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21.
Shi Liu Ron Jacob David Piwnica-Worms Melvyn Lieberman 《Molecular and cellular biochemistry》1989,89(2):147-150
We have recently reported the presence of an electroneutral (Na + K + 2 Cl) cotransport mechanism that is bumetanide-sensitive and maintains Cli above its electrochemical equilibrium in cultured chick heart cells. In steady state, (Na + K + 2 Cl) cotransport is inwardly directed and so contributes to the Na influx that must be counterbalanced by the activity of the Na/K pump to maintain Nai homeostasis. We now show that manipulating (Na + K + 2 Cl) cotransport by restoring Clo to a Cl-free solution indirectly influences Na/K pump activity because the bumetanide-sensitive recovery of a
infNa
supi
to its control level and the accompanying hyperpolarization could be blocked by 10–4M ouabain. In another protocol, when the Na/K pump was reactivated by restoring Ko (from 0.5 mM to 5.4 mM) and removing ouabain, the recovery of aNa was attenuated by 10–4M bumetanide. The relatively slow rate of ouabain dissociation coupled with the activation of Na influx by (Na + K + 2 Cl) cotransport clearly establishes the interaction of these transport mechanisms in regulating Nai. Although (Na + K + 2 Cl) cotransport is electroneutral, secondary consequences of its activity can indirectly affect the electrophysiological properties of cardiac cells. 相似文献
22.
Increased breakdown of myocardial phospholipids to fatty acids and lysophosphoglycerides is an early feature of myocardial ischemic injury and many investigators believe that enhanced phospholipase action is an important factor in the process. Several recent reports indicate that inhibitors of phospholipase A, such as mepacrine, chloroquine and chlorpromazine, can prevent heart phosphoglyceride breakdown in vivo. We isolated the phospholipases A from rat heart cytosol and sarcoplasmic reticulum and examined the effects of various cardioprotective substances on their activity. Most of the cardioprotective agents studied inhibited the heart phospholipases in vitro, providing further evidence that phospholipid degradation in ischemic myocardial injury may be modulated by pharmacologic agents. 相似文献
23.
C. M. B. Duwel F. C. Visser M. J. van Eenige J. P. Roos 《Molecular and cellular biochemistry》1989,88(1-2):191-194
Summary Under normal and ischemic conditions backdiffusion of radiolabeled non-esterified fatty acids (NEFA) has been demonstrated. In the fasted normal canine heart the extraction fraction (EF) during interventions with glucose or lactate loading, vasodilation, and metabolic level augmentation was determined, and compared with the control EF. Backdiffusion alterations were deduced from the EF changes. After iv injection of 17-iodo-131 heptadecanoic acid (IHDA), 11 blood samples were drawn from aorta and coronary sinus in a time period of 60 minutes. In the control and vasodilation group the EF slowly decreased from 40 to 10%. In contrast, the EF in the noradrenaline group was constant. During glucose and lactate infusion the EF became negative within 10 min and remained negative. These results suggest that during physiological circumstances backdiffusion is determined by the metabolic level of the heart and its substrate availability. 相似文献
24.
The combined effects of chlorine and ammonia on litter breakdown in outdoor experimental streams 总被引:2,自引:0,他引:2
The response of Potamogeton crispus L. breakdown to controlled doses of different levels of chlorine and chlorine + ammonia was investigated over two years in
outdoor experimental streams. In 1985, downstream riffles of 2 streams were dosed (observed in-stream concentrations) at ca.
10 μg/L Total Residual Chlorine (TRC), one stream at 64 μg/L TRC and one stream at 230 μg/L TRC. Two control streams were
not dosed and the upstream riffles of each stream served as within stream controls. In 1986, the downstream riffle of one
stream was dosed at 70 μg/L TRC and a second stream was dosed at 200 μg/L TRC. Four streams were also dosed with 2.5 mg/L
NH3-N: one stream with no chlorine, one stream with ca. 10 μg/L TRC, one with 56 μg/L TRC, and one with 150 μg/L TRC. A seventh
stream was dosed for 2 h at 2000 μg/L TRC and 2.5 mg/L ammonia and then allowed to recover (recovery stream). Each year, litter
decomposition (degree day k values) was measured during two 35 day trials (Jun–Jul and Aug–Sep). In 1985, when streams were dosed with chlorine alone,
decomposition was significantly reduced with the high (230 μg/L TRC) chlorine dose. Downstream decomposition was 27% (Jun–Jul)
and 59% (Aug–Sep) of the upstream (control) rate. No other chlorine effects were found during this period. In Jun–Jul 1986,
there was significantly lower decomposition in the downstream dosed sites of the 200 μg/L TRC alone stream, the 146 μg/L TRC
+ ammonia stream and the recovery stream; downstream decay rates were (respectively) 56%, 42% and 64% of the upstream control
sites. No other up-down pairs were different in July 1986. In Aug–Sep, all three streams with chlorine + ammonia (6, 56 and
146 μg/L TRC + 2,5 mg/L ammonia) and the 70 μg/L TRC alone stream had significantly lower decomposition rates in the downstream
dosed sites. For these streams, downstream decay rates ranged from 46% (high chlorine + ammonia) to 73% (low chlorine + ammonia)
of the upstream control rates. No other up-down pairs were different during this trial. Up and downstream sites of the stream
dosed with 2.5 mg/L ammonia alone were nearly identical for both trials (< 3% difference). These results indicate that TRC
at less than 250 μg/L can significantly reduce litter decomposition and strongly suggest that addition of ammonia to chlorinated
water can increase the toxic effect of chlorine.
