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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Changes of brain tissue calcium in the focal ischemia model of Wistar rat were investigated by three different methods; atomic absorption spectrophotometer, calcium stain with alizarin red S, and new histochemical method using aequorin, a calcium ion sensitive photoprotein. Tissue pH and tissue ATP were concomitantly investigated by histochemical method. Rat brain was frozen in situ at 15, 60 or 240 minutes after left middle cerebral artery was occluded. Coronal brain sections of 16 microns thickness was made and the brain slices applied for calcium stain and histochemical studies. The residual brain block was applied for atomic absorption spectrophotometric study. Tissue calcium content of left hemisphere increased from 1.34 +/- 0.09 (mean +/- SEM) (n = 7) to 1. 54 +/- 0.16 (n = 12), 2.07 +/- 0.12 (n = 9). 1.69 +/- 0.11 (n = 10) mumol/g wet weight after 15, 60 and 240 minutes respectively. Calcium stain with alizarin red S showed that the increase of calcium was observed in the peripheral part of the ischemic lesion where ATP was left in a spotty fashion, and calcium deposits disappeared with correspondence to exhaustion of ATP. Tissue calcium ion content studied by newly histochemical method, showed heterogeneous change. At an early stage of the ischemia, the increase of tissue calcium ion was shown only in the peripheral part of the ischemic lesion, and it gradually extended to the central part. Calcium ion increased in density in an area corresponding to that of the ATP decrease. Within the area of calcium ion increase, regional differences were noted; a greater increase at the border with the intact area and in the parts where ATP was heterogeneously preserved. In the non-ischemic area close to the ischemic area, where ATP was preserved with mild acidosis, calcium ion decreased more than in the surrounding area where ATP was preserved.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Changes in cerebral energy and calcium metabolisms on focal cerebral ischemia]. 179 92

To determine features of the steady state [Ca2+]-tension relationship in intact heart, we measured steady force and intracellular [Ca2+] ([Ca2+]i) in tetanized ferret papillary muscles. [Ca2+]i was estimated from the luminescence emitted by muscles that had been microinjected with aequorin, a Ca2+-sensitive, bioluminescent protein. We found that by raising extracellular [Ca2+] and/or by exposing muscles to the Ca2+ channel agonist Bay K 8644, tension development could be varied from rest to an apparently saturating level, at which increases in [Ca2+]i produced no further rise in force. 95% of maximal Ca2+-activated force was reached at a [Ca2+]i of 0.85 +/- 0.06 microM (mean +/- SEM; n = 7), which suggests that the sensitivity of the myofilaments to [Ca2+]i is far greater than anticipated from studies of skinned heart preparations (or from previous studies using Ca2+-sensitive microelectrodes in intact heart). Our finding that maximal force was reached by approximately 1 microM also allowed us to calculate that the steady state [Ca2+]i-tension relationship, as it might be observed in intact muscle, should be steep (Hill coefficient of greater than 4), which is consistent with the Hill coefficient estimated from the entire [Ca2+]i-tension relationship derived from families of variably activated tetani (6.08 +/- 0.68; n = 7). Finally, with regard to whether steady state measurements can be applied directly toward understanding physiological contractions, we found that the relation between steady force and [Ca2+]i obtained during tetani was steeper than that between peak force and peak [Ca2+]i observed during physiological twitches.
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PMID:Relationship between force and intracellular [Ca2+] in tetanized mammalian heart muscle. 241 83

Direct measurements of free intracellular calcium (Ca)i are needed for an understanding of the regulation of contractility. An on-line measurement of (Ca)i with Ca-selective microelectrodes in intact muscle strips provides a suitable means of investigating this problem, although considerable methodologic difficulties exist. Measurements of (Ca)i concentrations during muscle contraction have been carried out by different methods such as Ca-binding techniques and aequorin luminescence, but remain unsatisfying, since they were not performed on intact muscle strips. The authors' measurements were carried out with Ca-selective microelectrodes on rat papillary muscles (stretched to optimal length in a perfusion bath of 1.54 mL at 30 degrees C). The impalement of electrodes was considered adequate when the heights of Ca-electrode potential and membrane potential remained constant for more than twenty minutes. For provoking contractile responses, the authors replaced the normal Tyrode solution by a caffeine-containing contracture solution (content in mM: 0 NaCl [choline], 4 CaCl2, 30 KCl, 25 caffeine, 1.05 MgCl2). Ca-selective microelectrodes were calibrated before and after each measurement and only those impalements were taken as adequate that showed identical calibration curves before and after the experiment. They measured the (Ca)i at 20%, 50%, and 80% of maximal contractile force and obtained (Ca)i concentrations of 1.1 +/- 0.3 microM (at 20%), 3.6 +/- 1.2 microM (at 50%), and 11.8 +/- 0.27 microM (at 80%) (n = 6, +/- SEM). These results represent the fist on-line measurements of the myocardial (Ca)i concentrations with Ca++-selective microelectrodes in intact muscle strips during various degrees of contraction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Free calcium in rat papillary muscle at contraction assessed with Ca-selective microelectrodes. 275 65

Injection of inositol 1,4,5 trisphosphate (InsP3) into Limulus ventral photoreceptors causes an elevation of intracellular free Ca concentration (Cai) and depolarizes the photoreceptors. When measured with the photoprotein aequorin, the InsP3-induced Cai increase follows the time course of depolarization and declines within 1-2 s. However, sensitivity to further injections of InsP3 remains suppressed for several tens of seconds. The possibility that the suppression of Ca release (feedback inhibition) is due to a small lingering elevation of Cai, below the existing detection limit of aequorin, was investigated by measuring Cai with Ca-sensitive electrodes. Double-barreled, Ca-selective microelectrodes were used to pressure inject InsP3 and measure Cai at the same point. Light or InsP3 injections into the light-sensitive compartment depolarized the photoreceptors and induced an elevation of Cai that persisted for tens of seconds. Injections of InsP3 during the decay of Cai showed that sensitivity to InsP3 recovered as resting Cai approached the prestimulus level. The relationship between elevated Cai and feedback inhibition was very steep. An elevation of Cai of 1 microM or more was associated with inhibitions of 79 +/- 12.4% (SEM; n = 7) for the InsP3-induced Cai increase and of 76 +/- 8% for depolarizations. With a residual Cai elevation of 0.01 microM or less, the mean inhibition was 10 +/- 7.4% for InsP3-induced Cai increase and 6.6 +/- 4% for InsP3-induced depolarization. Injections of InsP3 into a light-insensitive compartment within the cell induced elevations of Cai with no associated depolarizations or feedback inhibition. To verify that a sustained elevation of Cai is necessary for inhibition of InsP3-induced Cai increase and depolarization, we injected ethyleneglycol-bis-(beta-aminoethylether)-N,N'-tetraacetic acid (EGTA) between two injections of InsP3. Injection of 1 mM EGTA or the related Ca chelator BAPTA, delivered 750 ms after the first injection of InsP3, restored the peak depolarization caused by the second injection of InsP3 to > 80 +/- 3% of control, compared with 13 +/- 8% without an intervening injection of EGTA. Measurement of Cai with aequorin showed that an intervening injection of EGTA partially restored the InsP3-induced Cai increase. The results suggest that feedback inhibition of InsP3-induced Cai increase and depolarization is mediated by a lingering elevation of Cai and not by depletion of intracellular Ca stores.
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PMID:A lingering elevation of Cai accompanies inhibition of inositol 1,4,5 trisphosphate-induced Ca release in Limulus ventral photoreceptors. 843 42