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1.
N. N. Khaertdinov D. R. Ahmetshina A. L. Zefirov G. F. Sitdikova 《Biochemistry (Moscow) Supplemental Series A: Membrane and Cell Biology》2013,7(1):52-57
Hydrogen sulfide (H2S) is an endogenously synthesized gaseous molecule which, along with nitric oxide and carbon monoxide, induces a number of effects in cardiovascular system under normal and pathological conditions. In the present work, the effects and underlying mechanisms of the H2S donor sodium hydrosulfide (NaHS) on the isometric force of frog myocardium contraction have been studied. NaHS at the concentration of 100 μM induced negative inotropic effect and reduced the maximum velocity of the contraction and relaxation of the isolated ventricle strips. The substrate of H2S synthesis, L-cysteine (200 μM and 1 mM), induced the same effect, while the inhibitors of cystathionin-γ-lyase, the H2S-producing enzyme in heart, β-cyanoalanine (500 μM) and propargylglycine (500 μM), increased the amplitude of contraction. Inhibition of cystathionin-γ-lyase by β-cyanoalanine prevented the negative inotropic effect of L-cysteine. After the inhibition of adenylate cyclase by MDL-12,330A (3 μM) or phosphodiesterases by IBMX (200 μM), the effect of NaHS was less than that in the control. In the presence of membrane-penetrating analogous of cAMP, 8Br-cAMP (100 μM) and pCPT-cAMP (100 μM), the negative inotropic effect of NaHS was completely retained. The effect of NaHS significantly decreased after preliminary application of the NO donor, SNAP (10 μM), and did not change after the inhibition of NO synthases by L-NAME (100 μM). The results suggest the possibility of endogenous synthesis of H2S in frog myocardium and regulation of its contractility by the activation of phosphodiesterases hydrolyzing cAMP, which leads to a decrease in the activation of cAMP-dependent protein kinases and phosphorylation of voltage-dependent L-type Ca channels. As a result, the reduction of calcium entry into cardiomyocytes decreases the contractility of frog myocardium. 相似文献
2.
Phillip R. Bennett M.B. Murdoch G. Elder M.D. Leslie Myatt Ph.D. 《Prostaglandins & other lipid mediators》1987,33(6)
The effects of the lipoxygenase products of arachidonic acid, 5- and 12-hydroxyeicosatetraenoic acid (5- and 12-HETE) and leukotriene B4 (LTB4), on the spontaneous contractility of lower uterine segment human myometrial strips obtained prior to labour have been studied
. 5-HETE gave a dose- dependent (10–500ng) increase in both the rate of contractions and overall contractility of myometrial strips while 12-HETE and LTB4 had no effect at the same concentrations. Prostaglandin F2
(50ng) contracted all myometrial strips in a similar pattern to 5-HETE but was approximately 10 times more potent. The effect of 5-HETE may be direct or perhaps indirect via interaction with the cyclo-oxygenase pathway. The findings do not disprove the contention that the onset of parturition may be characterized by a switch in arachidonic acid metabolism in intra-uterine tissues from lipoxygenase to cyclo-oxygenase products. 相似文献
3.
Background
Diastolic dysfunction is the hemodynamic hallmark of hypertensive heart disease. Tau (τ) has been used to describe left ventricle relaxation. The relationship between τ and afterload has been controversial. Our goal was to demonstrate this relationship in mice, because genetically-modified mouse models have been used extensively for studies in cardiovascular diseases.Methods
Increased arterial load was produced by phenylephrine administration (50 µg/kg iv) (n = 10). A series of pressure-volume loops was recorded with a Millar conductance catheter in vivo as the left ventricle pressure reached the maximum. The arterial load was expressed as Ea (effective arterial elastance). Tau values were computed using three mathematical methods: τWeiss, τGlantz, and τLogistic.Results
A correlation plot between τ and Ea showed a biphasic relationship a flat phase I and an inclined phase II. The existence of an inflection point was proved mathematically with biphasic linear regression. Pressure-volume area (PVA), a parameter linearly related to myocardial O2 consumption (MVO2), was found to be directly proportional to Ea. The plot of τ versus PVA was also biphasic.Conclusion
We concluded that a small increase of the arterial load by phenylephrine increased PVA (index of MVO2) but had little effect on τ. However, after an inflection point, further increase of arterial load and PVA resulted in the linear increase of τ. 相似文献4.
