髓腹外侧部的神经元活动有调变作用。  相似文献   

11.
We measured renal functions and hormones associated with fluid regulation after a bolus injection of aldosterone (Ald) during head-down tilt (HDT) bed rest to test the hypothesis that exposure to simulated microgravity altered renal responsiveness to Ald. Six male rhesus monkeys underwent two experimental conditions (HDT and control, 72 h each) with each condition separated by 9 days of ambulatory activities to produce a crossover counterbalance design. One test condition was continuous exposure to 10 degrees HDT; the second was a control, defined as 16 h per day of 80 degrees head-up tilt and 8 h prone. After 72 h of exposure to either test condition, monkeys were moved to the prone position, and we measured the following parameters for 4 h after injection of 1-mg dose of Ald: urine volume rate (UVR); renal Na(+)/K(+) excretion ratio; renal clearances of creatinine, Na(+), osmolality, and free water; and circulating hormones [Ald, renin activity (PRA), vasopressin (AVP), and atrial natriuretic peptide (ANP)]. HDT increased Na(+) clearance, total renal Na(+) excretion, urine Na(+) concentration, and fractional Na(+) excretion, compared with the control condition, but did not alter plasma concentrations of Ald, PRA, and AVP. Administration of Ald did not alter UVR, creatinine clearance, Ald, PRA, AVP, or ANP but reduced Na(+) clearance, total renal Na(+) excretion, urinary Na(+)/K(+) ratio, and osmotic clearance. Although reductions in Na(+) clearance and excretion due to Ald were greater during HDT than during control, the differential (i.e., interaction) effect was minimal between experimental conditions. Our data suggest that exposure to microgravity increases renal excretion of Na(+) by a natriuretic mechanism other than a change in renal responsiveness to Ald.  相似文献   

12.
目的观察D-半乳糖(D-gal)致亚急性衰老大鼠在尿液排泄方面的特点并探讨其多尿症状机制。方法在初筛合格的SD大鼠颈背部皮下注射浓度为5%的D-gal生理盐水溶液125mg/(kg·d)连续8周。观察动物在造模期间和停止造模后两周内24h总尿量及水负荷后排尿情况的变化;通过测定模型动物尿中K+、Na+、CL-浓度,血中ALD、ADH、ANP浓度及肾脏病理形态学观察,探讨模型动物24h总尿量增加的机制。结果与正常对照组相比较,模型组动物24h总尿量明显增加;水负荷后6h内排尿潜伏期明显缩短,排尿次数明显增多,但总尿量没有明显差异;模型动物尿中Na+、CL-浓度明显升高,K+浓度明显降低;血浆ALD、ADH含量显著降低,ANP含量显著增加,肾脏出现一系列硬化特征。结论 D-gal致亚急性衰老大鼠出现的总尿量增加和排尿次数增多的情况可能与其ADH、ALD、ANP合成与分泌异常及肾脏病理形态学改变有关。  相似文献   

13.
There is little information regarding the effect of hypoxia on alveolar fluid clearance capacity. We measured alveolar fluid clearance, lung water volume, plasma catecholamine concentrations, and serum osmolality in rats exposed to 10% oxygen for up to 120 h and explored the mechanisms responsible for the increase in alveolar fluid clearance. The principal results were 1) alveolar fluid clearance did not change for 48 h and then increased between 72 and 120 h of exposure to hypoxia; 2) although nutritional impairment during hypoxia decreased basal alveolar fluid clearance, endogenous norepinephrine increased net alveolar fluid clearance; 3) the changes of lung water volume and serum osmolality were not associated with those of alveolar fluid clearance; 4) an administration of beta-adrenergic agonists further increased alveolar fluid clearance; and 5) alveolar fluid clearance returned to normal within 24 h of reoxygenation after hypoxia. In conclusion, alveolar epithelial fluid transport capacity increases in rats exposed to hypoxia. It is likely that a combination of endogenous norepinephrine and nutritional impairment regulates alveolar fluid clearance under hypoxic conditions.  相似文献   

