Biomedical subjects

T Okamura

Publications and source records attributed to T Okamura.

At least 145 records · Page 8Linked to original sources

PubMed2000

[A successful case of post operative management using nitrogen gas inhalation for a one-month old infant with high pulmonary blood flow].

We report a successful case of post operative management by inhaling nitrogen gas for a one-month old infant with high pulmonary blood flow after Blalock-Taussig shunt and plasty of the pulmonary artery. The operation was performed under extracorporial circulation. Nitrogen gas inhalation was dramatically effective for this infant to stabilize his post operative hemodynamic state. This therapy appears to be a very useful and easy handling technique in postoperative management for a patient with high pulmonary blood flow.

Abnormalities, Multiple↗

PubMed1999

Inhibition by adrenomedullin of amine release from adrenergic nerves in dog mesenteric arteries.

Adrenomedullin and calcitonin gene-related peptide (CGRP) inhibited the pressor response to transmural electrical stimulation in perfused isolated canine mesenteric arteries. The response was abolished by treatment with either prazosin or tetrodotoxin. Adrenomedullin-(22-52), an adrenomedullin receptor antagonist, reduced the inhibitory effect of adrenomedullin (10(-10) to 10(-8) mol/l), but did not alter the action of CGRP. CGRP-(8-37), a CGRP(1) receptor antagonist, did not affect the inhibition induced by adrenomedullin, but reversed the CGRP-induced inhibition. In helical strips of the arteries, adrenomedullin (up to 10(-8) mol/l) did not influence the contraction induced by noradrenaline, whereas CGRP attenuated the response. Adrenomedullin decreased the release of noradrenaline from adrenergic nerves elicited by transmural electrical stimulation, but CGRP had no effect. Adrenomedullin-(22-52) reversed the decrease in noradrenaline release induced by adrenomedullin. The adrenomedullin-induced relaxation of vascular strips precontracted with prostaglandin F(2alpha) was suppressed by CGRP-(8-37) but was unaffected by adrenomedullin-(22-52). These findings suggest that adrenomedullin impairs noradrenaline release from adrenergic nerves by acting on adrenomedullin receptors located in the nerve terminals, whereas arterial relaxation caused by adrenomedullin and CGRP is due to activation of CGRP(1) receptors in vascular smooth muscle.

Adrenergic Fibers↗

PubMed1999

Cytogenetic alterations in pituitary adenomas detected by comparative genomic hybridization.

Pituitary adenomas are benign monoclonal tumors that are either hormonally functional or nonfunctional. Although their histologic and immunocytologic characteristics have been studied extensively, cytogenetic studies are scarce. We have investigated the cytogenetic alterations and DNA ploidy patterns of 12 sporadic pituitary adenomas, including 2 growth-hormone-secreting tumors, 1 prolactinoma, and 9 nonfunctional adenomas, by comparative genomic hybridization (CGH) and laser scanning cytometry (LSC). CGH revealed that the mean number of sites of copy gain was significantly higher in functioning adenomas than in nonfunctioning tumors (P < 0.01). The most frequent change detected was loss of 13q (5 cases), with a minimal common overlapping region at 13q14. These findings suggest that a putative tumor suppressor gene on 13q14 may play an important role in the development of pituitary adenomas. DNA aneuploidy was detected by LSC in 3 of the 12 cases. The DNA aneuploid adenomas showed cytogenetic changes more frequently than did the DNA diploid tumors (P < 0.02).

Adenoma↗

PubMed1999

Promoting effects of intravesical instillation of saline on bladder lesion development in rats pretreated with N-butyl-N-(4-hydroxybutyl) nitrosamine are inhibited by bacillus Calmette-Guerin.

The promoting effects of intravesical instillation of saline and the efficacy of bacillus Calmette-Guerin (BCG) for prophylaxis of bladder carcinogenesis were assessed. Rats were given 0.05% N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) for 10 weeks; they were then given 6 weekly intravesical instillations of BCG, saline or distilled water starting 1 week or 15 weeks after the BBN treatment. At 32 weeks, both the incidences and numbers of bladder cancers were elevated in animals receiving the saline. An exception was the early phase BCG group. Significant increases in tumor size were also noted for the saline, but not the distilled water group. The results indicate that intravesical instillation of saline promotes urinary bladder carcinogenesis. However, the inhibitory influence of BCG was suggested if administered at the early, but not the late phase, of carcinogenesis.