Lymphatic absorption is a highly regulated process driven by both an extrinsic mechanism (external force) and an intrinsic mechanism (lymphatic vessel contractility). The lymphatic muscle is a specialized smooth muscle with unique mechanical properties. To understand the molecular mechanism and relative contribution of smooth muscle contraction in lymphatic absorption, we analyzed mice with a smooth muscle-specific deletion of Mylk, a critical gene for smooth muscle contraction. Interestingly, the knockout mice were significantly resistant to anesthesia reagents. Upon injection in the feet with FITC-dextran, the mutant mice displayed a 2-fold delay of the absorption peak in the peripheral circulation. Examining the ear lymphatic vessels of the mutant mice revealed a reduction in the amount of fluid in the lumens of the lymphangions, suggesting an impairment of lymph formation. The Mylk-deficient lymphatic muscle exhibited a significant reduction of peristalsis and of myosin light chain phosphorylation in response to depolarization. We thus concluded that MLCK and myosin light chain phosphorylation are required for lymphatic vessel contraction. Lymphatic contractility is not an exclusive requirement for lymphatic absorption, and external force appears to be necessary for absorption. 相似文献
5.
Keita Saku Takamori Kakino Takahiro Arimura Takafumi Sakamoto Takuya Nishikawa Kazuo Sakamoto Masataka Ikeda Takuya Kishi Tomomi Ide Kenji Sunagawa 《PloS one》2016,11(4)
BackgroundLeft ventricular assist device (LVAD) mechanically unloads the left ventricle (LV). Theoretical analysis indicates that partial LVAD support (p-LVAD), where LV remains ejecting, reduces LV preload while increases afterload resulting from the elevation of total cardiac output and mean aortic pressure, and consequently does not markedly decrease myocardial oxygen consumption (MVO2). In contrast, total LVAD support (t-LVAD), where LV no longer ejects, markedly decreases LV preload volume and afterload pressure, thereby strikingly reduces MVO2. Since an imbalance in oxygen supply and demand is the fundamental pathophysiology of myocardial infarction (MI), we hypothesized that t-LVAD minimizes MVO2 and reduces infarct size in MI. The purpose of this study was to evaluate the differential impact of the support level of LVAD on MVO2 and infarct size in a canine model of ischemia-reperfusion.MethodsIn 5 normal mongrel dogs, we examined the impact of LVAD on MVO2 at 3 support levels: Control (no LVAD support), p-LVAD and t-LVAD. In another 16 dogs, ischemia was induced by occluding major branches of the left anterior descending coronary artery (90 min) followed by reperfusion (300 min). We activated LVAD from the beginning of ischemia until 300 min of reperfusion, and compared the infarct size among 3 different levels of LVAD support.Resultst-LVAD markedly reduced MVO2 (% reduction against Control: -56 ± 9%, p<0.01) whereas p-LVAD did less (-21 ± 14%, p<0.05). t-LVAD markedly reduced infarct size compared to p-LVAD (infarct area/area at risk: Control; 41.8 ± 6.4, p-LVAD; 29.1 ± 5.6 and t-LVAD; 5.0 ± 3.1%, p<0.01). Changes in creatine kinase-MB paralleled those in infarct size.ConclusionsTotal LVAD support that minimizes metabolic demand maximizes the benefit of LVAD in the treatment of acute myocardial infarction. 相似文献
6.
Raffaele Acierno Claudio Agnisola Rita Venzi Bruno Tota 《Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology》1990,160(4):365-371
Summary An in vitro preparation of the heart of the teleostConger conger, isolated without the pericardium, was set up. The procedure allowed subambient pressures to develop in the perfusion chamber during contraction, mimicking the in vivo situation with the pericardium intact. The ventricle produced a cardiac output of about 15 ml·min-1·kg wet body weight-1 at subambient input pressure, and was able to double the stroke work with an increase of preload up to about 0.2 kPa. Using this preparation it was found that prostacyclin has a positive inotropic effect on the atrium and ventricle, but it does not affect the heart rate. Semilogarithmic doseresponse curves of prostacyclin on the atrium are reported, showing a threshold concentration of about 10-9
M. The isolated and perfusedConger conger heart provides a useful model for a detailed analysis of the action of prostacyclin on myocardial contractility. 相似文献
7.
