SEARCH · PubMed Health

Results for “intracellular calcium levels”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources

PubMed1990

Histamine increases vascular tone and intracellular calcium level using both intracellular and extracellular calcium in porcine coronary arteries.

Effects of histamine on the tone and intracellular calcium level (Ca2+i) in porcine coronary arteries were simultaneously investigated by use of the fura-2 microscopic fluorometric method. Histamine (10(-6)-10(-4) M) induced concentration-dependent increases in tone and Ca2+i, but these responses were not sustained. Histamine induced a larger contraction than did KCl with a similar increase in Ca2+i. Depletion of the caffeine-sensitive Ca2+ store with ryanodine (3 x 10(-5) M) and repetitive applications of caffeine (2.5 x 10(-2) M) scarcely affected contractile and Ca2+i responses to histamine. In Ca2(+)-free medium or in the presence of verapamil (10(-6) M), histamine produced a briefer increase in Ca2+i and a smaller contraction than in normal medium. When histamine or caffeine was repetitively applied in Ca2(+)-free medium, the first application produced an increase in Ca2+i but the second application produced no increase. Although caffeine increased Ca2+i after repetitive histamine applications, histamine failed to increase Ca2+i after repetitive caffeine applications in Ca2(+)-free medium. These results indicate that vascular contraction induced by histamine may involve the following mechanisms: an increase in Ca2+ influx through Ca2+ channels, release of Ca2+ from the intracellular Ca2+ store which has an interaction with the caffeine-sensitive Ca2+ store, and sensitization of contractile proteins to Ca2+.

Animals↗

PubMed1991

Effects of elevated intracellular calcium levels on the cytoskeleton and tau in cultured human cortical neurons.

Considerable evidence suggests that altered neuronal calcium homeostasis plays a role in the neuronal degeneration that occurs in an array of neurological disorders. A reduction in microtubules, the accumulation of 8-15 nm straight filaments, and altered antigenicity toward antibodies to the microtubule-associated protein tau and ubiquitin, as well as granulovacuolar degeneration, are observed in many human neurodegenerative disorders. Progress toward understanding how and why human neurons degenerate has been hindered by the inability to examine living human neurons under controlled conditions. We used cultured human fetal cerebral cortical neurons to examine ultrastructural and antigenic changes resulting from elevations in intracellular calcium levels. Elevation of intracellular calcium by exposure to a calcium ionophore or a reduced level of extracellular Na+ for periods of hours to days caused a loss of microtubules, an increase in 8-15 nm straight filaments, and increased immunostaining with Alz-50 and 5E2 (tau antibodies) and ubiquitin antibodies. Granulovacuolar degeneration was also observed. Antigenic changes in tau were sensitive to phosphatases, and the electrophoretic mobility of tau was altered in cells exposed to calcium ionophore, indicating that tau was excessively phosphorylated as the result of elevated intracellular calcium levels. Colchicine also caused an accumulation of straight filaments and altered tau immunoreactivity, suggesting that a disruption of microtubules secondary to altered calcium homeostasis may be a key event leading to altered tau disposition and neuronal degeneration. These data demonstrate that aberrant rises in intraneuronal calcium levels can result in changes in the neuronal cytoskeleton similar to those seen in neurodegenerative disorders, and suggest that this experimental system will be useful in furthering our understanding of the cellular and molecular mechanisms of human neurological disorders.

Antibodies↗

PubMed2002

The kappa-opioid agonist U-69593 affects intracellular calcium level in R1.1 mouse thymoma cell line.

In this study, the effect of the kappa-opioid agonist U-69593 on the intracellular calcium level in R1.1. cells was investigated using FURA 2-AM dye. In the previous study, calcium transport into R1.1 cells was not affected by the kappa-opioid agonist (-)U50,488 [Int. J. Immunopharmacol. 21 (1999) 133]. In this study, the kappa-opioid agonist U-69593 (10(-10)-10(-6) M), decreased intracellular calcium level in unstimulated cells. This decrease could not be reversed by the kappa-opioid antagonist NBI (10(-5) or 10(-6) M). Ionophore A23187 was used to increase intracellular calcium level. Stimulation of intracellular calcium level by Ionophore A23187 was potentiated by the kappa-opioid agonist U-69593. Thus, we have shown that basal intracellular calcium level was decreased in R1.1 by the kappa-opioid agonist U-69593 and increased in R1.1 cells stimulated by Ionophore A23187.

