碱性成纤维细胞生长因子对大鼠肾小球系膜细胞原癌基因c-fos和c-myc表达的影响

在建立大鼠肾小球系膜细胞（ＭＣ）体外培养方法的基础上,通过３Ｈ－ＴｄＲ参入实验,ＲＮＡ印迹分析和斑点杂交观察ｂＦＧＦ对ＭＣＤＮＡ合成及原癌基因ｃ－ｆｏｓ和ｃ－ｍｙｃ表达的影响．结果表明,ｂＦＧＦ作用于ＭＣ１８ｈ,ＭＣ的３Ｈ－ＴｄＲ参入率明显增加（Ｐ＜０．０５）,２４ｈ达到高峰（Ｐ＜０．０１）;ｂＦＧＦ显著诱导原癌基因ｃ－ｆｏｓ和ｃ－ｍｙｃ表达,其表达活性分别于３０ｍｉｎ和１ｈ达到高峰．提示ｂＦＧＦ是ＭＣ的强效丝裂原,其对ＭＣＤＮＡ合成的促进作用与诱导原癌基因ｃ－ｆｏｓ和ｃ－ｍｙｃ表达有关．     

乙酰胆碱对大鼠头端延髓腹外侧区前交感神经元放电的作用

实验采用细胞外记录和微电泳等电生理方法,研究乙酰胆碱（ＡＣｈ）对氨基甲酸乙酯麻醉的大鼠头端延髓腹外侧区（ＲＶＬＭ）前交感神经元放电频率的影响。在ＲＶＬＭ共记录到３５个前交感神经元,微电泳ＡＣｈ能增加其放电（Ｐ〈０．０５）,并且具有剂量依赖性。其中２２个神经元微电泳Ｍ型胆碱受体阻断剂阿托品（ＡＴＲ）后能明显降低前交感神经元的基础放电（Ｐ〈０．０５）和完全阻断ＡＣｈ引起的神经元兴奋作用;分别向其余７和     

三七总皂甙对动物脑缺血性损伤的保护作用

观察三七总皂甙（ＳａｐｏｎｉｎｓｏｆＰａｎａｘｎｏｔｏｇｉｎｓｅｎｇＰＮＳ）对小鼠全脑缺血和大鼠局灶性脑缺血（ＭＣＡＯ）的影响。结果发现ＰＮＳ（５０、１００ｍｇ．ｋｇ－１×３ｄ,ｉｐ）明显延长断头或ｉｖ饱和ＭｇＣｌ２后喘息持续时间。ＰＮＳ２００ｍｇ．ｋｇ－１术前３０ｍｉｎ或ＭＣＡＯ术后１５ｍｉｎｉｐ能减少ＭＣＡＯ术后２４ｈ脑梗塞面积,改善神经功能障碍及行为异常,减轻神经细胞缺血性损害。提示ＰＮＳ对缺血性脑损伤有保护作用。     

外源性肺表面活性物质替代治疗对烟雾吸入所致肺组织细胞 …

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     

乙酰胆碱对大鼠体外抗体生成的影响

目的：观察不同浓度乙酰胆碱（ＡＣｈ,１０－１０～１０－５ｍｏｌ／Ｌ）对大鼠体外抗体生成的影响,并初步探讨其作用机制,从细胞水平了解乙酰胆碱与免疫功能之间的关系。方法：用体外抗体生成的检测方法,用绵羊红细胞（ＳＲＢＣ）刺激大鼠肠系膜淋巴结Ｂ细胞转化成抗体形成细胞（ＡＦＣ）,然后检测其抗体生成量。结果：①１０－１０～１０－７ｍｏｌ／ＬＡＣｈ能显著抑制体外抗体生成,其中１０－８和１０－７ｍｏｌ／ＬＡＣｈ的作用较强,而１０－６和１０－５ｍｏｌ／ＬＡＣｈ无明显的抑制作用;②Ｍ型胆碱能受体激动剂毛果芸香碱（１０－８和１０－７ｍｏｌ／Ｌ）能明显减弱体外抗体生成,而Ｎ型受体激动剂烟碱（１０－８和１０－７ｍｏｌ／Ｌ）没有显著的减弱作用,Ｍ型受体拮抗剂阿托品（１０－７和１０－６ｍｏｌ／Ｌ）可完全阻断ＡＣｈ抑制体外抗体生成的作用;③ＡＣｈ分别在Ｂ细胞用ＳＲＢＣ刺激后３～４８ｈ中的６个不同时间与淋巴细胞作用,其抗体生成仍然是减少的。结论：ＡＣｈ可非浓度依赖性地抑制大鼠的体外抗体生成;此作用可能由Ｂ细胞上的Ｍ型胆碱能受体介导;且ＡＣｈ可能主要影响Ｂ细胞转化的后期过程。     