currently at the Department of Fisheries and Wildlife
currently at the Department of Fisheries and Wildlife 相似文献
25.
Ian M. C. Dixon Masanori Kaneko Tomoji Hata Vincenzo Panagia Naranjan S. Dhalla 《Molecular and cellular biochemistry》1990,99(2):125-133
Although cardiac dysfunction due to ischemia-reperfusion injury is considered to involve oxygen free radicals, the exact manner by which this oxidative stress affects the myocardium is not clear. As the occurrence of intracellular Ca2+ overload has been shown to play a critical role in the genesis of cellular damage due to ischemia-reperfusion, this study was undertaken to examine whether oxygen free radicals are involved in altering the sarcolemmal Ca2+-transport activities due to reperfusion injury. When isolated rat hearts were made globally ischemic for 30 min and then reperfused for 5 min, the Ca2+ -pump and Na+-Ca2+ exchange activities were depressed in the purified sarcolemmal fraction; these alterations were prevented when a free radical scavenger enzymes (superoxide dismutase plus catalase) were added to the reperfusion medium. Both the Ca2+- pump and Na+- Ca2+ exchange activities in control heart sarcolemmal preparations were depressed by activated oxygen-generating systems containing xanthine plus xanthine oxidase and H2O2; these changes were prevented by the inclusion of superoxide dismutase and catalase in the incubation medium. These results support the view that oxidative stress during ischemia-reperfusion may contribute towards the occurrence of intracellular Ca2+ overload and subsequent cell damage by depressing the sarcolemmal mechanisms governing the efflux of Ca2+ from the cardiac cell. 相似文献
26.
辣椒素引起脊髓P物质释放及其对血压的影响 总被引:5,自引:0,他引:5
为进一步研究脊髓 P 物质(SP)在调节心血管活动中的作用,在大鼠脊髓蛛网膜下腔注射(ith)辣淑素(cap),以刺激脊髓 SP 能神经末梢释放 SP,结果引起血浆去甲肾上腺素(NA)和肾上腺素(AD)含量增高,及具有剂量依赖性的动脉血压上升,心率升高。ith 具有高度特异性的 SP 受体拮抗剂或 SP 抗血清均可阻断 cap 引起的升压效应,免疫组化测定也观察到注入的cap 剂量越大,脊髓胸段 SP 样免疫阳性反应物的致密度越低,这些观察结果支持 cap 可以引起脊髓内 SP 的释放的说法。在第一颈段(C_1)横断脊髓后 ith cap 所引起的升压效应与完整动物 ith cap 的升压效应无显著差异。以上结果提示脊髓 SP 能神经末梢释放的 SP 可以通过交感肾上腺髓质系统引起心血管兴奋效应,SP 可能是引起交感节前神经元兴奋的神经递质。 相似文献
27.
大鼠缰核与下丘脑外侧区在调节心血管活动方面的机能联系 总被引:6,自引:0,他引:6
电刺激大鼠下丘脑外侧区(LH),动脉压明显升高,心率加快,在刺激电极同侧缰核(Hb)内微量注射盐酸利多卡因、电刺激LH引起的升压反应可被阻断38.9%,心率增快反应可被阻断44.4%,双侧Hb内微量注射盐酸利多卡因,电刺激LH引起的升压反应可被阻断40.7%,心率增快反应可被阻断41.2% ,单侧或双侧Hb内微量注射人工脑脊液均不能阻断电刺激LH引起的心血管反应。电刺激大鼠Hb,动脉压明显升高,心率无明显改变,在刺激电极同侧LH内微量注射盐酸利多卡因,电刺激Hb引起的升压反应可被阻断63.2%,双侧LH内微量注射盐酸利多卡因,电刺激Hb引起的升压反应可被阻断62.6%,单侧或双侧LH内微量注射人工脑脊液均不能阻断电刺激Hb引起的心血管反应。本实验提示Hb与LH在调节心血管活动方面有协同作用。 相似文献
28.