Rianne Nederlof Ebru Gürel-Gurevin Otto Eerbeek Chaoqin Xie G. Sjoerd Deijs Moritz Konkel Jun Hu Nina C. Weber Cees A. Schumacher Antonius Baartscheer Egbert G. Mik Markus W. Hollmann Fadi G. Akar Coert J. Zuurbier 《Journal of physiology and biochemistry》2016,73(3):323-333
Ischemia/reperfusion (I/R) of the heart becomes injurious when duration of the ischemic insult exceeds a certain threshold (approximately ≥20 min). Mitochondrial bound hexokinase II (mtHKII) protects against I/R injury, with the amount of mtHKII correlating with injury. Here, we examine whether mtHKII can induce the transition from non-injurious to injurious I/R, by detaching HKII from mitochondria during a non-injurious I/R interval. Additionally, we examine possible underlying mechanisms (increased reactive oxygen species (ROS), increased oxygen consumption (MVO2) and decreased cardiac energetics) associated with this transition. Langendorff perfused rat hearts were treated for 20 min with saline, TAT-only or 200 nM TAT-HKII, a peptide that translocates HKII from mitochondria. Then, hearts were exposed to non-injurious 15-min ischemia, followed by 30-min reperfusion. I/R injury was determined by necrosis (LDH release) and cardiac mechanical recovery. ROS were measured by DHE fluorescence. Changes in cardiac respiratory activity (cardiac MVO2 and efficiency and mitochondrial oxygen tension (mitoPO2) using protoporphyrin IX) and cardiac energetics (ATP, PCr, ?GATP) were determined following peptide treatment. When exposed to 15-min ischemia, control hearts had no necrosis and 85% recovery of function. Conversely, TAT-HKII treatment resulted in significant LDH release and reduced cardiac recovery (25%), indicating injurious I/R. This was associated with increased ROS during ischemia and reperfusion. TAT-HKII treatment reduced MVO2 and improved energetics (increased PCr) before ischemia, without affecting MVO2/RPP ratio or mitoPO2. In conclusion, a reduction in mtHKII turns non-injurious I/R into injurious I/R. Loss of mtHKII was associated with increased ROS during ischemia and reperfusion, but not with increased MVO2 or decreased cardiac energetics before damage occurs. 相似文献
8.
The physiological basis of uterine contractility in laying hens is not well understood, but a better understanding is important for understanding the mechanisms governing egg laying. The characteristics of uterine contractility arising spontaneously or by prostaglandin F2α (PGF2α) stimulation were therefore examined and the underlying mechanisms investigated. Uterine strips were isolated from laying hens 4 h before oviposition and force measured. These strips remained healthy in vitro and produced regular spontaneous contractions. The contractions were phasic and could be recorded for several hours. Exposure to nifedipine, the specific L-type Ca channel blocker, led to the abolition of force. The contraction amplitude and frequency were significantly increased when Bay K8644, an agonist of L-type Ca channels, was applied or when the concentration of extracellular Ca was elevated. Spontaneous contractions were also significantly inhibited by wortmannin, the specific inhibitor of myosin light chain kinase (MLCK). When 1 μM PGF2α was applied to spontaneously contracting uterus, it significantly increased their amplitude and frequency of the contractions. As with spontaneous contractions, PGF2α-induced force production was abolished by nifedipine and wortmannin. In the absence of extracellular Ca, a small but tonic force was generated upon application of PGF2α which was not affected by wortmannin. Thus, extracellular Ca entry and MLCK phosphorylation are essential for uterine force production occurring spontaneously or by PGF2α stimulation. Our data supports the conclusion that the pathway dependent on extracellular Ca entry and MLCK phosphorylation predominates during PGF2α stimulation but suggests some involvement of an alternative force-producing pathway, presumably Ca-sensitization. 相似文献
9.
