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1.
The biotic and abiotic factors that modulate the life historyof C. finmarchicus are not well described, and Xabier Irigoien(Irigoien, 2004) suggests some interesting hypotheses aboutwhat role lipids might play. He does, however, make some questionableassumptions about the role of lipids during overwintering. First,he states that lipid storage determines the 相似文献
2.
Differential distribution of ERalpha and ERbeta mRNA in intrauterine tissues of the pregnant rhesus monkey 总被引:3,自引:0,他引:3
Wu WX Ma XH Smith GC Nathanielsz PW 《American journal of physiology. Cell physiology》2000,278(1):C190-C198
Twoestrogen receptor (ER) isoforms, ER and ER, have been described.However, no information is available in any species regarding thecomparison of ER and ER levels in pregnant intrauterine tissues.We investigated 1) distribution of ER and ER mRNA in myometrium, amnion, choriodecidua, and placenta; 2) theirabundance in intrauterine tissues at term not in labor (NIL) and inspontaneous term labor (STL); and 3) immunolocalization ofER and ER in pregnant rhesus monkey myometrium. Myometrium,amnion, choriodecidua, and placenta were obtained at cesarean sectionfrom monkeys in STL at 156-166 days gestational age(GA) (n = 4) and from control monkeys NIL at140-152 days GA (n = 4). RT-PCR was conducted to determineER and ER and glyceraldehyde-3-phosphate dehydrogenase mRNAabundance in four intrauterine tissues of the pregnant rhesus monkey.The cloned ER PCR fragment was subjected to sequence analysis. ERand ER were localized in the myometrium by immunohistochemistry. Wedemonstrated that 1) rhesus monkey ER shares >97%identity with human ER in the region sequenced; 2) both ERswere expressed in myometrium, amnion, and choriodecidua but not inplacenta in the current study; 3) ER and ER weredifferentially distributed in myometrium and amnion; 4) ERand ER were immunolocalized in myometrial smooth cells and smoothmuscle and endothelial cells of the myometrial blood vessels. Thebiological significance of these quantitative differences in ERsubtypes merits further study. 相似文献
3.
Li, M. H., J. Hildebrandt, and M. P. Hlastala.Quantitative analysis of transpleural flux in the isolated lung.J. Appl. Physiol. 82(2): 545-551, 1997.In this study, the loss of inert gas through the pleura of anisolated ventilated and perfused rabbit lung was assessed theoreticallyand experimentally. A mathematical model was used to represent an idealhomogeneous lung placed within a box with gas flow(box) surrounding the lung. Thealveoli are assumed to be ventilated with room air(A) andperfused at constant flow () containinginert gases (x) with various perfusate-air partition coefficients(p,x).The ratio of transpleural flux of gas(plx)to its total delivery to the lung via pulmonary artery( ),representing fractional losses across the pleura, can be shown todepend on four dimensionless ratios:1)p,x,2) the ratio of alveolar ventilation to perfusion(A/), 3) the ratioof the pleural diffusing capacity(Dplx) to the conductance ofthe alveolar ventilation (Dplx /Ag,where g is the capacitancecoefficient of gas), and 4) theratio of extrapleural (box) ventilation to alveolar ventilation(box/A).Experiments were performed in isolated perfused and ventilated rabbitlungs. The perfusate was a buffer solution containing six dissolvedinert gases covering the entire 105-fold range ofp,x usedin the multiple inert gas elimination technique. Steady-state inert gasconcentrations were measured in the pulmonary arterial perfusate,pulmonary venous effluent, exhaled gas, and box effluent gas. Theexperimental data could be described satisfactorily by thesingle-compartment model. It is concluded that a simple theoreticalmodel is a useful tool for predicting transpleural flux from isolatedlung preparations, with known ventilation and perfusion, for inertgases within a wide range of . 相似文献
4.