一氧化氮等在体外循环下心肌缺血再灌注损伤中的改变

近年来,一氧化氮（ｎｉｔｒｉｃｏｘｉｄｅ,ＮＯ）在心肌缺血再灌注损伤（ｍｇｏｃａｒｄｉａｌｉｓｃｈｅｍｉａｒｅｐｅｒｆｓｉｏｎｉｎｊｕｒｙ,ＭＩＲＩ）中的作用日益为人们所重视。本研究通过观察１６例心内直视手术患者主动脉阻断前,阻断３０ｍｉｎ、开放３０ｍｉｎ、１ｈ、２ｈ、４ｈ及８ｈ不同时相点血浆ＮＯ水平、ＬＤＨ及ＣＰＫ活性的动态变化,探讨ＮＯ在体外循环（ＣＰＢ）下ＭＩＲＩ中的作用、意义及其可能的机制,更好地为ＭＩＲＩ的防治提供可靠的理论依据。１　材料与方法（１）观察对象　先天性心脏病（室间隔缺损…     

大鼠液压冲击脑损伤脑干c-fos mRNA表达的定位观察

目的：研究大鼠中度侧位液压冲击脑损伤时脑干ｃ－ｆｏｓ ｍＲＮＡ及其表达产物Ｆｏｓ变化规律。方法：雄性ＳＤ大鼠,随机分为正常对照组、手术对照组和损伤组。损伤组动物均给以０．２ＭＰａ液压冲击脑损伤,按冲击后处死时间不同再分为５ｍｉｎ、１５ｍｉｎ、３０ｍｉｎ、１ｈ、２ｈ、４ｈ、８ｈ和１２ｈ组。应用免疫组织化学和原位杂交方法观察ｃ－ｆｏｓ在脑干的表达。结果：脑冲击后１５ｍｉｎ－１２ｈ,Ｆｏｓ阳性细胞数逐渐     

外源性肺表面活性物质替代治疗对烟雾吸入所致肺组织细胞损害的影响

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     

支链氨基酸对心肌缺血大鼠线粒体损伤的保护作用

目的和方法：本文用异丙肾上腺素（Ｉｓｏ） 造成大鼠心肌缺血动物模型,观察支链氨基酸（ＢＣＡＡ）对大鼠心肌缺血时线粒体结构和功能损伤的预防作用。结果：ＢＣＡＡ 能显著降低心肌缺血后心肌线粒体中丙二醛（ＭＤＡ） 水平、维持线粒体模平均微粘度（－η） 、线粒体呼吸链中细胞色素氧化酶及心肌肌球蛋白ＡＴＰａｓｅ活力。结论：给予ＢＣＡＡ对保护大鼠心肌线粒体的结构和功能免受缺血性损伤具有一定效果     