Cardiac dysfunction is a frequently reported complication of clinical and experimental diabetes mellitus. Streptozotocin (STZ) – induced diabetes in rat is associated with a variety of cardiac defects including disturbances to heart rhythm and prolonged time-course of cardiac muscle contraction and/or relaxation. The effects of carbenoxolone (CBX), a selective gap junction inhibitor, on heart rhythm and contractility in STZ-induced diabetic rat have been investigated. Heart rate was significantly (P < 0.05) reduced in Langendorff perfused spontaneously beating diabetic rat heart (171±12 BPM) compared to age-matched controls (229± 9 BPM) and further reduced by 10−5 M CBX in diabetic (20%) and in control (17%) hearts. Action potential durations (APDs), recorded on the epicardial surface of the left ventricle, were prolonged in paced (6 Hz) diabetic compared to control hearts. Perfusion of hearts with CBX caused further prolongation of APDs and to a greater extent in control compared to diabetic heart. Percentage prolongation at 70% from the peak of the action potential amplitude after CBX was 18% in diabetic compared to 48% in control heart. CBX had no significant effect on resting cell length or amplitude of ventricular myocyte shortening in diabetic or control rats. However, resting fura-2 ratio (indicator for intracellular Ca2+ concentration) and amplitude of the Ca2+ transient were significantly (P < 0.05) reduced by CBX in diabetic rats but not in controls. In conclusion the larger effects of CBX on APD in control ventricle and the normalizing effects of CBX on intracellular Ca2+ in ventricular myocytes from diabetic rat suggest that there may be alterations in gap junction electrophysiology in STZ-induced diabetic rat heart. 相似文献
10.
Structural interactions between the myosin converter and relay domains have been proposed to be critical for the myosin power stroke and muscle power generation. We tested this hypothesis by mutating converter residue 759, which interacts with relay residues I508, N509, and D511, to glutamate (R759E) and determined the effect on Drosophila indirect flight muscle mechanical performance. Work loop analysis of mutant R759E indirect flight muscle fibers revealed a 58% and 31% reduction in maximum power generation (PWL) and the frequency at which maximum power (fWL) is generated, respectively, compared to control fibers at 15°C. Small amplitude sinusoidal analysis revealed a 30%, 36%, and 32% reduction in mutant elastic modulus, viscous modulus, and mechanical rate constant 2πb, respectively. From these results, we infer that the mutation reduces rates of transitions through work-producing cross-bridge states and/or force generation during strongly bound states. The reductions in muscle power output, stiffness, and kinetics were physiologically relevant, as mutant wing beat frequency and flight index decreased about 10% and 45% compared to control flies at both 15°C and 25°C. Thus, interactions between the relay loop and converter domain are critical for lever-arm and catalytic domain coordination, high muscle power generation, and optimal Drosophila flight performance. 相似文献
11.
V. G. Solomonova P. P. Avdonin E. S. Vinichenko I. F. Sukhanova P. V. Avdonin 《Journal of Evolutionary Biochemistry and Physiology》2007,43(1):35-42
Thrombin acts on mammalian cells through the specific, so-called protease-activated receptors (PARs). The thrombin action is mediated via three out of four known types of these receptors—PAR1,3,4. Mammalian thrombin receptors, apart from performance of other functions, control cardiac and vascular contractility. It is not known whether receptors of such kind exist in invertebrate animals. In the present work we have showed for the first time that thrombin in the concentration range of 0.01–1 units/ml increases amplitude of contractions of the isolated heart ventricle of the edible snail Helix pomatia. Its effect is reproduced by peptide ligands of receptors PAR1 and PAR4 that have sequences Ser-Phe-Leu-Leu-Arg-Asn (SFLLRN) and Glu-Tyr-Pro-Gly-Lys-Phe (QYPGKF), respectively. A potent activator of cardiac contractility of H. pomatia is serotonin. A comparative study of the mechanisms of action of serotonin and thrombin on the edible snail heart was carried out. cAMP participates in transduction of signal from serotonin receptors. On the membrane preparation from the H. pomatia heart, it was shown that thrombin and peptide ligands PAR1 and PAR4, unlike serotonin, did not increase adenylyl cyclase activity. Thus, mechanism of activation of cardiac contractility of H. pomatia by thrombin differs from that of serotonin. It is suggested that molluscs have receptors homologous to protease-activated mammalian receptors. 相似文献
12.