Role of gelsolin in the actin filament regulation of cardiac L-type calcium channels 总被引:7,自引:0,他引:7
Lader Alan S.; Kwiatkowski David J.; Cantiello Horacio F. 《American journal of physiology. Cell physiology》1999,277(6):C1277
The actin cytoskeleton is an important contributor to themodulation of the cell function. However, little is known about theregulatory role of this supermolecular structure in the membrane eventsthat take place in the heart. In this report, the regulation of cardiacmyocyte function by actin filament organization was investigated inneonatal mouse cardiac myocytes (NMCM) from both wild-type mice andmice genetically devoid of the actin filament severing protein gelsolin(Gsn/). Cardiac L-type calcium channel currents(ICa) wereassessed using the whole cell voltage-clamp technique. Addition of theactin filament stabilizer phalloidin to wild-type NMCM increasedICa by 227% overcontrol conditions. The basalICa ofGsn/ NMCM was 300% higher than wild-type controls. Thisincrease was completely reversed by intracellular perfusion of theGsn/ NMCM with exogenous gelsolin. Further, cytoskeletal disruption of either Gsn/ or phalloidin-dialyzedwild-type NMCM with cytochalasin D (CD) decreased the enhancedICa by 84% and 87%, respectively. The data indicate that actin filament stabilization by either a lack of gelsolin or intracellular dialysis with phalloidin increase ICa,whereas actin filament disruption with CD or dialysis ofGsn/ NMCM with gelsolin decreaseICa. We concludethat cardiac L-type calcium channel regulation is tightly controlled byactin filament organization. Actin filament rearrangement mediated by gelsolin may contribute to calcium channel inactivation. 相似文献
5.
Buhagiar Kerrie A.; Hansen Peter S.; Bewick Nerida L.; Rasmussen Helge H. 《American journal of physiology. Cell physiology》2001,281(3):C1059
A reduction in angiotensinII (ANG II) in vivo by treatment of rabbits with theangiotensin-converting enzyme inhibitor, captopril, increasesNa+-K+ pump current (Ip)of cardiac myocytes. This increase is abolished by exposure of myocytesto ANG II in vitro. Because ANG II induces translocation of the-isoform of protein kinase C (PKC), we examined whether thisisozyme regulates the pump. We treated rabbits with captopril, isolatedmyocytes, and measured Ip of myocytes voltageclamped with wide-tipped patch pipettes. Ip ofmyocytes from captopril-treated rabbits was larger thanIp of myocytes from controls. ANG II superfusionof myocytes from captopril-treated rabbits decreasedIp to levels similar to controls. Inclusion ofPKC-specific blocking peptide in pipette solutions used to perfusethe intracellular compartment abolished the effect of ANG II. Inclusionof RACK, a PKC-specific activating peptide, in pipettesolutions had an effect on Ip that was similarto that of ANG II. There was no additive effect of ANG II andRACK. We conclude that PKC regulates the sarcolemmalNa+-K+ pump. 相似文献
6.
Xiao GQ Qu Y Sun ZQ Mochly-Rosen D Boutjdir M 《American journal of physiology. Cell physiology》2001,281(5):C1477-C1486
Investigation of the role ofindividual protein kinase C (PKC) isozymes in the regulation ofNa+ channels has been largely limited by the lack ofisozyme-selective modulators. Here we used a novel peptide-specificactivator (V1-7) of PKC and other peptide isozyme-specificinhibitors in addition to the general PKC activator phorbol12-myristate 13-acetate (PMA) to dissect the role of individual PKCs inthe regulation of the human cardiac Na+ channel hH1,heterologously expressed in Xenopus oocytes. Peptides wereinjected individually or in combination into the oocyte. Whole cellNa+ current (INa) was recorded usingtwo-electrode voltage clamp. V1-7 (100 nM) and PMA (100 nM)inhibited INa by 31 ± 5% and 44 ± 8% (at 20 mV), respectively. These effects were not seen with thescrambled peptide for V1-7 (100 nM) or the PMA analog4-phorbol 12,13-didecanoate (100 nM). However, V1-7-and PMA-induced INa inhibition was abolished byV1-2, a peptide-specific antagonist of PKC. Furthermore,PMA-induced INa inhibition was not altered by100 nM peptide-specific inhibitors for -, -, -, or PKC. PMAand V1-7 induced translocation of PKC from soluble toparticulate fraction in Xenopus oocytes. This translocationwas antagonized by V1-2. In native rat ventricular myocytes,PMA and V1-7 also inhibited INa; thisinhibition was antagonized by V1-2. In conclusion, the resultsprovide evidence for selective regulation of cardiac Na+channels by PKC isozyme. 相似文献
7.