Analgesics, Opioid↗

PubMed2005

Involvement of phospholipase C in Yersinia enterocolitica heat stable enterotoxin (Y-STa) mediated rise in intracellular calcium level in rat intestinal epithelial cells.

In response to Yersinia enterocolitica heat stable enterotoxin (Y-STa) intracellular calcium level was increased with a prolong sustained phase in presence of calcium chloride in extracellular environment in rat intestinal epithelial cells. Chelation of extracellular calcium with EGTA (extracellular calcium chelator) and suspension of cells in calcium free buffer demonstrated a rapid but transient rise in calcium level, which suggested that Y-STa induced rise in intracellular calcium concentration was the combination of both intracellular calcium store depletion and calcium influx from extracellular environment. Moreover, in response to Y-STa phosphoinositide specific phospholipase C activity and inositol tri phosphate (IP3) level was increased and U73122, a phospholipase C inhibitor could completely inhibit Y-STa induced calcium rise. However, treatment of rat enterocytes with dantrolene IP3, a mediated calcium release inhibitor from intracellular store resulted partial inhibition of Y-STa induced rise in intracellular calcium level. Similar observation was noted with IP3 receptor antagonist 2ABP (2-amino-ethoxydiphenylborate). These results suggested that beside phospholipase C IP3 pathway, phospholipase C might have an independent role in Y-STa induced calcium influx. Rise in phospholipase Cgamma isoform activity in response to Y-STa suggested that gamma isoform of phospholipase C might have a role in Y-STa mediated rise in intracellular calcium level.

Animals↗

PubMed1998

Effect of extracellular calcium on the intracellular calcium level of newborn rat skin basal cells.

The effect of extracellular calcium on the intracellular calcium level of newborn rat skin basal cells was examined. The intracellular calcium level of basal cells was affected by the extracellular calcium concentration on culture of the cells on a collagen-coated filter, but not on a plate. The intracellular calcium ion concentration ([Ca2+]i) of cells on a collagen-coated filter with 0.05 mM external CaCl2 was 15 nM and increased to 20-22 nM on culture with 2.0 mM extracellular CaCl2. From these results we concluded that the culture matrix (e.g. culture plates, or collagen-coated filters) affects the response of the basal cells to changes in the extracellular calcium content. The intracellular calcium level of Swiss 3T3 cells cultured both on plates and collagen-coated filters were affected by the extracellular calcium concentration. Their [Ca2+]i was determined as 49-50 nM in the presence of 0.05 mM external CaCl2, and 54-56 nM in the presence of 2.0 mM CaCl2. These different responses to extracellular Ca2+ may be due to differences in the proliferative profiles of basal cells and fibroblasts.

Animals↗

PubMedDate not supplied

The effect of δ-opioid agonists on intracellular calcium level in MOLT-4 T-cell line.

δ-opioid agonists were reported to affect T cell functions: proliferation, cytotoxicity, cytokine production. Changes in intracellular calcium level are important in T-cell activation. In this study the effect of the synthetic δ-opioid agonist DADLE and an endogenous δ-opioid pentapeptide Met-enkephalin on the intracellular calcium level in human T-lymphoblastic leukemia MOLT-4 cells is reported. Intracellular calcium level was monitored using QUIN 2-AM as a fluorescent dye in MOLT-4 cells after short treatment (2 and 15 min) with DADLE and Met-enkephalin. DADLE (10-8M) mildly (average 28%) decreased the intracellular calcium level after 1 min treatment. The suppressive effect of DADLE (10-8M) on the intracellular calcium level was enhanced by longer (15 min) treatment of MOLT-4 cells (average 40%). Met-enkephalin (10-9M - 10-7M) decreased (average 33 %) the intracellular calcium level after 2 min treatment (average 33% - 37%). However, Met-enkephalin (10-7M) increased (average 31%) the intracellular calcium level after longer (15 min) treatment. Ionophore A23187 (10-7M, 10-6M) was used as a positive control to enhance intracellular calcium level. Thus, δ-opioid agonist DADLE decreased basal intracellular calcium level in MOLT-4 cells after short treatment, while endogenous Met-enkephalin altered intracellular calcium level in a bidirectional way by decreasing and increasing it.

Journal Article↗

PubMed1997

High intracellular calcium levels during and after electrical discharges in molluscan peptidergic neurons.

