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Biomedical subjects

F Kashiwagi

Publications and source records attributed to F Kashiwagi.

At least 19 recordsLinked to original sources
PubMed2006

Finding cases of angle-closure glaucoma in clinic setting using a newly developed instrument.

PURPOSE: To validate the applicability of a newly developed, noncontact scanning peripheral anterior chamber depth analyzer (SPAC) for screening eyes at the risk of angle-closure glaucoma (ACG). SUBJECTS AND METHODS: All glaucoma patients who visited the University of Yamanashi Hospital from February through May 2003 were enrolled, except those with aphakic eye or pseudophakic eye. Of the 552 enrolled patients, 48 with ACG or narrow angles requiring laser iridotomy (LI) were categorized as patients with high-risk ACG eyes, and those with open angle were categorized as patients with control eyes. In all, 20 patients with ACG or narrow angles requiring prophylactic LI, who were followed up by an independent private ophthalmic clinic, were enrolled for threshold analysis. Nonophthalmologists measured anterior chamber depth and the averaged values of three measurements were employed for analysis. Threshold analysis and discriminant analysis were employed for determining the sensitivity and specificity of SPAC for diagnosing eyes with high-risk ACG. RESULTS: SPAC distinguished well the high-risk ACG eyes from the control eyes, and one of the most useful criteria for screening is as follows: any of the four measured points should exceed 95% confidence interval, and sensitivity and specificity should be 97.6 and 83.5%, respectively. CONCLUSION: SPAC is thought to be useful for detecting eyes at the risk of ACG by nonophthalmologists.

Anterior Chamber↗
PubMed2004

A newly developed peripheral anterior chamber depth analysis system: principle, accuracy, and reproducibility.

AIM: To develop a new, non-contact system for measuring anterior chamber depth (ACD) quantitatively, and to investigate its accuracy as well as interobserver and intraobserver reproducibility. METHODS: The system scanned the ACD from the optical axis to the limbus in approximately 0.5 second and took 21 consecutive slit lamp images at 0.4 mm intervals. A computer installed program automatically evaluated the ACD, central corneal thickness (CT), and corneal radius of curvature (CRC) instantly. A dummy eye was used for investigating measurement accuracy. The effects of CT and CRC on the measurement results were examined using a computer simulation model to minimise measurement errors. Three examiners measured the ACD in 10 normal eyes, and interobserver and intraobserver reproducibility was analysed. RESULTS: The ACD values measured by this system were very similar to theoretical values. Increase of CRC and decrease in CT decreased ACD and vice versa. Data calibration using evaluated CT and CRC successfully reduced measurement errors. Intraobserver and interobserver variations were small. Their coefficient variation values were 7.4% (SD 2.3%) and 6.7% (0.7%), and these values tended to increase along the distance from the optical axis. CONCLUSION: The current system can measure ACD with high accuracy as well as high intraobserver and interobserver reproducibility. It has potential use in measuring ACD quantitatively and screening subjects with narrow angle.

Adult↗
PubMed2000

Effects of brain-derived neurotrophic factor and neurotrophin-4 on isolated cultured retinal ganglion cells: evaluation by flow cytometry.

PURPOSE: Effects of brain-derived neurotrophic factor (BDNF) and neurotrophin (NT)-4 on retinal ganglion cells (RGCs) isolated and cultured in a serum-free medium are evaluated objectively by using flow cytometry. METHODS: RGCs from the retinas of 2-day-old rats were isolated in a two-step panning and cultured in a serum-free medium. BDNF (1, 10, and 100 pg/ml or 1, 10, and 100 ng/ml), NT-4 (0.1, 1, 10, and 100 ng/ml) or their vehicle, phosphate-buffered saline, were individually added to aliquots of the medium to be cultured for 48 hours. Then, after adding 5-chloromethylfluorescein diacetate, the survival of RGCs was evaluated using flow cytometry. RESULTS: The method used allowed the authors to analyze 10,000 RGCs per sample in approximately 2 minutes, so that a much larger number of cells was evaluated in a shorter period than with previously reported methods. RGCs were classified into either large or small RGCs, and the survival of each of these groups was determined objectively by the amount of fluorescent emission. BDNF improved the survival rate of RGCs concentration-dependently. In particular, the survival rate of small RGCs was greatly improved. BDNF at 100 ng/ml increased the survival rate of small RGCs by 17.4% and that of large RGCs by 7.8% in comparison to the controls. NT4 did not significantly improve the survival rates of either large or small RGCs. CONCLUSIONS: BDNF improved the survival rate of RGCs, particularly of small RGCs, concentration-dependently, but NT-4 had little influence on the survival rate. The current method was useful in evaluating the effects of neuroprotective factors or neurotoxic factors on cultured RGCs.