Potent inhibition of the aortic smooth muscle maxi-K channel by clinical doses of ethanol 总被引:2,自引:0,他引:2
Walters FS Covarrubias M Ellingson JS 《American journal of physiology. Cell physiology》2000,279(4):C1107-C1115
We investigated the effects ofclinically relevant ethanol concentrations (5-20 mM) on thesingle-channel kinetics of bovine aortic smooth muscle maxi-K channelsreconstituted in lipid bilayers (1:1palmitoyl-oleoyl-phosphatidylethanolamine:palmitoyl-oleoyl-phosphatidylcholine). Ethanol at 10 and 20 mMdecreased the channel open probability (Po) by75 ± 20.3% mainly by increasing the mean closed time (+82 to+960%, n = 7). In some instances, ethanol alsodecreased the mean open time (40.8 ± 22.5%). ThePo-voltage relation in the presence of 20 mMethanol exhibited a rightward shift in the midpoint of voltageactivation (V1/2 17 mV), a slightlysteeper relationship (change in slope factor, k, 2.5 mV), and a decreased maximum Po (from~0.82 to ~0.47). Interestingly, channels inhibited by ethanol atlow Ca2+ concentrations (2.5 µM) were veryresistant to ethanol in the presence of increased Ca2+ ( 20 µM). Alcohol consumption in clinically relevant amounts may alterthe contribution of maxi-K channels to the regulation of arterial tone. 相似文献
8.
The following is the abstract of the article discussed in thesubsequent letter:Venegas, José G., R. Scott Harris, and BrettA. Simon. A comprehensive equation for the pulmonarypressure-volume curve. J. Appl. Physiol. 84(1): 389-395, 1998.Quantification of pulmonary pressure-volume (P-V) curves isoften limited to calculation of specific compliance at a given pressureor the recoil pressure (P) at a given volume (V). These parameters can be substantially different depending on the arbitrary pressure orvolume used in the comparison and may lead to erroneous conclusions. Weevaluated a sigmoidal equation of the form, V = a + b[1 + e(Pc)/d]1, for its ability to characterize lung and respiratory system P-V curves obtained under a variety of conditions including normal andhypocapnic pneumoconstricted dog lungs (n = 9), oleicacid-induced acute respiratory distress syndrome (n = 2), andmechanically ventilated patients with acute respiratory distresssyndrome (n = 10). In this equation, a corresponds tothe V of a lower asymptote, b to the V difference between upperand lower asymptotes, c to the P at the true inflection pointof the curve, and d to a width parameter proportional to the Prange within which most of the V change occurs. The equation fittedequally well inflation and deflation limbs of P-V curves with a meangoodness-of-fit coefficient (R2) of 0.997 ± 0.02 (SD). When the data from all analyzed P-V curves were normalized by thebest-fit parameters and plotted as (V a)/b vs.(P c)/d, they collapsed into a single and tightrelationship (R2 = 0.997). These resultsdemonstrate that this sigmoidal equation can fit with excellentprecision inflation and deflation P-V curves of normal lungs and oflungs with alveolar derecruitment and/or a region of gastrapping while yielding robust and physiologically useful parameters. 相似文献
9.