Intracellular calcium levels ([Ca2+]i) during and following electrical activity of the neuroendocrine caudodorsal cells of the pond snail (Lymnaea stagnalis) were measured in situ and in dissociated cells by combining electrical recordings and Fura-2 measurements. Caudodorsal cells are typical neuroendocrine cells that control egg laying via the release of a set of peptides during a stereotyped discharge of action potentials. Single action potentials or short trains of spikes in dissociated caudodorsal cells induced only small but consistent increases in [Ca2+]i. With longer or repeated spike trains, larger [Ca2+]i transients were measured, indicating accumulation of calcium. The calcium channel blocker Ni2+ suppressed the calcium elevation, suggesting that calcium influx occurred through voltage-activated calcium channels. Calcium levels in caudodorsal cells in situ were measured before, during and after the stereotyped firing pattern, a approximately 35-min discharge of regular spiking. Basal calcium levels in caudodorsal cells in situ were about 125 nM. During the initial phase of the discharge, the intracellular calcium level increased to approximately 250 nM. Maximal calcium levels (300-600 nM) were only reached at the final phase of the discharge or several minutes after the cessation of firing. Calcium levels remained elevated for up to 1 h after the end of the discharge. During this time, caudodorsal cells were characterized by very low excitability. We suggest that the prolonged, elevated level of calcium following the discharge need not be directly dependent on action potentials. The long-lasting [Ca2+]i elevation may cause the release of neuropeptides to outlast the duration of electrical activity, thus uncoupling release from spiking. In addition, it may cause reduced excitability of neuroendocrine cells following a period of spiking, thereby inducing a refractory period.

Action Potentials↗

PubMed1997

High intracellular calcium levels during and after electrical discharges in molluscan peptidergic neurons.

Intracellular calcium levels ([Ca2+]i) during and following electrical activity of the neuroendocrine caudodorsal cells of the pond snail (Lymnaea stagnalis) were measured in situ and is dissociated cells by combining electrical recordings and Fura-2 measurements. Caudodorsal cells are typical neuroendocrine cells that control egg laying via the release of a set of peptides during a stereotyped discharge of action potentials. Single action potentials or short trains of spikes in dissociated caudodorsal cells induced only small but consistent increases in [Ca2+]i. With longer or repeated spike trains, larger [Ca2+]i transients were measured, indicating accumulation of calcium. The calcium channel blocker Ni2+ suppressed the calcium elevation, suggesting that calcium influx occurred through voltage-activated calcium channels. Calcium levels in caudodorsal cells in situ were measured before, during and after the stereotyped firing pattern, a approximately 35-min discharge of regular spiking. Basal calcium levels in caudodorsal cells in situ were about 125 nM. During the initial phase of the discharge, the intracellular calcium level increased to approximately 250 nM. Maximal calcium levels (300-600 nM) were only reached at the final phase of the discharge or several minutes after the cessation of firing. Calcium levels remained elevated for up to 1 h after the end of the discharge. During this time, caudodorsal cells were characterized by very low excitability. We suggest that the prolonged, elevated level of calcium following the discharge need not be directly dependent on action potentials. The long-lasting [Ca2+]i elevation may cause the release of neuropeptides to outlast the duration of electrical activity, thus uncoupling release from spiking. In addition, it may cause reduced excitability of neuroendocrine cells following a period of spiking, thereby inducing a refractory period.

Action Potentials↗

PubMed2000

Muscarinic receptors modulate intracellular calcium level in chick sensory neurons.

In the present work we have studied the variation of intracellular calcium levels induced by muscarinic agonists in chick dorsal root ganglia neurons. Muscarinic agonists such as muscarine and oxotremorine cause an increase of intracellular calcium levels in fura-2AM-loaded DRG neurons of E18 chick embryos. This increase was abolished following treatment with 1 microM atropine but not by 1 microM mecamylamine, indicating that the observed intracellular calcium increase, was dependent on muscarinic receptor activation. Stimulation in absence of external calcium or pre-incubation of the DRG cultures with thapsigargin or Mn(2+) demonstrated that [Ca(2+)](i) increase is mainly due to its release from intracellular stores. The use of selective antagonists of muscarinic receptor subtypes also indicated that M(1) and to a lesser extent M(3) receptor subtypes are responsible for the observed intracellular calcium mobilization. Finally pre-treatment of DRG cultures with pertussis toxin showed that the variation of [Ca(2+)](i) levels was dependent on PTX-insensitive G-protein. Moreover muscarinic agonists induce in DRG also the increase of IPs level, suggesting that the variations of intracellular calcium levels may be due at least in part to the activation of the phosphoinositide transduction pathway. In conclusion the reported observations demonstrate the activity of muscarinic receptors in sensory neurons, suggesting a functional role for acetylcholine in sensory transduction.