人主动脉硫酸乙酰肝素蛋白聚糖对培养的人血管壁细胞生长的作用

通过培养的人主动脉平滑肌细胞（ｈＡＳＭＣ）及脐静脉内皮细胞（ｈＵＶＥＣ）,应用＾３Ｈ－ＴｄＲ参入、Ｎｏｒｔｈｅｒｎ ｂｌｏｔ分析、逆转录多聚酶链反应（ＲＴ－ＰＣＲ）、放射免疫分析（ＲＩＡ）、和紫外比色法等技术观察了人主动脉中硫酸乙酰肝素蛋白聚糖（ＨＳＰＧ）对ｈＡＳＭＣ和ｈＵＶＥＣ ＤＮＡ合成的作用及对血小板源生长因子（ＰＧＤＦ）、ＰＧＤＦ受体、转化生长因子β（ＴＧＦ－β）、内皮素－１（ＥＴ－１）或     

Cutaneous blood flow and sweat rate responses to exogenous administration of acetylcholine and methacholine.

The aim of this study was to evaluate cutaneous vasodilation and sweating responses to exogenous administration of acetylcholine (ACh) and methacholine (MCh), which have different sensitivities to endogenous cholinesterase. Four intradermal microdialysis probes were placed in dorsal forearm skin: two sites were perfused with ACh (1 x 10(-7)-1 M) and the other two with the same molar concentrations of MCh. Sweat rate (SR) and cutaneous blood flow were simultaneously assessed directly over each microdialysis membrane. Dose-response curves were constructed, and the effective concentration of the drug resulting in 50% of the maximal response (EC(50)) was identified. For SR and cutaneous vascular conductance (CVC), there were no significant differences in EC(50) between sites receiving the same drug: -1.52 +/- 0.18 and -1.19 +/- 0.09 log-molar concentration of ACh at distal and proximal sites, respectively, and -2.35 +/- 0.24 and -2.42 +/- 0.23 log-molar concentration of MCh at distal and proximal sites, respectively, for SR (P > 0.05) and -3.87 +/- 0.32 and -3.97 +/- 0.27 log-molar concentration of ACh at distal and proximal sites, respectively, and -4.78 +/- 0.17 and -4.46 +/- 0.16 log-molar concentration of MCh at distal and proximal sites, respectively, for CVC (P > 0.05). However, the EC(50) for CVC and SR was significantly lower at the MCh than at the ACh sites. A second procedure was performed to confirm that differences in responses between ACh and MCh could be attributed to different cholinesterase sensitivities. Similarly, four microdialysis membranes were placed in dorsal forearm skin: two sites were perfused with ACh and other two with MCh. However, one of each of the ACh and MCh sites was also perfused with 10 microM neostigmine (an acetylcholinesterase inhibitor). Neostigmine at the ACh site induced a leftward shift (i.e., lower EC(50)) of the SR and CVC dose-response curves compared with the site treated with ACh alone, resulting in no difference in the EC(50) for SR and CVC between the ACh + neostigmine and the MCh site. These results suggest that elevations in SR and CVC occur earlier with MCh than with ACh treatment because of differences in cholinesterase susceptibility between these drugs.     

Maintaining nitric oxide-induced airway relaxation with superoxide dismutase

BACKGROUND: We have previously shown that the protective effect of inhaled nitric oxide (iNO) against methacholine-induced bronchoconstriction is negated in airways subjected to hyperosmotic stress. In this study, hypothesizing that the impaired efficiency of iNO was caused by release of reactive oxygen radicals, we examined the effect of the radical scavenging enzyme superoxide dismutase (SOD). METHODS: Hemodynamic and respiratory measurements were performed on anesthetized rabbits after (1) inhalation of methacholine (MCh), (2) iNO (80ppm), followed by MCh, (3) inhalation of hypertonic saline (HS), followed by iNO and MCh and (4) pre-treatment with inhalation of SOD, followed by HS, iNO and MCh. We analyzed plasma for a marker of oxidative stress, 8-iso-prostaglandin (PG)F(2alpha) and for a marker of activation of COX-mediated inflammatory cascades, PGF(2alpha) metabolite. RESULTS: Pre-treatment with SOD restored the bronchoprotective response to iNO in hyperosmotic airways. No direct effect was seen by SOD treatment on levels of 8-iso-PGF(2alpha), but this marker of oxidative stress correlated positively with increased bronchoconstriction. Hyperosmotic challenge elevated levels of PGF(2alpha) metabolite, and pre-treatment with SOD protected against this activation of the inflammatory cascade. CONCLUSION: SOD pre-treatment restores the relaxant effects of iNO in hyperosmotically challenged airways by attenuating oxidative stress and activation of COX-mediated inflammatory cascades.     