Windchill and the risk of tissue freezing 总被引:1,自引:0,他引:1
Danielsson, Ulf. Windchill and the risk of tissuefreezing. J. Appl. Physiol. 81(6): 2666-2673, 1996.Low air temperatures and high wind speeds are associated with anincreased risk of freezing of the exposed skin. P. A. Siple and C. F. Passel (Proc. Am. Phil. Soc. 89: 177-199, 1945) derivedtheir windchill index from cooling experiments on a water-filledcylinder to quantify the risk of frostbite. Their results arereexamined here. It is found that their windchill index does notcorrectly describe the convective heat transfer coefficient(hc) for such a cylinder; theeffect of the airspeed (v) isunderestimated. New risk curves have been developed, based on theconvection equations valid for cylinders in a cross flow,hc v0.62, and tissuefreezing data from the literature. An analysis of the data reveals alinear relationship between the frequency of finger frostbite and thesurface temperature. This relation closely follows a normaldistribution of finger-freezing temperatures, with an SD of 1°C. Asthe skin surface temperature falls from 4.8 to 7.8°C,the risk of frostbite increases from 5 to 95%. These data indicatethat the risk of finger frostbite is minor above an air temperature of10°C, irrespective of v,but below 25°C there is a pronounced risk, even at lowv. 相似文献
10.
Tenotomy decreases reporter protein synthesis via the 3'-untranslated region of the beta-myosin heavy chain mRNA 总被引:1,自引:0,他引:1
We tested thehypothesis that the -myosin heavy chain (-MHC) 3'-untranslatedregion (UTR) mediates decreased protein expression after tenotomy ofthe rat soleus. We also tested the hypothesis that decreased proteinexpression is the result of RNA-protein interactions within the 3'-UTR.-MHC was chosen for study because of its critical role in thefunction of postural muscles such as soleus. Adult rat soleus muscleswere directly injected with luciferase (LUC) reporter constructscontaining either the -MHC or SV40 3'-UTR. After 48 h oftenotomy, there was no significant effect on LUC expression in the SV403'-UTR group. In the -MHC 3'-UTR group, LUC expression was 37.3 ± 4% (n = 5, P = 0.03) of that in shamcontrols. Gel mobility shift assays showed that a protein factorspecifically interacts with the -MHC 3'-UTR and that tenotomysignificantly increases the level of this interaction (25 ± 7%,n = 5, P = 0.02). Thus the -MHC3'-UTR is directly involved in decreased protein expression that isprobably due to increased RNA-protein binding within the UTR. 相似文献
11.
Sweeney WE Kusner L Carlin CR Chang S Futey L Cotton CU Dell KM Avner ED 《American journal of physiology. Cell physiology》2001,281(5):C1695-C1705
To study the pathophysiology ofautosomal recessive polycystic kidney disease (ARPKD), we soughtto develop conditionally immortalized control and cystic murinecollecting tubule (CT) cell lines. CT cells were isolated fromintercross breedings between BPK mice(bpk+/), a murine model of ARPKD,and the Immorto mice(H-2Kb-ts-A58+/+).Second-generation outbred offspring (BPK × Immorto) homozygous for the BPK mutation (bpk/;Im+/±; cysticBPK/H-2Kb-ts-A58), were phenotypicallyindistinguishable from inbred cystic BPK animals(bpk/). CysticBPK/H-2Kb-ts-A58 mice developed biliary ductalectasia and massively enlarged kidneys, leading to renal failure anddeath by postnatal day 24. Principal cells (PC) wereisolated from outbred cystic and noncystic BPK/H-2Kb-ts-A58 littermates at specificdevelopmental stages. Epithelial monolayers were under nonpermissiveconditions for markers of epithelial cell polarity and PC function.Cystic and noncystic cells displayed several properties characteristicof PCs in vivo, including amiloride-sensitive sodium transport andaquaporin 2 expression. Cystic cells exhibited apical epidermal growthfactor receptor (EGFR) mislocalization but normal expression of ZO-1 and E-cadherin. Hence, these cell lines retain the requisitecharacteristics of PCs, and cysticBPK/H-2Kb-ts-A58 PCs retained the abnormal EGFRmembrane expression characteristic of ARPKD. These cell lines representimportant new reagents for studying the pathogenesis of ARPKD. 相似文献
12.
With Wild Orchids of the Prairies and Great Plains Region ofNorth America, published by University Press of Florida, PaulMartin Brown offers the sixth in his series of regional orchidbooks. The others are: Wild Orchids of the Northeastern UnitedStates; Wild Orchids of Florida; Wild Orchids of SoutheasternUnited States North of Peninsular Florida; Wild Orchids of thePacific Northwest and Canadian Rockies; and Wild Orchids ofthe Canadian Maritimes and Northern Great Lakes Region. Allbut the first were published by the University Press of Florida.It is straightforward to deduce that Brown eventually intendsto produce regional orchid floras covering the United Statesand Canada. If so, a significant increase 相似文献
13.