Animals↗

PubMed1999

Influence of denervation on neurogenic inhibitory response of corpus cavernosum and nitric oxide synthase histochemistry.

Aims of this study were to functionally and histologically determine the localization of ganglia that distribute inhibitory nerves to the penile corpus cavernosum in dogs. In isolated corpus cavernosa from seven control dogs contracted with endothelin-1, transmural electrical stimulation (5 Hz for 40 s) elicited contractions which were reversed to relaxations by prazosin. The relaxation was abolished by NG-nitro-l-arginine (l-NNA), a nitric oxide (NO) synthase inhibitor, and restored by l-arginine. Parts of bilateral pelvic nerve plexuses running to the penis were surgically denervated in anesthetized three dogs, or the bilateral neuronal tissues close to the corpus cavernosum were removed for denervation in seven dogs. One week after the operation, the dogs were sacrificed. Denervation of pelvic plexus did not attenuate neurogenic relaxations, whereas denervation of the distal portion abolished the responses. In the tissues close to the corpus cavernosum excised for denervation, ganglia containing abundant nerve cells and fibers stained by nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase method were histochemically detected. One week after the denervation, there were no NADPH diaphorase-positive nerve fibers in the trabecula of corpus cavernosum. It is concluded that neurogenic relaxations of canine corpus cavernosum are mediated by NO synthesized from l-arginine in nerve terminals, and this nerve is originated from ganglia located close to the corpus cavernosum but not directly from the pelvic nerve plexus.

Adenosine Triphosphate↗

PubMed1999

Clonal change of infiltrating T-cells in children with familial hemophagocytic lymphohistiocytosis: possible association with Epstein-Barr virus infection.

BACKGROUND: Although familial hemophagocytic lymphohistiocytosis (FHL) has been considered a T-cell disorder, to the authors' knowledge there are no previous reports on the clonal basis of FHL. In the current study the authors analyzed the clonality of T-cells in two FHL patients at the time of disease onset and at disease progression. METHODS: Patient 1 had FHL and died of recurrent disease 4 months after bone marrow transplantation (BMT). His liver and spleen showed massive infiltrations of CD3+, CD4-, and CD8+ T-cells. The Epstein-Barr virus (EBV) genome was detected by in situ hybridization. Patient 2 also had FHL and died of progressive disease 9 weeks after the onset of disease despite chemotherapy. A polymerase chain reaction (PCR) analysis showed positive EBV genome in the peripheral blood, liver, and spleen of Patient 2. In the two patients, T-cell receptor-beta and alpha-chain variable region (TCR Vbeta and V alpha) repertoires in peripheral mononuclear cells were analyzed at the time of disease onset and at disease progression by the inverse PCR method. When a high usage (> 15%) of a specific Vbeta family member was observed, a clonal analysis was performed by PCR using beta-chain joining region (Jbeta) primers. The clonality of specific Vbeta-Jbeta fragments was confirmed by a single strand confirmation polymorphism (SSCP) analysis. RESULTS: Although there was no preferential usage of Vbeta in Patient 1, the exclusive expression of Jbeta1.2 for Vbeta13 was observed. A high frequency of Vbeta13 also was observed at the time of disease progression, but the Jbeta fragment for Vbeta13 was polyclonal. In Patient 2, the restricted usage of Jbeta1.6 for Vbeta5a was observed at the time of disease onset, whereas Jbeta1.1 and 1.2 for Vbeta4 were observed exclusively at the time of disease progression. The clonality of Vbeta13-Jbeta1.2 in Patient 1 and Vbeta5a-Jbeta1.6 and Vbeta4-Jbeta1.1/Jbeta1.2 in Patient 2 was confirmed by SSCP analysis. CONCLUSIONS: These findings suggest that the polyclonal T-cell lymphoproliferative disease associated with EBV was induced after BMT in Patient 1, and that the clonal change of expanded T-cells also was induced by EBV in Patient 2. The clonal analysis of T-cells is a useful tool to clarify the pathogenesis of FHL.

Disease Progression↗

PubMed1999

Mechanisms underlying the neurogenic relaxation of isolated porcine sphincter pupillae.