Role of dopamine and arterial chemoreceptors in thermal tachypnea in conscious cats

In mammals submitted to a warm environment, intracerebral injection of dopamine (DA) produces no change or an increase in body temperature accompanied by an increase in metabolic heat production, but its effect on heat loss mechanisms such as vasodilation and tachypnea is not clear. Because the principal mechanism of heat loss in the conscious cat is thermal tachypnea, we studied the influence of DA on thermal tachypnea in response to heat stress (ambient temperature = 33-36 degrees C) in five conscious cats. We first studied the steady-state response to a DA agonist, apomorphine, which crosses the blood-brain barrier. Intravenous injection of apomorphine greatly reduced thermal tachypnea by decreasing respiratory frequency (from 94.9 to 52.5 breaths/min) and increasing tidal volume (from 13.2 to 20.4 ml). The subsequent injection of the DA antagonist haloperidol, which also crosses the blood-brain barrier, restored the initial tachypnea. To further investigate the mechanism involved in thermal tachypnea, we studied the influence of peripheral chemoreceptors by transiently stimulating or inhibiting carotid body (CB) activity during tachypneic breathing. CB stimulation by intravenous injection of NaCN or domperidone reduced thermal tachypnea mainly by decreasing the respiratory frequency, whereas CB inhibition by DA tended to increase frequency and thus tachypnea. It is concluded that 1) in a warm environment, central DA receptors are also greatly involved in heat loss mechanisms, 2) arterial chemoreceptor input appears to counteract this tachypneic breathing, and 3) thermal and hypoxic tachypnea may be controlled by the same mechanism in which a DA-like system has a key role.     

Effects of salbutamol and Ro-20-1724 on airway and parenchymal mechanics in rats.

We investigated the effects of a selective beta(2)-agonist, salbutamol, and of phosphodiesterase type 4 inhibition with 4-(3-butoxy-4-methoxy benzyl)-2-imidazolidinone (Ro-20-1724) on the airway and parenchymal mechanics during steady-state constriction induced by MCh administered as an aerosol or intravenously (iv). The wave-tube technique was used to measure the lung input impedance (ZL) between 0.5 and 20 Hz in 31 anesthetized, paralyzed, open-chest adult Brown Norway rats. To separate the airway and parenchymal responses, a model containing an airway resistance (Raw) and inertance (Iaw), and a parenchymal damping (G) and elastance (H), was fitted to ZL spectra under control conditions, during steady-state constriction, and after either salbutamol or Ro-20-1724 delivery. In the Brown Norway rat, the response to iv MCh infusion was seen in Raw and G, whereas continuous aerosolized MCh challenge produced increases in G and H only. Both salbutamol, administered either as an aerosol or iv, and Ro-20-1724 significantly reversed the increases in Raw and G when MCh was administered iv. During the MCh aerosol challenge, Ro-20-1724 significantly reversed the increases in G and H, whereas salbutamol had no effect. These results suggest that, after MCh-induced changes in lung function, salbutamol increases the airway caliber. Ro-20-1724 is effective in reversing the airway narrowings, and it may also decrease the parenchymal constriction.     

Lysophosphatidic acid enhances airway response to acetylcholine in guinea pigs.

