American Journal of Physiology最新文献_第6页

Cardiovascular response to exercise. 心血管对运动的反应。

American Journal of Physiology Pub Date : 1999-12-01 DOI: 10.1152/advances.1999.277.6.S244

M H Laughlin

{"title":"Cardiovascular response to exercise.","authors":"M H Laughlin","doi":"10.1152/advances.1999.277.6.S244","DOIUrl":"https://doi.org/10.1152/advances.1999.277.6.S244","url":null,"abstract":"This article is intended for instructors who teach cardiovascular physiology. In our physiology course exercise physiology is used as a tool to review and integrate cardiovascular and respiratory physiology. It is assumed that the students already have mastered the fundamentals of cardiovascular and respiratory physiology. Because this paper is part of a cardiovascular refresher course, I have deleted much of the respiratory physiology. The objectives of this presentation are for the student to 1) understand the relationship between maximal oxygen consumption and endurance during sustained exercise and be able to define \"maximal oxygen consumption\"; 2) understand the determinants of of maximal oxygen consumption; 3) understand the effects of dynamic exercise on the cardiovascular system and mechanisms for these effects; 4) understand the relationships between exercise intensity and major cardiorespiratory parameters, including heart rate, cardiac output, blood flow distribution, left ventricular stroke volume, arterial pressures, total peripheral resistance, and arterial and venous blood oxygen content; 5) be able to compare and contrast the cardiovascular effects of dynamic and isometric exercise in man and the mechanisms responsible for the major differences; and 6) be able to apply knowledge of the cardiovascular effects of exercise to understanding the causes of cardiovascular symptoms in disease and in diagnosis of disease states. This material contains many areas that stimulate discussion with students and allow exploration of concepts that are challenging for the student. This give and take between teachers and student is difficult to summarize in an article of this sort. Therefore, subjects that in my experience often stimulate questions and discussion with the students are indicated in the text.","PeriodicalId":7590,"journal":{"name":"American Journal of Physiology","volume":"277 6 Pt 2","pages":"S244-59"},"PeriodicalIF":0.0,"publicationDate":"1999-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1152/advances.1999.277.6.S244","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21499810","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 173

Nitric oxide is the predominant mediator of cerebellar hyperemia during somatosensory activation in rats. 一氧化氮是大鼠体感觉激活期间小脑充血的主要介质。

American Journal of Physiology Pub Date : 1999-12-01 DOI: 10.1152/ajpregu.1999.277.6.R1760

G Yang, G Chen, T J Ebner, C Iadecola

{"title":"Nitric oxide is the predominant mediator of cerebellar hyperemia during somatosensory activation in rats.","authors":"G Yang, G Chen, T J Ebner, C Iadecola","doi":"10.1152/ajpregu.1999.277.6.R1760","DOIUrl":"https://doi.org/10.1152/ajpregu.1999.277.6.R1760","url":null,"abstract":"Crus II is an area of the cerebellar cortex that receives trigeminal afferents from the perioral region. We investigated the mechanisms of functional hyperemia in cerebellum using activation of crus II by somatosensory stimuli as a model. In particular, we sought to determine whether stimulation of the perioral region increases cerebellar blood flow (BFcrb) in crus II and, if so, whether the response depends on activation of 2-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)-kainate receptors and nitric oxide (NO) production. Crus II was exposed in anesthetized rats, and the site was superfused with Ringer. Field potentials were recorded, and BFcrb was measured by laser-Doppler flowmetry. Crus II was activated by electrical stimulation of the perioral region (upper lip). Perioral stimulation evoked the characteristic field potentials in crus II and increased BFcrb (34 +/- 6%; 10 Hz-25 V; n = 6) without changing arterial pressure. The BFcrb increases were associated with a local increase in glucose utilization (74 +/- 8%; P < 0.05; n = 5) and were attenuated by the AMPA-kainate receptor antagonist 2, 3-dihydroxy-6-nitro-7-sulfamoylbenzo-[f]quinoxaline (-71 +/- 3%; 100 microM; P < 0.01; n = 5). The neuronal NO synthase inhibitor 7-nitroindazole (7-NI, 50 mg/kg; n = 5) virtually abolished the increases in BFcrb (-90 +/- 2%; P < 0.01) but did not affect the amplitude of the field potentials. In contrast, 7-NI attenuated the increase in neocortical cerebral blood flow produced by perioral stimulation by 52 +/- 6% (P < 0.05; n = 5). We conclude that crus II activation by somatosensory stimuli produces localized increases in local neural activity and BFcrb that are mediated by activation of glutamate receptors and NO. Unlike in neocortex, in cerebellum the vasodilation depends almost exclusively on NO. The findings underscore the unique role of NO in the mechanisms of synaptic function and blood flow regulation in cerebellum.","PeriodicalId":7590,"journal":{"name":"American Journal of Physiology","volume":"277 6","pages":"R1760-70"},"PeriodicalIF":0.0,"publicationDate":"1999-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1152/ajpregu.1999.277.6.R1760","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21457783","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 93