Alba Vecchini Luciano Binaglia Paolo Di Nardo Marilena Minieri Giuseppe Tallarida 《Molecular and cellular biochemistry》1992,110(1):47-54
The activity of phospholipid base exchange enzymes has been evaluated in cardiac sarcolemmal membranes from Syrian Golden
hamsters and from a hamster strain (UM-X7.1) characterized by a genetic form of hypertrophic cardiomyopathy. No choline base
exchange activity and only a little serine base exchange activity were detected, whereas the ethanolamine base exchange enzyme
was found highly active in membranes from both strains. For this reason, the present study is focussed on the ethanolamine
base exchange enzyme. The apparent Km for ethanolamine of ethanolamine base exchange enzyme from Syrian Golden membranes and
from UM-X7.1 strain membranes are 18 and 32 μM, respectively. The specific activity of the sarcolemmal ethanolamine base exchange
enzyme is lower in the UM-X7.1 strain than in Syrian Golden hamsters. The calcium-dependence of the enzyme appears different
when the membranes from the two strains are compared. Indeed, after removal of the membrane-bound divalent cations, comparable
activities are found in both membrane preparations, whereas, upon addition of Ca2+ to the incubation mixtures, the activity of the enzyme is enhanced in the membranes from Syrian Golden strain more than in
those from UM-X7.1 strain. The cholesterol content of sarcolemmal membranes is higher in the cardiomyopathic strain than in
the Syrian Golden hamsters. A possible relation between changes of the membrane lipid composition and of the ethanolamine
base exchange activity is discussed. 相似文献
29.
Effects of endotoxin administration on the ATP-dependent Ca2+ transport in canine cardiac sarcolemma were investigated. The results show that the sidedness of the sarcolemmal vesicles was not affected but the ATP-dependent Ca2+ transport in cardiac sarcolemma was decreased by 22 to 46% (p < 0.05) at 4 h following endotoxin administration. The kinetic analysis indicates that the Vmax for ATP and for Ca2+ were decreased by 50% (p < 0.01) and 32% (p < 0.01), respectively, while the Km values for ATP and Ca2+ were not significantly affected after endotoxin administration. Magnesium (1–5 mM) stimulated while vanadate (0.25–3.0 M) inhibited the ATP-dependent Ca2+ transport, but the Mg2+-stimulated and the vanadate-inhibitable activities remained significantly lower in the endotoxin-treated animals. These data demonstrate that endotoxin administration impairs the ATP-dependent Ca2+ transport in canine cardiac sarcolemma and that the impairment is associated with a mechanism not affecting the affinity towards ATP and Ca2+. Additional experiments show that the Ca2+ sensitivity of the Ca2+-ATPase activity was indifferent between the control and endotoxic groups suggesting that endotoxic injury impairs Ca2+ pumping without affecting Ca2+-ATPase activity. Since sarcolemmal ATP-dependent Ca2+ transport plays an important role in the regulation of cytosolic Ca2+ homeostasis, an impairment in the sarcolemmal ATP-dependent Ca2+ transport induced by endotoxin administration may have a pathophysiological significance in contributing to the development of myocardial dysfunction in endotoxin shock. 相似文献
30.
K. Prasad J. B. Gupta J. Kalra B. Bharadwaj 《Molecular and cellular biochemistry》1992,111(1-2):55-59
It has been suggested that oxygen free radicals (OFR) depress the excitation-contraction coupling in cardiac muscle. It is possible that a decrease in the cardiac contractility in the failing heart may be due to an increased OFR producing activity of polymorphonuclear (PMN) leukocytes. We studied the OFR producing activity (chemiluminescence) of PMN leukocytes from blood in dogs with heart failure due to chronic volume overload. The animals were divided into two groups: I) normal, (n = 10): II) dogs with mitral insufficiency (MI) of 6 to 9 months duration, (n = 10). Hemodynamic studies were done to establish the presence of heart failure. Blood samples were collected to measure PMN leukocyte chemiluminescence. There was a decrease in the cardiac index and index of myocardial contractility (dp/dt/IIP) and an increase in the left ventricular end-diastolic pressure in dogs with MI indicating left ventricular failure. The peak chemiluminescent activity of the PMN leukocytes in blood of dogs with failure was about four folds greater than that in the blood from normal dogs. These results suggest that there may be an increased OFR generation in dogs with volume overload heart failure. The decrease in the myocardial contractility in the failing heart might be due to an increase in the OFR produced by the PMN leukocytes. 相似文献