Yorek Mark A.; Dunlap Joyce A.; Thomas Michael J.; Cammarata Patrick R.; Zhou Cheng; Lowe William L. Jr. 《American journal of physiology. Cell physiology》1998,274(1):C58
Previously we have shown that hyperosmolarity increasesNa+-myo-inositolcotransporter (SMIT) activity and mRNA levels in cultured endothelialcells. Because hyperosmolarity and cytokines, such as tumor necrosisfactor- (TNF-), activate similar signal transduction pathways, weexamined the effect of TNF- on SMIT mRNA levels andmyo-inositol accumulation. In contrastto the effect of hyperosmolarity, TNF- caused a time- andconcentration-dependent decrease in SMIT mRNA levels andmyo-inositol accumulation. The effectof TNF- on myo-inositolaccumulation was found in large-vessel endothelial cells (derived fromthe aorta and pulmonary artery) and cerebral microvessel endothelialcells. In bovine aorta and bovine pulmonary artery endothelial cells,TNF- activated nuclear factor (NF)-B. TNF- also increasedceramide levels, and C2-ceramidemimicked the effect of TNF- on SMIT mRNA levels andmyo-inositol accumulation in bovineaorta endothelial cells. Pyrrolidinedithiocarbamate, genistein, and7-amino-1-chloro-3-tosylamido-2-hepatanone, compounds that can inhibitNF-B activation, partially prevented the TNF--induced decrease inmyo-inositol accumulation. The effectof TNF- on myo-inositolaccumulation was also partially prevented by the protein kinase Cinhibitor calphostin C but not by staurosporine. These studiesdemonstrate that TNF- causes a decrease in SMIT mRNA levels andmyo-inositol accumulation in culturedendothelial cells, which may be related to the activation of NF-B. 相似文献
14.
Chemokine expression in CF epithelia: implications for the role of CFTR in RANTES expression 总被引:5,自引:0,他引:5
Schwiebert Lisa M.; Estell Kim; Propst Stacie M. 《American journal of physiology. Cell physiology》1999,276(3):C700
To delineate themechanisms that facilitate leukocyte migration into the cystic fibrosis(CF) lung, expression of chemokines, including interleukin-8 (IL-8),monocyte chemoattractant protein-1 (MCP-1), andRANTES, was compared between CF and non-CF airway epithelia. Thefindings presented herein demonstrate that, under either basalconditions or tumor necrosis factor- (TNF-)- and/or interferon- (IFN-)-stimulated conditions, a consistent pattern ofdifferences in the secretion of IL-8 and MCP-1 between CF and non-CFepithelial cells was not observed. In contrast, CF epithelial cellsexpressed no detectable RANTES protein or mRNA under basal conditionsor when stimulated with TNF- and/or IFN-(P 0.05), unlike their non-CFcounterparts. Correction of the CF transmembrane conductance regulator(CFTR) defect in CF airway epithelial cells restored the induction ofRANTES protein and mRNA by TNF- in combination with IFN-(P 0.05) but had little effect onIL-8 or MCP-1 production compared with mock controls. Transfection studies utilizing RANTES promoter constructs suggested that CFTR activates the RANTES promoter via a nuclear factor-B-mediated pathway. Together, these results suggest that1) RANTES expression is altered inCF epithelia and 2) epithelialexpression of RANTES, but not IL-8 or MCP-1, is dependent on CFTR. 相似文献
15.