The contractile response to three different prostanoids of the isolated human myometrium and the different layers of the utero-tubal junction (UTJ) was studied . The prostaglandin endoperoxide, PGH2, stimulated contractility of both the myometrium and the outer and inner muscle layers of the UTJ, whereas the intermediate layer of the UTJ was inhibited. Thromboxane A2 generated from PGH2 and a thromboxane synthase preparation caused a stimulation of both the myometrium and all three layers of the UTJ. The stimulatory response to TxA2 occurred at concentrations as low as 50–70 pg/ml. The sodium salt of PGI2 was found to relax both the myometrium and all the layers of the UTJ. Intravenous administration of PGI2 in repeated doses between 2–8 μg induced facial flushing and headache but had little if any effect on uterine contractility. At least under conditions, these short-lived prostanoids and/or their metabolites apparently have a specific action on uterine contractility, an action which is manifested at comparatively low concentrations. 相似文献
13.
The contraction-relaxation cycle of the heart represents the combined action of a variety of different components of the myocytes. For many years an ‘index’ of contractility has been sought as a means of describing and integrating the large amount of information available from the studies of heart muscle contraction. This review will undertake to show that dF/dt, recorded from the whole heart, and dT/dt, recorded in isometric studies of isolated heart muscle preparations, should not be considered as the ‘index’ of contractility. Examples will be presented in which an increasing dT/dt is paradoxically accompanied by a lower tension, while a decreasing dT/dt can occur concomitantly with an increased contractile tension. Arguments are further presented in support of the concept that Ca2+, in conjunction with troponin C, is the main determinant of cardiac contractility and that dT/dt reflects a dynamic equilibrium between free and troponin-bound Ca2+. Peak tension is thus the net result of overlapping events competing for Ca2+ during the latter part of contraction, that is, during Phase II of contraction as defined below. These suggestions are based upon the following considerations: (a) The Ca2+ pumps are active even during rest and serve to maintain low cytosolic Ca2+ levels, (b) As cytosolic Ca2+ concentration increases, Ca2+ pump activity also increases, (c) In addition, the Na+Ca2+ exchange is activated by elevated Ca2+ concentrations and serves to decrease cytosolic Ca2+ levels, (d) The net result is a decline in free Ca2+ concentration during Phase II and a reduction in the rate of cross-bridge formation until peak tension is reached. Thus, the Ca2+ handling elements of the myocyte serve as a finely tuned feedback device, regulating troponin C-Ca2+ interactions controlling the Ca2+ concentration of the cytosol and as a result, the actin and myosin interaction. Factors which influence the function of these elements will change the contractility of the heart. 相似文献
14.
Rachad M. Shoucri Jacques R. Rouleau John G. Kingma Jr Jean G. Dumesnil Gilles R. Dagenais 《Bulletin of mathematical biology》1989,51(4):475-484
There is still controversy as to which characteristics of the pressure-volume relation should be used to define myocardial
contractility. In the present study a mathematical model for the left ventricle as a two-dimensional cylinder contracting
radially and symmetrically was used to establish a relation between a calculated intramyocardial pressure (Dh) and theP-V relation (PVR) at end-systole. Four new indices are introduced that allow a better assessment of change in inotropic state
of the myocardium, namely the calculated intramyocardial pressure (Dh), the calculated resultant pressure across the inner surface of the myocardium (Dh-P) (P=cavity pressure), the workW
t related to the pressure (Dh) and the workW
d related to the pressure (Dh-P). A relation betweenW
t andW
d and different parts of the area under the PVR is established. Indices derived in this manner from the PVR to study changes
in myocardial contractility appear to have a clear physical meaning. 相似文献
15.