14.
To test the hypothesis that exogenous atrial natriuretic peptide (ANP) prevents the acute pulmonary pressor response to hypoxia, ANP (20-micrograms/kg bolus followed by 1-microgram.kg-1.min-1 infusion) or vehicle was administered intravenously to conscious rats beginning 3 min before exposure to hypoxia or room air for 90 min. Exogenous ANP abolished the acute pulmonary pressor response to hypoxia in association with marked and parallel increases in plasma ANP and guanosine 5'-cyclic monophosphate (cGMP) and with a significant increase in lung cGMP content. To examine whether endogenous ANP modulates the acute pulmonary pressor response to hypoxia, rats were pretreated with a monoclonal antibody (Ab) to ANP and exposed to hypoxia. Mean pulmonary arterial pressure (MPAP) in the Ab-treated rats was not different from control over the first 6 h of hypoxic exposure. Thereafter, the Ab-treated group had significantly higher MPAP than control. Our data suggest that 1) exogenous ANP blocks the pulmonary pressor response to acute hypoxia via stimulation of cGMP accumulation in the pulmonary vasculature, and 2) endogenous ANP may modulate the subacute, but not acute, phase of hypoxic pulmonary hypertension.  相似文献   

15.
Atrial natriuretic peptide in hypoxia   总被引:4,自引:0,他引:4  
Chen YF 《Peptides》2005,26(6):1068-1077
A growing number of mammalian genes whose expression is inducible by hypoxia have been identified. Among them, atrial natriuretic peptide (ANP) synthesis and secretion is increased during hypoxic exposure and plays an important role in the normal adaptation to hypoxia and in the pathogenesis of cardiopulmonary diseases, including chronic hypoxia-induced pulmonary hypertension and vascular remodeling, and right ventricular hypertrophy and right heart failure. This review discusses the roles of ANP and its receptors in hypoxia-induced pulmonary hypertension. We and other investigators have demonstrated that ANP gene expression is enhanced by exposure to hypoxia and that the ANP so generated protects against the development of hypoxic pulmonary hypertension. Results also show that hypoxia directly stimulates ANP gene expression and ANP release in cardiac myocytes in vitro. Several cis-responsive elements of the ANP promoter are involved in the response to changes in oxygen tension. Further, the ANP clearance receptor NPR-C, but not the biological active NPR-A and NPR-B receptors, is downregulated in hypoxia adapted lung. Hypoxia-sensitive tyrosine kinase receptor-associated growth factors, including fibroblast growth factor (FGF) and platelet derived growth factor (PDGF)-BB, but not hypoxia per se, inhibit NPR-C gene expression in pulmonary arterial smooth muscle cells in vitro. The reductions in NPR-C in the hypoxic lung retard the clearance of ANP and allow more ANP to bind to biological active NPR-A and NPR-B in the pulmonary circulation, relaxing preconstricted pulmonary vessels, reducing pulmonary arterial pressure, and attenuating the development of hypoxia-induced pulmonary hypertension and vascular remodeling.  相似文献   

16.
We tested the physiological reliability of plasma renin activity (PRA) and plasma concentrations of arginine vasopressin (P[AVP]), aldosterone (P[ALD]), and atrial natriuretic peptide (P[ANP]) in the early follicular phase and midluteal phases over the course of two menstrual cycles (n = 9 women, ages 25 +/- 1 yr). The reliability (Cronbach's alpha >/=0.80) of these hormones within a given phase of the cycle was tested 1) at rest, 2) after 2.5 h of dehydrating exercise, and 3) during a rehydration period. The mean hormone concentrations were similar within both the early follicular and midluteal phase tests; and the mean concentrations of P[ALD] and PRA for the three test conditions were significantly greater during the midluteal compared with the early follicular phase. Although Cronbach's alpha for resting and recovery P[ANP] were high (0.80 and 0.87, respectively), the resting and rehydration values for P[AVP], P[ALD], and PRA were variable between trials for the follicular (alpha from 0.49 to 0.55) and the luteal phase (alpha from 0.25 to 0. 66). Physiological reliability was better after dehydration for P[AVP] and PRA but remained low for P[ALD]. Although resting and recovery P[AVP], P[ALD], and PRA were not consistent within a given menstrual phase, the differences in the concentrations of these hormones between the different menstrual phases far exceeded the variability within the phases, indicating that the low within-phase reliability does not prevent the detection of menstrual phase-related differences in these hormonal variables.  相似文献   

17.
As a result of our recently published studies we have thought that altitude diuresis resulting from hypoxic stimulation of the arterial chemoreceptors reduces the cardiac volume overload. To test this hypothesis, cardiovascular, endocrine and renal responses to stepwise acute exposure to simulated altitude (6,000 m) were compared in ten acclimatized recumbent mountaineers a mean of 24 days, SD 11, after descending from Himalayan altitudes of at least 4,000 m, with those found in ten non-acclimatized recumbent volunteers. The results showed that natriuresis and diuresis typified the renal responses to altitude exposure of both the acclimatized as well as non-acclimatized subjects, as long as altitude was well tolerated. It was concluded that the renal effects were mediated by atrial natriuretic peptide release and slight suppression of arginine-vasopressin (AVP) secretion, that the increased urine flow at altitude offset the cardiac (volume) overload resulting from hypoxic stimulation of the arterial chemoreceptors, and that enhanced AVP secretion, as found in the non-acclimatized subjects at and above 4,000 m, coincided with subjective and objective distress, i.e. with inadequate altitude adjustment owing to insufficient chemoreflex effects and central hypoxia.  相似文献   