Cholecystokinin induction of mob-1 chemokine expression in pancreatic acinar cells requires NF-kappa B activation 总被引:1,自引:0,他引:1
Inflammatory mediators are involved in the early phase of acutepancreatitis, but the cellular mechanisms responsible for theirgeneration within pancreatic cells are unknown. We examined the role ofnuclear factor-B (NF-B) in cholecystokinin octapeptide (CCK-8)-induced mob-1 chemokineexpression in pancreatic acinar cells in vitro. Supraphysiological, butnot physiological, concentrations of CCK-8 increased inhibitory B(IB-) degradation, NF-B activation, andmob-1 gene expression in isolatedpancreatic acinar cells. CCK-8-induced IB- degradation wasmaximal within 1 h. Expression ofmob-1 was maximal within 2 h. Neitherbombesin nor carbachol significantly increasedmob-1 mRNA or induced IB-degradation. Thus the concentration, time, and secretagogue dependenceof mob-1 gene expression and IB-degradation were similar. Inhibition of NF-B with pharmacologicalagents or by adenovirus-mediated expression of the inhibitory proteinIB- also inhibited mob-1 geneexpression. These data indicate that the NF-B signaling pathway isrequired for CCK-8-mediated induction ofmob-1 chemokine expression inpancreatic acinar cells. This supports the hypothesis that NF-Bsignaling is of central importance in the initiation of acute pancreatitis. 相似文献
16.
Bumetanide blocks CFTR GCl in the native sweat duct 总被引:1,自引:0,他引:1
Bumetanide is wellknown for its ability to inhibit the nonconductiveNa+-K+-2Clcotransporter. We were surprised in preliminary studies to find thatbumetanide in the contraluminal bath also inhibited NaCl absorption inthe human sweat duct, which is apparently poor in cotransporteractivity. Inhibition was accompanied by a marked decrease in thetransepithelial electrical conductance. Because the cystic fibrosistransmembrane conductance regulator (CFTR) Cl channel is richlyexpressed in the sweat duct, we asked whether bumetanide acts byblocking this anion channel. We found that bumetanide1) significantly increased wholecell input impedance, 2)hyperpolarized transepithelial and basolateral membrane potentials, 3) depolarized apical membranepotential, 4) increased the ratio ofapical-to-basolateral membrane resistance, and5) decreased transepithelialCl conductance(GCl).These results indicate that bumetanide inhibits CFTRGClin both cell membranes of this epithelium. We excluded bumetanideinterference with the protein kinase A phosphorylation activationprocess by "irreversibly" phosphorylating CFTR [by usingadenosine5'-O-(3-thiotriphosphate) in thepresence of a phosphatase inhibition cocktail] before bumetanideapplication. We then activated CFTRGClby adding 5 mM ATP. Bumetanide in the cytoplasmic bath(103 M) inhibited ~71%of this ATP-activated CFTRGCl,indicating possible direct inhibition of CFTRGCl.We conclude that bumetanide inhibits CFTRGClin apical and basolateral membranes independent of phosphorylation. Theresults also suggest that>105 M bumetanide cannotbe used to specifically block theNa+-K+-2Cl cotransporter. 相似文献
17.
The effect of the substituted pyridazinone herbicides, Sandoz9785 and Sandoz 6706, on lipid metabolism was studied in greeningbarley leaves. The herbicides had no effect on chlorophyll formationbut caused an altered chloroplast morphology during greening.In leaves supplied with {14C} acetate, Sandoz 9785 decreasedincorporation of radioactivity into linolenate while Sandoz6706 decreased incorporation into both linolenate and trans-3-hexadecenoate.Decreased linolenate labelling was accompanied by an accumulationof {14C}linolenate in diacylgalactosylglycerol. {14C}Palmitateaccumulated in phosphatidylglycerol when synthesis of trans-3-hexadecenoatewas inhibited. The results are discussed in relation to thefunction of acyl lipids in fatty acid desaturation and the roleof lipids in chloroplast morphology. Key words: Chloroplast structure, Lipid synthesis, Substituted pyridazinones, Fatty acid desaturation 相似文献
18.