Two circadian rhythms in the human electroencephalogram during wakefulness. 人清醒时脑电图的两种昼夜节律。

American Journal of Physiology Pub Date : 1999-12-01 DOI: 10.1152/ajpregu.1999.277.6.R1771

D Aeschbach, J R Matthews, T T Postolache, M A Jackson, H A Giesen, T A Wehr

{"title":"Two circadian rhythms in the human electroencephalogram during wakefulness.","authors":"D Aeschbach, J R Matthews, T T Postolache, M A Jackson, H A Giesen, T A Wehr","doi":"10.1152/ajpregu.1999.277.6.R1771","DOIUrl":"https://doi.org/10.1152/ajpregu.1999.277.6.R1771","url":null,"abstract":"The influence of the circadian pacemaker and of the duration of time awake on the electroencephalogram (EEG) was investigated in 19 humans during approximately 40 h of sustained wakefulness. Two circadian rhythms in spectral power density were educed. The first rhythm was centered in the theta band (4.25-8.0 Hz) and exhibited a minimum approximately 1 h after the onset of melatonin secretion. The second rhythm was centered in the high-frequency alpha band (10.25-13.0 Hz) and exhibited a minimum close to the body temperature minimum. The latter rhythm showed a close temporal association with the rhythms in subjective alertness, plasma melatonin, and body temperature. In addition, increasing time awake was associated with an increase of power density in the 0.25- to 9.0-Hz and 13.25- to 20. 0-Hz ranges. It is concluded that the waking EEG undergoes changes that can be attributed to circadian and homeostatic (i.e., sleep-wake dependent) processes. The distinct circadian variations of EEG activity in the theta band and in the high-frequency alpha band may represent electrophysiological correlates of different aspects of the circadian rhythm in arousal.","PeriodicalId":7590,"journal":{"name":"American Journal of Physiology","volume":"277 6","pages":"R1771-9"},"PeriodicalIF":0.0,"publicationDate":"1999-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1152/ajpregu.1999.277.6.R1771","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21457784","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 157

Integrin signaling, free radicals, and tyrosine kinase mediate flow constriction in isolated cerebral arteries. 整合素信号、自由基和酪氨酸激酶介导离体脑动脉的血流收缩。

American Journal of Physiology Pub Date : 1999-12-01 DOI: 10.1152/ajpheart.1999.277.6.H2264

J A Madden, N J Christman

{"title":"Integrin signaling, free radicals, and tyrosine kinase mediate flow constriction in isolated cerebral arteries.","authors":"J A Madden, N J Christman","doi":"10.1152/ajpheart.1999.277.6.H2264","DOIUrl":"https://doi.org/10.1152/ajpheart.1999.277.6.H2264","url":null,"abstract":"Isolated, cannulated, and pressurized (100 mmHg) middle cerebral arteries from adult cats were perfused intraluminally at rates from 0 to 4 ml/min with heated and gassed physiological saline solution. An electronic system held pressure constant by changing outflow resistance. The arteries constricted 18.1 +/- 0.95% in response to flow and depolarized from -54 +/- 0.51 to -40 +/- 1.26 mV (P < 0.05). Constriction was independent of a functional endothelium but was eliminated by superoxide dismutase or tyrosine kinase inhibitors. Luminal perfusion with a synthetic extracellular matrix Arg-Gly-ASP (RGD) peptide that binds with integrin significantly reduced constriction to flow. Neither reducing intraluminal pressure nor increasing tone or shear stresses altered constriction to flow. Flow-induced constriction did not impede the ability of the arteries to dilate to hypercapnia, and inhibiting flow-induced constriction did not alter contractile responses to other agonists. These data suggest that, in vitro, middle cerebral arteries constrict to flow through a mechanism involving free radicals and tyrosine kinase and that flow shear stresses resulting in constriction are transduced by integrin signaling.","PeriodicalId":7590,"journal":{"name":"American Journal of Physiology","volume":"277 6","pages":"H2264-71"},"PeriodicalIF":0.0,"publicationDate":"1999-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1152/ajpheart.1999.277.6.H2264","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21458513","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 55