18.
We tested the hypotheses that hypoxic exposure is associated with exacerbated pulmonary hypertension and right ventricular (RV) enlargement, reduced atrial natriuretic peptide (ANP) clearance receptor (NPR-C) expression, and enhanced B-type natriuretic peptide (BNP) expression in the absence of ANP. Male wild-type [ANP(+/+)], heterozygous [ANP(+/-)], and homozygous [ANP(-/-)] mice were studied after a 5-wk hypoxic exposure (10% O(2)). Hypoxia increased RV ANP mRNA and plasma ANP levels only in ANP(+/+) and ANP(+/-) mice. Hypoxia-induced increases in RV pressure were significantly greater in ANP(-/-) than in ANP(+/+) or ANP(+/-) mice (104 +/- 17 vs. 45 +/- 10 and 63 +/- 7%, respectively) as were increases in RV mass (38 +/- 4 vs. 26 +/- 5 and 29 +/- 4%, respectively). NPR-C mRNA levels were greatly reduced in the kidney, lung, and brain by hypoxia in all three genotypes. RV BNP mRNA and lung and kidney cGMP levels were increased in hypoxic mice. These findings indicate that disrupted ANP expression worsens hypoxic pulmonary hypertension and RV enlargement but does not alter hypoxia-induced decreases in NPR-C and suggest that compensatory increases in BNP expression occur in the absence of ANP.  相似文献   

19.
The effect of short lasting hypoxia on blood pressure, plasma atrial natriuretic peptide level and number of specific atrial granules were studied in 26 male spontaneously hypertensive and 24 normotensive Wistar rats. A great difference occurred in ANP secretion between hypertensive and normotensive rats. In the hypertensive animals elevated plasma ANP concentration (130 +/- 27 pg/ml) and decreased granularity in the right atria (73 +/- 2) were found on the first day of hypoxia with a slight elevation in urinary sodium content versus normotensive controls. The blood pressure also decreased although not significantly (190 +/- 14 mm Hg). In Wistar rats increased plasma ANP (130 +/- 34 pg/ml) and decreased atrial granularity versus normotensive controls (72 +/- 10 in the left and 113 +/- 16 in the right atrium) were observed only on the third day of hypoxia without changes in blood pressure and natriuresis. In SHR the rapid but short timed ANP release might be of right atrial origin and probably the consequence of a continuous and perhaps increased secretion of the peptide in normoxic conditions too. In Wistar rats the plasma ANP elevation could be secondary due to the increased plasma level of different vasoactive hormones to hypoxia. In the altered effect of ANP in hypertensive and normotensive hypoxic animals, structural and functional changes in the vascular bed may play a role.  相似文献   

20.
High-altitude exposure changes the distribution of body water and electrolytes. Arginine vasopressin (AVP) may influence these alterations. The purpose of this study was to examine the effect of a 24-h water deprivation trial (WDT) on AVP release after differing altitude exposures. Seven healthy males (age 22 +/- 1 yr, height 176 +/- 2 cm, mass 75.3 +/- 1.8 kg) completed three WDTs: at sea level (SL), after acute altitude exposure (2 days) to 4,300 m (AA), and after prolonged altitude exposure (20 days) to 4,300 m (PA). Body mass, standing and supine blood pressures, plasma osmolality (Posm), and plasma AVP (PAVP) were measured at 0, 12, 16, and 24 h of each WDT. Urine volume was measured at each void throughout testing. Baseline Posm increased from SL to altitude (SL 291.7 +/- 0.8 mosmol/kgH2O, AA 299.6 +/- 2.2 mosmol/kgH2O, PA 302.3 +/- 1.5 mosmol/kgH2O, P < 0.05); however, baseline PAVP measurements were similar. Despite similar Posm values, the maximal PAVP response during the WDT (at 16 h) was greater at altitude than at SL (SL 1.7 +/- 0.5 pg/ml, AA 6.4 +/- 0.7 pg/ml, PA 8.7 +/- 0.9 pg/ml, P < 0.05). In conclusion, hypoxia appeared to alter AVP regulation by raising the osmotic threshold and increasing AVP responsiveness above that threshold.  相似文献   

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