Animals↗

PubMed1995

Multiple effects of opiates on intracellular calcium level and on calcium uptake in three neuronal cell lines.

The present study examines the modulation by opiates of intracellular calcium levels and calcium entry, using fura-2 imaging and 45Ca2+ uptake, in three neuronal cell lines. We show that opiates (10(-7)-10(-5) M morphine and 10(-9)-10(-7) M etorphine) exert both inhibitory and excitatory effects on KCl-induced elevation in intracellular calcium level in SK-N-SH, NG108-15 and NMB cell lines. In addition, opiates elevate basal (non KCl-stimulated) intracellular calcium level in all three cell cultures. 45Ca2+ uptake is augmented by opiates in SK-N-SH cells and this stimulatory effect is not blocked by pertussis toxin. In NMB cells, an additional inhibitory effect of opiates on basal calcium takes place: opiates reduce intracellular calcium level as measured by fura-2, and decrease calcium influx as detected by 45Ca2+ uptake. The heterogeneity in the opioid regulation of calcium could not be attributed to the type of opioid drug, neither to its concentration nor to the experimental conditions, since neighboring cells within the same culture responded differently.

Calcium↗

PubMed1998

Effect of graft reperfusion on intracellular calcium levels in mononuclear leucocytes during human orthotopic liver transplantation.

BACKGROUND: Orthotopic liver transplantation (OLT) is accompanied by local and systemic manifestations of the ischaemia-reperfusion syndrome. Local effects are mediated in part through changes in intracellular calcium levels in Kupffer cells. Arachidonic acid metabolites mediate increases in intracellular calcium concentration and thus potentiate the effect of free radicals. This study was carried out to characterize white blood cell (WBC) calcium changes as a mediator for white cell activation in human OLT. METHODS: Twenty consecutive patients had OLT using standard surgery and anaesthesia techniques. Blood samples were drawn for estimation of WBC cytosolic calcium content at induction of anaesthesia, 5 min before graft reperfusion and 15 min after reperfusion. The rate of rise in intracellular calcium concentration after the addition of a calcium chloride 1 mmol L(-1) solution to the extracellular milieu was used as an estimate of membrane calcium permeability. RESULTS: Both extracellular (P = 0.0002) and intracellular (P = 0.0008) calcium concentrations rose with time. However, at no time was there a correlation between extracellular and intracellular calcium levels or rate of calcium influx (r2 = 0.002, P = 0.78). There was a significant increase in intracellular calcium concentration (P = 0.0008) and in the rate of rise of intracellular calcium levels (P = 0.0009) after reperfusion. CONCLUSION: There was a significant increase in circulating monocyte membrane permeability for calcium and cytosolic calcium concentration following reperfusion in human OLT. This was independent of extracellular calcium concentration. These results are consistent with WBC activation by reperfusion and could be implicated in the systemic reperfusion syndrome seen in OLT in humans.

Adult↗

PubMedDate not supplied

Local modulation of intracellular calcium levels near a single-cell wound in human endothelial monolayers.

An endothelial cell monolayer with a single mechanically lysed cell was used as a model to examine the extent, kinetics, and nature of local calcium mobilization in the neighborhood of a wound. Individual endothelial cells from confluent monolayers were mechanically lysed with a minutien needle coupled to a micromanipulator while producing no observable mechanical trauma to the neighboring cells. Changes in calcium levels in individual cells surrounding the wound site were monitored by epifluorescence microphotometry with the calcium-sensitive fluorophore indo-1. Individual cells adjacent to the wound site showed a substantial increase in their intracellular calcium levels, almost as high as the calcium levels attained by ionophore controls. The magnitude of intracellular calcium mobilization in confluent monolayers decreased with distance from the wound site, and those cells located at a radius greater than seven cells from the wound site showed no change in their calcium levels. Thus, lysis of a single cell resulted in calcium mobilization in approximately 200 neighboring cells. The time necessary for intracellular calcium to reach maximum levels also increased with distance from the wound site. Calcium mobilization was partly intracellular and was inhibited by disrupting cell-cell coupling or by increasing gap junction resistance by heptanol. This mobilization was greatly attenuated in subconfluent endothelial monolayers, and it was not observed in fibroblasts or smooth muscle cells; furthermore, the effect was defective in monolayers intentionally contaminated with smooth muscle cells. This study examines the extent and possible mechanisms of local endothelial activation near a microscopic endothelial wound.