NADPH and heme redox modulate pulmonary artery relaxation and guanylate cyclase activation by NO. NADPH和血红素氧化还原通过NO调节肺动脉舒张和鸟苷酸环化酶活化。

American Journal of Physiology Pub Date : 1999-12-01 DOI: 10.1152/ajplung.1999.277.6.L1124

S A Gupte, T Rupawalla, D Phillibert, M S Wolin

{"title":"NADPH and heme redox modulate pulmonary artery relaxation and guanylate cyclase activation by NO.","authors":"S A Gupte, T Rupawalla, D Phillibert, M S Wolin","doi":"10.1152/ajplung.1999.277.6.L1124","DOIUrl":"https://doi.org/10.1152/ajplung.1999.277.6.L1124","url":null,"abstract":"The hemoprotein oxidant ferricyanide (FeCN) converts the iron of the heme on soluble guanylate cyclase (sGC) from Fe(2+) to Fe(3+), which prevents nitric oxide (NO) from binding the heme and stimulating sGC activity. This study uses FeCN to examine whether modulation of the redox status of the heme on sGC influences the relaxation of endothelium-removed bovine pulmonary arteries (BPA) to NO. Pretreatment of the homogenate of BPA with 50 microM FeCN resulted in a loss of stimulation of sGC activity by the NO donor 10 microM S-nitroso-N-acetylpenicillamine (SNAP). In the FeCN-treated homogenate reconcentrated to the enzyme levels in BPA, 100 microM NADPH restored NO stimulation of sGC, and this effect of NADPH was prevented by an inhibitor of flavoprotein electron transport, 1 microM diphenyliodonium (DPI). In BPA the relaxation to SNAP was not altered by FeCN, inhibitors of NADPH generation by the pentose phosphate pathway [250 microM 6-aminonicotinamide (6-AN) and 100 microM epiandrosterone (Epi)], or 1 microM DPI. However, the combination of FeCN with 6-AN, Epi, or DPI inhibited (P < 0.05) relaxation to SNAP without significantly altering the relaxation of BPA to forskolin. The inhibitory effects of 1 microM 1H-[1,2, 4]oxadiazolo[4,3-a]quinoxalin-1-one (a probe that appears to convert NO-heme of sGC to its Fe(3+)-heme form) on relaxation to SNAP were also enhanced by DPI. These observations suggest that a flavoprotein containing NADPH oxidoreductase may influence cGMP-mediated relaxation of BPA to NO by maintaining the heme of sGC in its Fe(2+) oxidation state.","PeriodicalId":7590,"journal":{"name":"American Journal of Physiology","volume":"277 6","pages":"L1124-32"},"PeriodicalIF":0.0,"publicationDate":"1999-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1152/ajplung.1999.277.6.L1124","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21458785","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 39

Cisplatin induces renal expression of P-glycoprotein and canalicular multispecific organic anion transporter. 顺铂诱导肾p -糖蛋白和小管多特异性有机阴离子转运蛋白的表达。

American Journal of Physiology Pub Date : 1999-12-01 DOI: 10.1152/ajprenal.1999.277.6.F832