Animals↗
PubMed1998

The effect of duration of cerebral ischemia on brain pyruvate dehydrogenase activity, energy metabolites, and blood flow during reperfusion in gerbil brain.

The objective of this study was to determine whether the duration of an ischemic insult effects the activity of the mitochondrial enzyme pyruvate dehydrogenase (PDH) in relation to the recovery of metabolites and regional cerebral blood flow (rCBF) immediately after ischemia and during reperfusion in gerbil cortex. Cerebral ischemia was induced, using the bilateral carotid artery occlusion method, for 20 or 60 min, followed by reperfusion up to 120 min. Immediately after ischemia PDH activity increased threefold regardless of ischemic duration. In the 60-min ischemic group, PDH remained activated, the recovery of high energy phosphates and the clearance of lactate were poor, and the rCBF was 48% of controls after 20-min reperfusion, decreasing gradually to 26% at 120-min reperfusion. In the 20-min ischemic group, PDH activity normalized quickly, the restoration of energy phosphates was good, there was a quick reduction in lactate within the first 60 min of reperfusion, and the rCBF was 65% of control at 20-min reperfusion, and remained over 48% of control throughout reperfusion. Recovery of metabolism after reperfusion did not parallel the changes in rCBF in either group, most noticeably in the 60-min ischemic group. The slow normalization of PDH activity reflected the poor recovery of metabolites in the 60-min ischemic group, indicating that PDH activity is important in the resynthesis of energy metabolites during reperfusion. In conclusion, prolonging the ischemic insult effected PDH activity during reperfusion, impaired recovery of energy metabolites, and worsened the recovery of rCBF.

Adenosine Triphosphate↗
PubMed1997

Prostaglandin action on ciliary smooth muscle extracellular matrix metabolism: implications for uveoscleral outflow.

The cellular mechanisms mediating intraocular pressure reduction following topical prostaglandin (PG) treatments are poorly understood. To determine if PG treatments might induce altered metabolism of extracellular matrix surrounding ciliary muscle cells, confluent human ciliary smooth muscle cell cultures were exposed to PGF 2 alpha' 17-phenyltrinor-PGF2 alpha' or 11-deoxy-PGE1 for one to four days and the distributions of collagen types I, III and IV as well as laminin were determined immunocytochemically. In addition, collagen type IV and promatrix metalloproteinase III (proMMP-3) content within treated cultures was determined using sandwich ELISAs. Compared with vehicle-treated cultures, there were substantial reductions in the density and branching of the collagen type IV-immunoreactive lattice accompanied by thickening of remaining strands in all PG-treated cultures. Similar changes were seen in the distribution of laminin within all PG-treated cultures. Reductions in collagen type III immunoreactivity were seen in cultures treated with either PGF2 alpha or 17-phenyltrinor-PGF2 alpha. No changes were observed in collagen type I immunoreactivity. Quantitative analyses revealed increased amounts of collagen type IV in both the culture medium and in extracts of the cell layer in all PG-treated cultures. In addition, there were substantial increases in the concentrations of proMMP-3 in all PG-treated cultures. These results indicate that PGs induce increased turnover and remodeling of ECM adjacent to ciliary muscle cells. Such changes may contribute to increased uveoscleral outflow in vivo following topical PG treatment.

Animals↗
PubMed1997

Calponin distribution in human ciliary muscle and other anterior segment tissues.