Inhalation of lysophosphatidic acid (LPA, 1-100 microg/ml) for 2 min enhanced the airway response induced by intravenous injection of ACh in guinea pigs. At 30 min after inhalation of LPA, the airway response to ACh was two fold higher than that before inhalation. This enhancement of airway response to ACh was partially inhibited by capsaicin desensitization or bilateral vagotomy. These results suggested that the enhancement of airway response to ACh induced by LPA may be due to the activation of capsaicin-sensitive fibers. It can be also contribute to bronchial asthma or other types of pulmonary disease such as cough variant asthma and atopic cough.     

Developmental nicotine exposure alters cholinergic control of respiratory frequency in neonatal rats

Prenatal nicotine exposure with continued exposure through breast milk over the first week of life (developmental nicotine exposure, DNE) alters the development of brainstem circuits that control breathing. Here, we test the hypothesis that DNE alters the respiratory motor response to endogenous and exogenous acetylcholine (ACh) in neonatal rats. We used the brainstem‐spinal cord preparation in the split‐bath configuration, and applied drugs to the brainstem compartment while measuring the burst frequency and amplitude of the fourth cervical ventral nerve roots (C4VR), which contain the axons of phrenic motoneurons. We applied ACh alone; the nicotinic acetylcholine receptor (nAChR) antagonist curare, either alone or in the presence of ACh; and the muscarinic acetylcholine receptor (mAChR) antagonist atropine, either alone or in the presence of ACh. The main findings include: (1) atropine reduced frequency similarly in controls and DNE animals, while curare caused modest slowing in controls but no consistent change in DNE animals; (2) DNE greatly attenuated the increase in C4VR frequency mediated by exogenous ACh; (3) stimulation of nAChRs with ACh in the presence of atropine increased frequency markedly in controls, but not DNE animals; (4) stimulation of mAChRs with ACh in the presence of curare caused a modest increase in frequency, with no treatment group differences. DNE blunts the response of the respiratory central pattern generator to exogenous ACh, consistent with reduced availability of functionally competent nAChRs; DNE did not alter the muscarinic control of respiratory motor output. © 2016 Wiley Periodicals, Inc. Develop Neurobiol 76: 1138–1149, 2016     

Effects of rapid saline infusion on lung mechanics and airway responsiveness in humans.

Lung mechanics and airway responsiveness to methacholine (MCh) were studied in seven volunteers before and after a 20-min intravenous infusion of saline. Data were compared with those of a time point-matched control study. The following parameters were measured: 1-s forced expiratory volume, forced vital capacity, flows at 40% of control forced vital capacity on maximal (Vm(40)) and partial (Vp(40)) forced expiratory maneuvers, lung volumes, lung elastic recoil, lung resistance (Rl), dynamic elastance (Edyn), and within-breath resistance of respiratory system (Rrs). Rl and Edyn were measured during tidal breathing before and for 2 min after a deep inhalation and also at different lung volumes above and below functional residual capacity. Rrs was measured at functional residual capacity and at total lung capacity. Before MCh, saline infusion caused significant decrements of forced expiratory volume in 1 s, Vm(40), and Vp(40), but insignificantly affected lung volumes, elastic recoil, Rl, Edyn, and Rrs at any lung volume. Furthermore, saline infusion was associated with an increased response to MCh, which was not associated with significant changes in the ratio of Vm(40) to Vp(40). In conclusion, mild airflow obstruction and enhanced airway responsiveness were observed after saline, but this was not apparently due to altered elastic properties of the lung or inability of the airways to dilate with deep inhalation. It is speculated that it was likely the result of airway wall edema encroaching on the bronchial lumen.     