I. V. Shemarova S. M. Korotkov V. P. Nesterov 《Journal of Evolutionary Biochemistry and Physiology》2013,49(4):423-428
The inotropic action of La3+ on frog myocardium was studied with taking into account its effect on mitochondria of cardiomyocytes (CM). It has been established that in the range of studied concentrations (0.2–6.0 mM), La3+ decreases dose-dependently the force of cardiac contractions (by 3.3–92.2%). In parallel experiments on isolated rat heart mitochondria (RHM), La3+ at a concentration of 25 μM has been shown to cause swelling of non-energized and energized mitochondria incubated in isotonic medium with 125 mM NH4NO3 and in hypotonic medium with 25 mM CH3COOK. The study of oxidative processes in mitochondria with aid of polarographic method of measurement of oxygen concentration has shown that La3+ at concentrations of 50 and 100 μM increases the oxygen consumption rate by mitochondria in the state 2. However, La3+ does not decrease the respiration rate of isolated mitochondria in the state 3, as this takes place in the case of use of Cd2+ or at the Ca2+-overloading of mitochondria. The rate of endogenous respiration of isolated mitochondria in the medium with La3+ was higher than in control, which suggests its effect on ion permeability of the inner membrane. The data obtained in this work indicate that the La3+-produced decrease of contractility of cardiac muscle is not only due to the direct blocking effect on the potential-controlled Ca2+-channels, but is also mediated by its unspecific action on the CM mitochondria. This action is manifested as an acceleration of the energy-dependent K+ transport in matrix and as an increase of ion permeability of the inner mitochondrial membrane (IMM). 相似文献
16.
Peter S. Davie Craig E. Franklin 《Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology》1992,162(3):256-262
Summary Oxygen consumption of an in-pericardium heart preparation from the spiny dogfish (Squalus acanthias) was linearly related to cardiac power output. Basal oxygen consumption, predicted from the regression, was 0.127 l · s-1 · g ventricle mass-1 and increased by 0.189 l · s-1 · g ventricle mass-1 per milliwatt of power generated. From the relationship between cardiac power output and mechanical efficiency, mechanical efficiency was predicted to increase with cardiac power output to a maximum of 21 %. Mechanical efficiency was measured during volume loading and pressure loading at two power outputs (50% and 72% of maximum power output). At 50% of maximum power output, mechanical efficiency increased significantly by 2.87%, from 11.9±0.3% to 14.8±0.5% (n=7), when flow was halved and output pressure doubled to achieve the same power output. Similarly, at 72% of maximum power output, mechanical efficiency increased from 14.74±0.92% to 17.61±0.84% (n=6) when flow was halved and output pressure doubled to generate the same higher level of power output. The increased mechanical efficiency at higher output pressures is believed to result from cardiac myocytes working within a length range where they are able to generate the most tension during contraction and are most efficient. We speculate that the loss of mechanical efficiency associated with large changes in sarcomere length, when stroke volume is large, is a driving force behind the use of frequency as the principal means of increasing cardiac output as observed in more active fishes, birds and mammals.Abbreviations BM
body mass
- CO
cardiac output
- HR
heart rate
-
P
i
mean cardiac input pressure
-
P
o
mean cardiac output pressure
-
PO
partial pressure of oxygen
- SV
stroke volume of heart
- VM
ventricle mass 相似文献
17.
Responses of a holothurian smooth muscle to a range of muscarinic (M1 to M5) acetylcholine receptor (mAChR) agonists and antagonists were surveyed using calcium (Ca2+)-selective electrodes and a mechanical recording technique. Most of the mAChR agonists and antagonists tested increased both
contractility and net Ca2+ efflux, with M1-specific agents like oxotremorine M being the most potent in their action. To investigate the possible sources of Ca2+ used during mAChR activation, agents that disrupt intracellular Ca2+ ion sequestration [cyclopiazonic acid (CPA), caffeine, ryanodine], the phosphoinositide signaling pathway [lithium chloride
(LiCl)], and L-type Ca2+ channels (diltiazem and verapamil) were used to challenge contractions induced by oxotremorine M. These contractions were
blocked by treatment with CPA, caffeine, LiCl, and by channel blockers, diltiazem and verapamil, but were unaltered by ryanodine.
Our data suggest that this smooth muscle had an M1,3,5-like receptor that was associated with the phosphoinositide signaling pathway that relied on intracellular Ca2+ stores, but secondarily used extracellular Ca2+ via the opening of L-type channels. 相似文献
18.