PURPOSE: Calponins are a family of actin-binding proteins known to regulate aortic and tracheal smooth muscle contraction. This investigation was undertaken to assess the presence, subtype, and distribution of calponin proteins in human ciliary muscle, iris, and other anterior segment tissues as well as expression in ciliary muscle cells in vitro. METHODS: The distribution of calponin immunoreactivity was assessed in paraffin sections of human anterior segment tissue. Human ciliary muscle proteins were analyzed by polyacrylamide gel electrophoresis and Western blotting. The regulation of calponin expression was compared with alpha-sm-actin expression in preconfluent and postconfluent ciliary muscle cell cultures by immunocytochemistry. To determine total cell counts, the cultures were counter-stained with ethidium homodimer. As control specimens, expression of calponin and alpha-sm-actin also was assessed in human Tenon fibroblast cultures. RESULTS: Strong calponin immunoreactivity was present in ciliary muscle, iris dilator and sphincter muscles, and blood vessel smooth muscle. Fine immunostained strands also were observed in the scleral spur. This distribution was similar to alpha-sm-actin. Western blotting showed a single band of calponin with a molecular weight of 32 kDa. In the cultured ciliary muscle cells, calponin stained straight cable-like fibers running parallel along the long axis of the cells. Although the proportion of calponin immunoreactive cells was reduced substantially in preconfluent cultures, virtually all cells were stained in confluent primary through fourth-passage cultures. Cultured human Tenon fibroblasts did not show either calponin or alpha-sm-actin immunoreactivity. CONCLUSIONS: Calponin is expressed in human ciliary muscle, iris smooth muscles, blood vessel smooth muscle, as well as within the scleral spur. In addition, calponin is expressed by ciliary smooth muscle cells in vitro. The role of calponin in contraction of these tissues should be investigated.

Adult↗
PubMed1997

Prostaglandins alter extracellular matrix adjacent to human ciliary muscle cells in vitro.

PURPOSE: This study investigates the possibility that prostaglandins (PGs) induce changes in extracellular matrix (ECM) adjacent to ciliary muscle cells. METHODS: Human ciliary smooth muscle cells were grown to confluence in monolayer cultures and were treated with PGF2alpha, 11-deoxy-PGE1, or PhXA85 (the nonesterified analogue of PhXA41) for 12 to 72 hours. The amount of collagens type I, III, and IV in the cultures was determined, using sandwich enzyme immunoassays. The distributions of these collagens were assessed in the PG-treated cultures by immunocytochemistry. RESULTS: Twenty-four-hour treatment with 20 nM PGF2alpha, 11-deoxy-PGE1, or PhXA85 reduced the amount of collagen type I in extracts of the cell layer by 65+/-10%, 56+/-7%, and 46+/-7%, respectively, when compared with levels of those substances in vehicle-treated cultures. In similar fashion, collagen type III in cell layer extracts was reduced by 41+/-5%, 33+/-9%, and 3+/-5%, respectively. When the concentration of PGs was increased to 200 nM, the amount of type III collagen in the cell layer extracts was reduced by 93+/-7%, 99+/-1%, and 99+/-1%, respectively. Changes in type IV collagen in cell layer extracts after treatment with 20 nM PGs were not statistically significant. When the concentration of PGF2alpha, 11-deoxy-PGE1, or PhXA85 was increased to 200 nM, the amount of collagen type IV in the cell layer extract increased by 101+/-16%, 14+/-5%, and 89+/-11%, respectively. There were minimal changes in the staining pattern for collagen type I after 24-hour treatment with 20 nM PGs. When the PG concentration was increased to 200 nM, there were reductions in the density of collagen type I fibrils and clumping of collagen type III immunoreactive elements. The delicate lacework of collagen type IV immunoreactivity was replaced by bundles or clumps of heavy immunoreactive strands, separated by areas without immunoreactivity. These changes were present in cultures exposed to 20 nM PGs and were marked when PG concentration was increased to 200 nM. CONCLUSION: These results indicate that PGs can induce substantial changes in the ECM around ciliary smooth muscle cells in vitro. These data support the possibility that changes in ciliary muscle ECM may contribute to increased uveoscleral outflow facility after topical PG administration.

Adult↗
PubMed1997

Prostaglandins increase matrix metalloproteinase release from human ciliary smooth muscle cells.