Antigen challenge of sensitized rats increases airway responsiveness to methacholine

We measured airway responsiveness to methacholine (MCh) of highly inbred rats before and after six inhalational challenges with antigen. Ten Brown-Norway rats (130-216 g) that were actively sensitized to ovalbumin (OA) received six challenges with OA at 5-day intervals beginning 19 days after sensitization. An aerosol of OA (5% wt/vol) was inhaled for 1, 2, 5, and 10 min or until pulmonary resistance (RL) increased by at least 50%. Challenges with aerosolized MCh were performed immediately before and 14 days after sensitization, 2 days after the 3rd OA exposure, and 2, 7, 12, and 17 days after the 6th OA challenge. Four unsensitized rats underwent inhalational challenges with MCh over an equivalent time period. Responsiveness to MCh was calculated as the concentration of MCh required to increase RL to 200% of the control value (EC200RL). Seven out of 10 rats in the experimental group reacted to the first OA challenge with an immediate increase in RL of greater than 50% of control (range 70-550%). Three animals were unreactive to OA. Base-line EC200RL for all rats undergoing sensitization was 2.13 mg/ml (geometric mean), and it did not change significantly after sensitization (2.05 mg/ml). However, EC200RL of the rats that reacted to OA (n = 7) decreased significantly after 3 (1.11 mg/ml; P less than 0.005) and 6 OA exposures (0.96 mg/ml; P less than 0.005). The increase in responsiveness to inhaled MCh was present 17 days after the last OA exposure (EC200RL = 1.40 mg/ml; P less than 0.05). EC200RL of neither the unreactive sensitized rats (n = 3) nor the control rats (n = 4) changed after OA challenges.(ABSTRACT TRUNCATED AT 250 WORDS)     

Airway constriction measured from tantalum bronchograms in conscious mice in response to methacholine

A single-projection X-ray technique showed an increase in functional residual capacity (FRC) in conscious mice in response to aerosolized methacholine (MCh) with little change in airway resistance (Raw) measured using barometric plethysmography (Lai-Fook SJ, Houtz PK, Lai Y-L. J Appl Physiol 104: 521-533, 2008). The increase in FRC presumably prevented airway constriction by offsetting airway contractility. We sought a more direct measure of airway constriction. Anesthetized Balb/c mice were intubated with a 22-G catheter, and tantalum dust was insufflated into the lungs to produce a well-defined bronchogram. After overnight recovery, the conscious mouse was placed in a sealed box, and bronchograms were taken at maximum and minimum points of the box pressure cycle before (control) and after 1-min exposures to 25, 50, and 100 mg/ml MCh aerosol. After overnight recovery, each mouse was studied under both room and body temperature box air conditions to correct for gas compression effects on the control tidal volume (Vt) and to determine Vt and Raw with MCh. Airway diameter (D), FRC, and Vt were measured from the X-ray images. Compared with control, D decreased by 24%, frequency decreased by 35%, FRC increased by 120%, and Raw doubled, to reach limiting values with 100 mg/ml MCh. Vt was unchanged with MCh. The limiting D occurred near zero airway elastic recoil, where the maximal contractility was relatively small. The conscious mouse adapted to MCh by breathing at a higher lung volume and reduced frequency to reach a limit in constriction.     

The process of cardiorespiratory autoresuscitation in intact newborn rats

To examine the process of spontaneous autoresuscitation and the recovery of the hypoxic ventilatory response (HVR) after prolonged anoxia, we monitored respiratory frequency (f, by body plethysmography) and heart rate (HR, by ECG) in intact newborn rats (n = 12, day 2-4) before, during, and after 100% N2 exposure. The rat before anoxia showed signs of HVR: f changes at acute hypoxia (10% O2) and hyperoxia (100% O2). During anoxia, the spontaneous respiratory movement "gasping" appeared for 21 min (mean). At O2 restoration (with 100% O2), gasping stopped and no respiratory flow was detected for 1 min. One rat failed to autoresuscitate and had heart arrhythmia during the transient apnea, but 11 rats recovered respiration after the HR acceleration. Despite the successful autoresuscitation, the rats did not show HVR at 10 min into the recovery period and the recovery of HVR required more than 30 min. The results indicate that O2 inhalation is useful to trigger autoresuscitation even when the rat has already been in a state of profound hypoxic depression, but the rat becomes transiently insensitive to HVR after autoresuscitation. We estimate that reform of the respiratory control system in newborn rats is not yet firmly established to track HVR early in the recovery phase after prolonged anoxia.