Interaction of cross-sectional area, driving pressure, and airflow of passive velopharynx 总被引:2,自引:0,他引:2
Isono Shiroh; Feroah Thom R.; Hajduk Eric A.; Brant Rollin; Whitelaw William A.; Remmers John E. 《Journal of applied physiology》1997,83(3):851-859
Isono, Shiroh, Thom R. Feroah, Eric A. Hajduk, Rollin Brant,William A. Whitelaw, and John E. Remmers. Interaction ofcross-sectional area, driving pressure, and airflow of passive velopharynx. J. Appl. Physiol. 83(3):851-859, 1997.Previous studies have shown that, when thepharyngeal muscles are relaxed, the velopharynx is a highly compliantsegment of the pharynx. Thus, under these circumstances,cross-sectional area of the velopharynx (AVP), drivingpressure across the velopharynx (P), and inspiratory airflow(I) willbe mutually interdependent variables. The purpose of the presentinvestigation was to describe the interrelation among these threevariables during inspiration. We studied 15 sleeping patients withobstructive sleep apnea/hypopnea when the pharyngeal muscles wererendered hypotonic by applying continuous positive airway pressure tothe nasal airway.AVP, determined by endoscopic imaging, was significantly greater at onset ofI limitationthan at minimum oropharyngeal pressure(P < 0.01). Snoring was neverobserved duringIlimitation. In a subgroup of six patients, values for P,I, andAVP were obtainedat 0.1-s intervals at various levels of mask pressure. For these sixpatients, the mathematical expressionI = 0.657(AVP/Amax) · P0.332,where Amax ismaximal AVP,described the relationship among the three variables(R2 = 0.962) forflow-limited and non-flow-limited inspirations. The impedance of thepassive velopharynx, defined asP0.33/,was inversely related toAVP and increaseddramatically when AVP was <0.3cm2. In summary, we observed aprogressive decrease inAVP during flow-limited inspiration in patients with obstructive sleep apnea. Thisconstriction of the velopharynx contributes to an increase invelopharyngeal impedance that, in turn, counterbalances the increase inP during flow limitation. 相似文献
19.
Ameredes Bill T.; Brechue William F.; Stainsby Wendell N. 《Journal of applied physiology》1998,84(6):1909-1916
Repetitiveisometric tetanic contractions (1/s) of the caninegastrocnemius-plantaris muscle were studied either at optimal length(Lo) or shortlength (Ls;~0.9 · Lo),to determine the effects of initial length on mechanical and metabolicperformance in situ. Respective averages of mechanical and metabolicvariables were(Lo vs.Ls, allP < 0.05) passive tension (preload) = 55 vs. 6 g/g, maximal active tetanic tension(Po) = 544 vs. 174 (0.38 · Po)g/g, maximal blood flow () = 2.0 vs. 1.4 ml · min1 · g1,and maximal oxygen uptake(O2) = 12 vs. 9 µmol · min1 · g1.Tension at Lodecreased to0.64 · Po over20 min of repetitive contractions, demonstrating fatigue; there were nosignificant changes in tension atLs. In separatemuscles contracting atLo, was set to that measured atLs (1.1 ml · min1 · g1),resulting in decreased O2(7 µmol · min1 · g1),and rapid fatigue, to0.44 · Po. Thesedata demonstrate that 1)muscles at Lohave higher andO2 values than those at Ls;2) fatigue occurs atLo with highO2, adjusting metabolic demand (tension output) to match supply; and3) the lack of fatigue atLs with lowertension, , andO2 suggestsadequate matching of metabolic demand, set low by shortmuscle length, with supply optimized by low preload. Thesedifferences in tension andO2 betweenLo andLs groupsindicate that muscles contracting isometrically at initial lengthsshorter than Loare working under submaximal conditions. 相似文献
20.
Much research has focused on understanding breeding synchronyin animals and its relationship to such issues as mating systemsand extrapair copulations in birds (Birkhead and Biggins, 1987;Emlen and Oring, 1977; Knowlton, 1979; Stutchbury and Morton,1995). To empirically examine synchrony, one needs an appropriatemeasure of the degree of synchrony in a population. Kempenaers(1993) presented an index of breeding synchrony (modified fromBjörklund and Westman, 1986) that has gained wide use asa simple representation of the degree to which breeding is synchronizedamong animals. This synchrony index (SI) is calculated as follows:
where F is the totalnumber of breeding females in the population; fi,p is the numberof fertile females, excluding 相似文献