PURPOSE: To identify matrix metalloproteinases (MMPs) released by ciliary smooth muscle cells in vitro and to determine whether MMP release is altered by exposure to prostaglandins (PGs). METHODS: Human ciliary smooth muscle cells were grown to confluence in monolayer cultures and treated with PGF2 alpha, 11-deoxy-PGE1, or PhXA85 (the nonesterified analogue of PhXA41) for 12 to 72 hours. The activity of MMP in the medium was assayed using gelatin and casein zymography. Identification of the specific MMP associated with each band was made by Western blot analysis. Band intensity, which reflects activity, was measured with a scanning laser densitometer. RESULTS: Three major bands appeared in the gelatin zymographs at positions corresponding to molecular weights of 62 kDa, 68 kDa, and 97 kDa. A single band at 50 kDa predominated in the casein zymograms. Substitution of EDTA for calcium and zinc in the development solution eliminated the appearance of these bands, indicating that they reflect MMP activity. Immunoblotting, using MMP-specific antibodies, confirmed that the three bands in the gelatin zymographs were MMP-1, MMP-2, and MMP-9, respectively; the single band in the casein zymographs was MMP-3. Treatment with 200 nM PGF2 alpha, 11-deoxy-PGE1, or PhXA85 for 72 hours increased the combined density scores for MMP-1 and MMP-2 by 37%, 64%, and 27%; the density scores for MMP-9 by 268%, 253%, and 125%; and the density scores for MMP-3 by 35%, 71%, and 22%, respectively. CONCLUSIONS: These results indicate that ciliary smooth muscle cells can secrete MMP-1, MMP-2, MMP-3, and MMP-9. In addition, exposure to PGF2 alpha, 11-deoxy-PGE1, or PhXA85 increases production of all four MMPs. These observations support the hypothesis that increased MMP production by ciliary muscle cells has a role in increasing uveoscleral outflow facility after topical PG administration.

Adult↗
PubMed1996

Prostaglandins increase proMMP-1 and proMMP-3 secretion by human ciliary smooth muscle cells.

PURPOSE: The mechanism by which prostaglandin(PG)F2 alpha increases uveoscleral outflow and lowers intraocular pressure in primates is not known. In cultured human ciliary muscle cells, PGF2 alpha induces the expression of the protooncogene c-fos which is known to induce the transcription of genes such as matrix metalloproteinase-1 (MMP-1) and MMP-3 in other cell systems. As these enzymes are initially secreted as proenzymes, the present study was undertaken to determine if PG treatment induces ciliary muscle cells to secrete either proMMP-1 or proMMP-3. METHODS: Human ciliary smooth muscle cells were grown to confluence in monolayer cell cultures and then treated with PGF2 alpha, 17-phenyltrinor-PGF2 alpha, or 11-deoxy-PGE1. Medium harvested at various times after treatment was assayed for proMMP-1 and proMMP-3 content using sandwich ELISAs. RESULTS: Three days after adding 10 nM PGF2 alpha, proMMP-1 and proMMP-3, concentrations in the culture medium were increased by 254 +/- 33% (mean +/- SE) and 128 +/- 13%, respectively. Compared with vehicle controls, 24 h treatment with 200 nM PGF2 alpha, 17-phenyltrinor-PGF2 alpha, or PGE1, increased proMMP-1 by 116 +/- 29%, 169 +/- 26%, and 273 +/- 16%, respectively. In parallel experiments, proMMP-3 was increased by 99 +/- 18%, 82 +/- 24%, and 214 +/- 16%, respectively. CONCLUSIONS: These results suggest that induction of MMPs in situ following topical PG treatment may degrade ciliary muscle extracellular matrix and possibly contribute to increased uveoscleral outflow, as well.

Alprostadil↗
PubMed1994

Effect of a new calcium antagonist (SM-6586) on experimental cerebral ischemia.

SM-6586 (SM) is a new derivative of dihydropyridine with potent calcium blocking activity and inhibitory activity of the Na+/H+ and Na+/Ca++ exchange transport. The effect of SM on survival rate, brain edema and metabolites was evaluated using two different models in spontaneously hypertensive rat (SHR). Global ischemia was induced by bilateral common carotid artery ligation (BLCL) and focal ischemia was induced by middle cerebral artery occlusion. The survival rate after BLCL was higher in the SM-treated group. The brain water content was lower, the ATP level was higher and lactate level was lower in the SM-treated group compared to the control group. In focal ischemia models, the SM-treated group showed a reduction of T1 relaxation time. The brain water content was significantly decreased in the SM-treated group. These results indicate that SM was effective in ameliorating the ischemic insult in global and focal cerebral ischemia models.

Animals↗
PubMed1994

Comparison of the effects of glycerol, mannitol, and urea on ischemic hippocampal damage in gerbils.