Calcium↗

PubMed1992

Intracellular calcium levels regulate the actions of nerve growth factor on calcium uptake in PC12 cells.

The uptake of divalent cations and the intracellular concentration of calcium in PC12 cells were studied by flow cytometric analysis using the calcium-sensitive dye, Fluo-3, under a variety of conditions. In particular the actions of nerve growth factor were analyzed. The data show that nerve growth factor stimulates the uptake of divalent cations and increases the intracellular calcium levels of cells attached to collagen-coated plates. The data further indicate that nerve growth factor-dependent increases in the uptake of divalent cations become less pronounced as the intracellular concentration of calcium increases. Intracellular calcium levels increase upon detachment of the cells from the plates and also with increasing cell density. Studies on the uptake of 45calcium confirmed the influence of intracellular calcium levels on nerve growth factor-stimulated calcium uptake. Thus, the effect of nerve growth factor on the uptake of divalent cations is dependent on the calcium levels in the cells, perhaps explaining why previous studies in this field have provided inconsistent results.

Animals↗

PubMed1996

Elevation of intracellular calcium levels in neurons by nicotinic acetylcholine receptors.

The recognition that intracellular free calcium serves as a ubiquitous intracellular signal has motivated efforts to elucidate mechanisms by which cells regulate calcium influx. One route of entry that may offer both spatial and temporal fine resolution for altering calcium levels is that provided by cation-permeable, ligand-gated ion channels. Biophysical measurements as well as calcium imaging techniques demonstrate that neuronal nicotinic acetylcholine receptors as a class have a high relative permeability to calcium; some subtypes equal or exceed all other known receptors in this respect. Activation of nicotinic receptors on neurons can produce substantial increases in intracellular calcium levels by direct passage of calcium through the receptor channel. When multiple classes of nicotinic receptors are expressed by the same neuron, each appears capable of increasing calcium in the cell but may differ with respect to location, temporal response, agonist sensitivity, or regulation in achieving it. As a result, nicotinic receptors must be considered strong candidates for signaling molecules through which neurons regulate a diverse array of cellular events.

Acetylcholine↗

PubMed1994

Synaptic-type acetylcholine receptors raise intracellular calcium levels in neurons by two mechanisms.

Nicotinic acetylcholine receptors (AChRs) located in the postsynaptic membrane on neurons are responsible for mediating fast, excitatory synaptic transmission. If synaptic AChRs are also highly permeable to calcium as reported recently for several kinds of neuronal AChRs, the synaptic receptors could regulate calcium-dependent events in the neurons in concert with normal transmission. Chick ciliary ganglion neurons have two classes of AChRs, one located predominantly in the synaptic membrane and responsible for synaptic signaling through the ganglion and the other located almost exclusively in nonsynaptic membrane and having no known function. The nonsynaptic receptors can readily elevate intracellular calcium concentrations. The experiments reported here indicate that synaptic-type receptors can raise intracellular calcium levels to the same extent as the nonsynaptic receptors and that they do so not only by being permeable to calcium themselves but also by activating voltage-dependent calcium channels (VDCCs). Currents of equivalent amplitude are obtained through the synaptic-type receptors when neurons are bathed in solutions containing either sodium or calcium as the sole extracellular cation. Measuring the effect of ion substitutions on the reversal potential of the receptors and applying the Goldman-Hodgkin-Katz constant field equation indicates the receptors are at least as permeable to calcium as to sodium. When neurons are loaded with the calcium-sensitive dye fluo-3 and challenged with nicotine, both the synaptic-type and nonsynaptic AChRs substantially elevate intracellular calcium levels under physiological conditions, and do so largely by activating VDCCs. Confirmation that synaptic-type AChRs can elevate intracellular calcium levels in the absence of contributions from VDCCs was obtained from voltage-clamp experiments on neurons loaded with fluo-3. The fluorescence signals indicate that the nicotine-induced calcium increases in neurons voltage clamped at rest are nearly as great as those induced in the same neurons when VDCCs are maximally activated by a voltage step. Calcium flux through AChRs may be particularly important for mediating local changes in calcium concentrations near the plasma membrane, which, in turn, could regulate specific membrane-associated calcium-dependent events.