M Demeule, M Brossard, R Béliveau

{"title":"Cisplatin induces renal expression of P-glycoprotein and canalicular multispecific organic anion transporter.","authors":"M Demeule, M Brossard, R Béliveau","doi":"10.1152/ajprenal.1999.277.6.F832","DOIUrl":"https://doi.org/10.1152/ajprenal.1999.277.6.F832","url":null,"abstract":"The expression of two members of the ATP-binding cassette family of transport proteins, P-glycoprotein (P-gp) and the canalicular multispecific organic anion transporter (cMOAT or Mrp2), was evaluated in renal brush-border membranes (BBM) and various rat tissues after cisplatin treatment. One administration of cisplatin (5 mg/kg) increased P-gp expression by >200-300% in renal BBM and in crude membranes from liver and intestine. The increase in P-gp expression in the kidney was also detected in photolabeling experiments, suggesting the induction of functional P-gp. cMOAT expression was increased by >10-fold in renal BBM after cisplatin administration, although it had no effect on liver cMOAT expression. The increase in the levels of both proteins was maximal at 2 days after cisplatin treatment and lasted for at least 8 days. These results indicate that a single administration of cisplatin induces overexpression of P-gp and cMOAT in specific tissues. This may be of significant relevance to the design of clinical trials using cisplatin as a single chemotherapeutic agent or in combination with other drugs.","PeriodicalId":7590,"journal":{"name":"American Journal of Physiology","volume":"277 6","pages":"F832-40"},"PeriodicalIF":0.0,"publicationDate":"1999-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1152/ajprenal.1999.277.6.F832","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21457788","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 64

Cardiac arrhythmias. 心律失常。

American Journal of Physiology Pub Date : 1999-12-01 DOI: 10.1152/advances.1999.277.6.S214

A M Katz

引用次数: 0

Teaching critical thinking skills in physiology. 教授生理学中的批判性思维技能。

American Journal of Physiology Pub Date : 1999-12-01 DOI: 10.1152/advances.1999.277.6.S268

A P McNeal, S Mierson

引用次数: 3

Teaching about disinhibition. 关于解除抑制的教学。

American Journal of Physiology Pub Date : 1999-12-01 DOI: 10.1152/advances.1999.277.6.S281

R Tannerthies

引用次数: 10

Role of a negative arterial-portal venous glucose gradient in the postexercise state. 负的动脉-门静脉葡萄糖梯度在运动后状态中的作用。

American Journal of Physiology Pub Date : 1999-12-01 DOI: 10.1152/ajpendo.1999.277.6.E1038

P Galassetti, Y Koyama, R H Coker, D B Lacy, A D Cherrington, D H Wasserman

{"title":"Role of a negative arterial-portal venous glucose gradient in the postexercise state.","authors":"P Galassetti, Y Koyama, R H Coker, D B Lacy, A D Cherrington, D H Wasserman","doi":"10.1152/ajpendo.1999.277.6.E1038","DOIUrl":"https://doi.org/10.1152/ajpendo.1999.277.6.E1038","url":null,"abstract":"Unlabelled: Prior exercise stimulates muscle and liver glucose uptake. A negative arterial-portal venous glucose gradient (a-pv grad) stimulates resting net hepatic glucose uptake (NHGU) but reduces muscle glucose uptake. This study investigates the effects of a negative a-pv grad during glucose administration after exercise in dogs.Experimental protocol: exercise (-180 to -30 min), transition (-30 to -20 min), basal period (-20 to 0 min), and experimental period (0 to 100 min). In the experimental period, 130 mg/dl arterial hyperglycemia was induced via vena cava (Pe, n = 6) or portal vein (Po, n = 6) glucose infusions. Insulin and glucagon were replaced at fourfold basal and basal rates. During the experimental period, the a-pv grad (mg/dl) was 3 +/- 1 in Pe and -10 +/- 2 in Po. Arterial insulin and glucagon were similar in the two groups. In Pe, net hepatic glucose balance (mg x kg(-1) x min(-1), negative = uptake) was 4.2 +/- 0.3 (basal period) and -1.2 +/- 0.3 (glucose infusion); in Po it was 4.1 +/- 0.5 and -3.2 +/- 0.4, respectively (P < 0.005 vs. Pe). Total glucose infusion (mg x kg(-1) x min(-1)) was 11 +/- 1 in Po and 8 +/- 1 in Pe (P < 0.05). Net hindlimb and whole body nonhepatic glucose uptakes were similar.Conclusions: the portal signal independently stimulates NHGU after exercise. Conversely, prior exercise eliminates the inhibitory effect of the portal signal on glucose uptake by nonhepatic tissues. The portal signal therefore increases whole body glucose disposal after exercise by an amount equal to the increase in NHGU.","PeriodicalId":7590,"journal":{"name":"American Journal of Physiology","volume":"277 6","pages":"E1038-45"},"PeriodicalIF":0.0,"publicationDate":"1999-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1152/ajpendo.1999.277.6.E1038","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21457867","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 12