The effects of glycerol and mannitol, as well as urea, on delayed neuronal death (DND) in the gerbil hippocampus were investigated. 20% solution of glycerol, mannitol and urea were prepared, and 6.5 ml/kg of each agent, or saline, was administered to male Mongolian gerbils intraperitoneally 30 min before ischemia. The animals were subjected to transient forebrain ischemia for 5 min. Seven days after the ischemic insult, the brains were fixed and stained for histopathological analysis. The number of normal neurons (neuronal density, ND) in a 1 mm linear length of hippocampal CA1 region was counted. ND of sham-operated group (n = 6) was 275.3 +/- 16.7 (mean +/- SD). ND in the saline-treated group (n = 6) was 14.8 +/- 5.0. ND of groups treated with glycerol (n = 6), mannitol (n = 6) and urea (n = 4) was 68.2 +/- 56.7 (p < 0.01), 52.8 +/- 54.4 (p < 0.01) and 12.0 +/- 2.5 (NS), respectively. The present study demonstrates that glycerol and mannitol have some protective effects against DND in the gerbil hippocampus, whereas urea has no effect.

Animals↗
PubMed1994

[Seasonal variation in intraocular pressure].

Generally speaking, physicians have the impression that intraocular pressure (IOP) in winter is higher than in summer, but it is very difficult to evaluate the difference between summer and winter IOP statistically, because the treatments of glaucoma patients are changed according to their conditions. We compared the winter and summer IOP of normal subjects and of several glaucoma patients who had no therapy or no change in therapy. The subjects were divided into four groups, i.e., 20 eyes of the normal group, 17 eyes of the ocular hypertensive group, 24 eyes of the primary open angle glaucoma group, and 52 eyes of the low tension glaucoma group. The difference in mean IOP between summer and winter were evaluated for each subject. In all groups, the mean difference in mean winter IOP was significantly higher. The ups and downs of IOP were greater in the ocular hypertensive group and the primary open angle glaucoma group than in the normal group and the low tension glaucoma group. These results suggest that the seasonal variation of IOP should be taken in consideration when treating glaucoma patients.

Adult↗
PubMed1993

The role of bradykinin in mediating ischemic brain edema in rats.

BACKGROUND AND PURPOSE: We investigated the hypothesis that bradykinin generation may induce ischemic brain edema in spontaneously hypertensive rats. METHODS: Cerebral ischemia lasting 3 hours was produced by bilateral common carotid artery occlusion in 67 rats. After the ischemic period, the rats were reperfused. Cerebral water content and energy metabolites (adenosine triphosphate, lactate, and pyruvate), as well as plasma and tissue bradykinin, were measured. Additionally, using the same experimental paradigm, bradykinin synthesis inhibitors (aprotinin [n = 7] and soybean trypsin inhibitor [n = 7]) were administered immediately after ischemia induction to determine the relation of bradykinin generation to the progression of ischemic brain edema. RESULTS: Cerebral water content increased during the 3-hour ischemic period, peaked at 30 minutes of reperfusion, and declined thereafter. Bradykinin levels in plasma and tissue rose markedly 30 minutes after reperfusion and fell thereafter. The progressive loss of adenosine triphosphate was mirrored by the rise in lactate. In the treated groups, aprotinin and soybean trypsin inhibitor administration significantly attenuated cerebral edema (p < 0.01 and p < 0.05, respectively). The treated groups also showed less lactate accumulation and more adenosine triphosphate preservation than did the controls. CONCLUSIONS: These results demonstrate that bradykinin levels in plasma and tissue corresponded to cerebral edema progression and that bradykinin suppression decreased edema formation. These novel findings indicate that bradykinin activation augments the progression of ischemic brain edema.

Adenosine Triphosphate↗
PubMed1992

Effect of a prostacyclin derivative (OP-41483) and a hyperosmotic agent (glycerol) on brain edema and metabolism in cerebral ischemia.