Animals↗

PubMed1997

Transforming growth factor alpha treatment alters intracellular calcium levels in hair cells and protects them from ototoxic damage in vitro.

To determine if transforming growth factor alpha (TGF alpha) pretreatment protects hair cells from aminoglycoside induced injury by modifying their intracellular calcium concentration, we assayed hair cell calcium levels in organ of Corti explants both before and after aminoglycoside (i.e. neomycin, 10(-3) M) exposure either with or without growth factor pretreatment. After TGF alpha (500 ng/ml) treatment, the intracellular calcium level of hair cells showed a five-fold increase as compared to the levels observed in the hair cells of control cultures. After ototoxin exposure, calcium levels in hair cells of control explants showed an increase relative to their baseline levels, while in the presence of growth factors pretreatment, hair cells showed a relative reduction in calcium levels. Pretreatment of organ of Corti explants afforded significant protection of hair cell stereocilia bundle morphology from ototoxic damage when compared to explants exposed to ototoxin alone. This study correlates a rise in hair cell calcium levels with the otoprotection of hair cells by TGF alpha in organ of Corti explants.

Animals↗

PubMed1992

The initial stages of neural regeneration are dependent upon intracellular calcium levels.

The earliest events of neuronal regeneration require resealing of the neurite's membrane after injury and the subsequent formation of a new growth cone. We have investigated these activities in vitro employing the large identified neurons of the snail Helisoma. Regeneration was elicited by transection of neurite processes and assessed by studying the formation of new growth cones from the proximal neurite stumps. Under normal conditions new growth cones formed rapidly in 100% of the preparations. This formation appeared to follow, however, a large rise in intracellular calcium and did not start until after the cells homeostatic machinery had re-established near baseline calcium levels. To test the hypothesis that elevated intracellular calcium levels delayed or inhibited growth cone formation, transections were performed after experimentally increasing intracellular calcium concentrations to different levels by either depolarization or by calcium ionophores. Under these conditions, regeneration was significantly retarded in a fashion dependent upon the intracellular calcium concentration. Another change in the extracellular milieu, namely lowering of the extracellular calcium concentration, also significantly retarded growth cone formation. Under these conditions neurons appeared unable to reseal their cut ends and eventually died. Taken together, these studies demonstrate the importance of both the extracellular and intracellular milieu at times immediately following neurite transection in determining whether or not the earliest stages of neuronal regeneration will occur.

Animals↗

PubMed1991

Intracellular calcium levels in canine basilar artery smooth muscle following experimental subarachnoid hemorrhage: an electron microscopic cytochemical study.

Changes in intracellular calcium levels in canine basilar arterial smooth muscle were semiquantitatively measured by an electron microscopic cytochemical technique using a combined oxalate-pyroantimonate method. Measurements made after subarachnoid hemorrhage were compared with those made after contraction induced by prostaglandin F2 alpha. Fifteen minutes after topical application of the drug, when the basilar artery was constricted by 20%, 15% of smooth muscle cells contained a large amount of intracellular calcium. One hour later, the diameter of the basilar artery and intracellular calcium precipitation returned almost to control levels. Fifteen minutes after the first intracisternal injection of autologous blood, when acute vasospasm was angiographically evident, 13% of smooth muscle cells contained a large amount of calcium. After 1 h, when acute vasospasm had already abated, the number of smooth muscle cells containing a large amount of calcium markedly increased to 37% and some smooth muscle cells showed early degenerative findings such as intracytoplasmic vacuoles including calcium accumulation. After 48 h, when delayed vasospasm had already started, the calcium deposits and early degenerative changes had decreased significantly. After 49 h and 4 days (1 h and 48 h after the second injection of blood), the change in the amount of calcium was the same as at 1 h and 48 h after the first injection, respectively, but degeneration of smooth muscle cells increased. Therefore, acute vasospasm after subarachnoid hemorrhage may be caused by an initial elevation of intracellular calcium levels, as is the case with drug-induced contraction.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