O. L. Lange T. G. A. Green H. Reichenberger A. Meyer 《Plant biology (Stuttgart, Germany)》1996,109(1):43-50
Abstract: Lichens, being poikilohydric, have varying thallus water contents (WC) and show a complex interaction between net photosynthesis (NP) and WC. NP can be depressed at low WC (desiccation effects) and, in some species, also at high WC. In the latter case the depression is normally ascribed to increased CO2 diffusion resistances through water blockage. Recently, an earlier explanation, that the depression at high WC is due to recycling of CO2 from increased dark respiration processes (DR), has been given renewed prominence. The two explanations were distinguished by the concurrent use of gas exchange and chlorophyll fluorescence techniques to investigate NP: WC relationships in the lichens Peltigera leucophlebia (green algal) and P. neckeri (cyanobacterial). Both species had a distinct optimal WC for NP with depressed values at low and high WC. The maximal quantum yield for both CO2 fixation (initial slope of light response curves of NP) and photosystem II (fluorescence signals of dark-adapted thalli) was depressed only at low WC and remained high at optimal and greater WC. In contrast, the relative electron transport rate (ETR, derived from fluorescence signals of thalli in the light) tracked NP and was depressed at low and high WC. The depression of both NP and ETR at high WC (not that at low WC) could be prevented by using elevated external CO2 concentrations. A single, linear relationship was found between all values of gross photosynthesis (NP + DR) and ETR regardless of external CO2 concentration or WC. Our results show that, for these lichens, the depression in NP at high WC is a real fall in photosynthetic rate of the photobionts and is not due to recycling of CO2. The removal of the depression in NP and ETR at high WC by using elevated external CO2 levels allows us to conclude that an additional CO2 diffusion resistance is present. 相似文献
19.
C. Lobaccaro-Henri M. Saintot B. Descomps H. Thaler-Dao F. Laffargue H.P. Zahradnik 《Prostaglandins & other lipid mediators》1992,44(5)
We studied the effect of antiprogesterone RU 486 on spontaneous uterine contractility and PGI2 release with human myometrial strips superfused “in vitro”. A decrease of PGI2 release into the superfusion medium was observed after 20 min superfusion. The inhibition was dose-dependent and reversible. After 20 min washing with tyrode medium without RU 486, the uterine strips recovered their initial rate of release. R5020, a progesterone agonist, did not affect PGI2 release nor dexamethasone and testosterone. Parallel to the decrease of PGI2 observed during RU 486 superfusion, the uterine spontaneous contraction frequency decreased, while the amplitude and duration of contractions increased. The alteration of uterine contractility was also rapid, dose-dependent and reversible. Modifications of uterine strip spontaneous contractility, similar to those induced by RU 486, were also observed with superfusions of R5020 at concentrations as low as 10−9M, dexamethasone (10−8M), but not with superfusions of testosterone. These observations are not in favour of a progesterone-receptor mediated effect of RU 486 in our model. The mechanism of action may be related to the antiprogesterone specific structure i.e. the bulky substituent at the C-11 position. The RU 486 effect on uterine strip contractility, mimicked by other steroids, could point to a non-specific lipid/membrane interaction. However, the fact that testosterone did not affect motility, may indicate a possible specificity of steroids having a 3 oxo pregnene structure. 相似文献
20.
The contractility of hearts from normal fed rats is decreased by 70% during perfusion with 50 μM chloroquine, which is a potent inhibitor of endogenous lipolysis. In triacylglycerol-rich hearts, obtained by feeding rats rapeseed-oil, chloroquine depresses lipolysis much less, while contractility was found to be inhibited only 30%. In both groups of hearts the effect of chloroquine was decreased by adding fatty acids, prostaglandin E1, the ionophore X-537A or more Ca2+ to the perfusion fluid. Norepinephrine and glucagon also stimulate chloroquine-depressed hearts. The conclusion is therefore reached that fatty acids act as Ca2+-vehicles in heart cells and that chloroquine, by inhibiting lipolysis, decreases Ca2+-transport by lowering unesterified fatty acid levels. 相似文献