A PGI2 derivative, OP-41483, and a hyperosmotic agent, glycerol, were tested for possible beneficial effects on brain edema, metabolism and pathological changes in cerebral ischemia. Combination treatment with these agents was also tested. Cerebral ischemia was produced in spontaneously hypertensive rats, using bilateral common carotid artery ligation (BLCL). OP-41483 was administered four times, hourly (500 ng/kg x 4, i.p.). Ten percent glycerol was administered intravenously (6.6 ml/kg). And, for the combination treatment, OP-41483 was administered three times, hourly (500 ng/kg x 3, i.p.), and 10% glycerol was administered intravenously (6.6 ml/kg) in the same manner as the glycerol treated group. In ischemic controls, saline was administered intravenously (6.6 ml/kg). After 3 h of ischemia, brain water content and metabolites were determined and pathological observation was conducted using electron microscopy. OP-41483 treated animals maintained higher levels of ATP concentration and reduced accumulation of lactate, but showed no difference in brain water content compared to saline treated controls. Glycerol treated animals showed significance in terms of reduction of brain water content and accumulation of lactate. Glycerol abated the depletion of ATP concentration. OP-41483+glycerol treated animals showed the most significant effect on the reduction of brain water content and accumulation of lactate. The combination treatment also maintained higher levels of ATP concentration. Additionally, swelling of astrocytic foot processes and mitochondria with destroyed crista were not observed pathologically in the combination treated animals. These results show that OP-41483, glycerol and combination treatment are beneficial in the treatment of cerebral ischemia. They also indicate that the combination treatment significantly enhances the protective effects compared to individual treatment.

Animals↗
PubMed1991

Effect of a new hyperosmotic agent, NIK-242 injection, on brain water content, metabolites and cerebral blood flow in cerebral ischemia in the spontaneously hypertensive rat.

We examined the effects of a new hyperosmotic agent (NIK-242inj.) on brain edema, energy metabolites and regional cerebral blood flow (r-CBF) during acute cerebral ischemia. Cerebral ischemia was induced by bilateral common carotid artery ligation (BLCL) using spontaneously hypertensive rats (SHR). The experimental animals were divided into 4 groups, A:20% NIK-242inj., B:20% mannitol, C:10% glycerol in 5% fructose, D:normal saline. All the animals were administered the agent or saline intravenously beginning at 1h after BLCL and continuing for 2h for a total dose of 6.8 ml/kg body weight. Brain water content and metabolites (ATP, lactate, pyruvate) were determined 3h after BLCL. Regional cerebral blood flow (r-CBF) in thalamus was also measured by the hydrogen clearance technique. The brain water content in the NIK-242inj. group was significantly lower than that of saline group. The concentration of brain ATP in the NIK-242inj. group remained higher than those of saline group. Accumulation of lactate in the NIK-242inj. group was less than in the mannitol and saline groups. The lactate/pyruvate ratio of the NIK-242 inj. group was significantly lower than that of the saline and mannitol groups. At 3h after BLCL, the reduction of r-CBF in the NIK-242inj. group was smaller than that of saline group. The present study suggests that NIK-242inj. as well as glycerol could ameliorate brain edema, disruption of brain energy metabolism and reduction of r-CBF in acutely induced cerebral ischemia.

Animals↗
PubMed1990

Role of platelets as a factor aggravating cerebral ischemia.

In order to clarify the role of platelets as a factor aggravating cerebral ischemia, an experimental model of ischemia was investigated using thrombocytopenic rats. In addition, the prostacyclin derivative (OP-41483) and the thromboxane A2 synthetase inhibitor (OKY-046), both of which inhibit platelet aggregation, were tested for possible beneficial effects on cerebral ischemia. Cerebral ischemia was produced in spontaneously hypertensive male rats using bilateral common carotid artery ligation (BLCL). Thrombocytopenia was produced with an antiplatelet antiserum which reduced the platelet count to less than 6 x 10(4)/microliters by 24 h. OP-41483 was administered four times hourly (500 ng/kg x 4, i.p.), beginning 1 h prior to BLCL. Similarly, OKY-046 was injected four times hourly (10 mg/kg x 4, i.p.). Brain metabolites such as ATP, lactate and pyruvate and water content were determined after 3 h of cerebral ischemia. Brain levels of ATP in the ischemic rats with thrombocytopenia were higher than those of the ischemic rats without thrombocytopenia. In addition, thrombocytopenia reduced the increase of lactate and water content in the ischemic brain. Animals treated with OP-41483 also maintained higher levels of ATP and lower levels of lactate and water compared to animals given a vehicle. OKY-046 significantly reduced brain water content, but had no effect on the ischemic alteration of brain metabolite levels. These results indicate that platelets play an important role in the progression of metabolic change during ischemia.

Adenosine Triphosphate↗