Mechanisms of relaxation induced by nerve stimulation were examined in isolated porcine iris sphincter muscle in reference to norepinephrine, nitric oxide (NO) and vasoactive intestinal polypeptide (VIP) and the functional interaction of inhibitory and excitatory nerves. Changes in isometric tension were recorded in strips of the sphincter pupillae, which were stimulated by transmurally applied electrical pulses. The presence of neurons containing acetylcholinesterase and tyrosine hydroxylase (TH) was determined histochemically. Transmural electrical stimulation (0.5-20 Hz) produced a frequency-related contraction, which was reversed to a relaxation by atropine in prostaglandin F2alpha-contracted strips. The relaxant response was abolished by timolol and suppressed by metoprolol, a beta1-adrenoceptor antagonist, but was not influenced by butoxamine, a beta2-receptor antagonist. Norepinephrine-induced relaxations were also attenuated only by timolol and metoprolol. Treatment with NG-nitro-L-arginine, a NO synthase inhibitor, and [D-p-Cl-Phe6,Leu17]VIP, a VIP receptor antagonist, did not inhibit the neurogenic relaxation. Contractions induced by nerve stimulation were potentiated by timolol and physostigmine but not by the NO synthase inhibitor. In the sphincter muscle, cholinesterase- and TH-positive nerve fibers and bundles were histologically detected. It is concluded that porcine iris sphincter is innervated by cholinergic excitatory and adrenergic inhibitory nerves. The neurogenic relaxation is associated solely with activation of beta1 adrenoceptors by norepinephrine but is not mediated by NO or VIP.

Acetylcholinesterase↗

PubMed1999

Thallium and FDG uptake by atelectasis with bronchogenic carcinoma.

We report a case of bronchogenic carcinoma with atelectasis studied by T1-SPECT and FDG-PET. In the carcinoma, abnormally high uptake of T1 and FDG were detected, but in the region of atelectasis, an abnormally high uptake of T1 with a relatively low uptake of FDG were observed. On quantitative analyses, the T1 retention indexes of the tumor and atelectasis were 29.7 and 42.0. The mean SUVs of FDG of the tumor and the atelectasis were 8.92 and 1.28. T1-SPECT could not distinguish the atelectasis from the carcinoma. FDG-PET was superior to T1-SPECT in this case in detecting malignancy and distinguishing it from atelectasis.

Biological Transport↗

PubMed1999

Two cases of chronic tonsillitis studied by FDG-PET.

We report two cases of chronic tonsillitis studied by FDG-PET. Symmetrical high FDG uptake by the tonsils was observed in both cases. On histopathologic examination of the resected tonsils, follicular hyperplasia was observed with proliferation of lymphocytes in the germinal centers. Increased glucose metabolism in active inflammation involving lymphocyte proliferation was thought to be a cause of high FDG uptake by tonsils in chronic tonsillitis.

Adolescent↗

PubMed1999

Cases of cutaneous and nasal CD56 (NCAM)-positive lymphoma in Japan have differences in immunohistology, genotype, and etiology.

CD56 (NCAM)-positive lymphoma frequently involves the skin and nasal area. This study shows it is likely that the clinicopathologic features of this lymphoma are distinctive to each of the primarily involved sites. Sixteen cutaneous and 11 nasal cases of CD56-positive lymphoma were examined. In 10 cutaneous cases, the lesions consisted of pleomorphic large-cell lymphoma that expressed CD3epsilon (CD3), CD2 (LFA2), CD4, CD122 (IL-2B receptor), TIA1, perforin, and granzyme B and displayed angiocentric/angiodestructive features. Lobular panniculitis was found in 8 of these cases, and 6 cases showed other organ involvement. The remaining 6 cutaneous cases consisted mostly of CD3epsilon- and CD4-positive, CD2-, CD122-, and TIA1-negative large blastic lymphoma, having less angiodestruction and panniculitis. Bone marrow invasion and leukemic changes were found in 4 of these cases during the clinical course. All 11 nasal cases showed pleomorphic small and medium-size lymphoma cells with angiodestructive features and were positive for CD3epsilon, CD2, CD122, TIA1, perforin, and granzyme B. CD4-positive lymphoma was found in 4 of these cases. Only 3 nasal cases showed other organ involvement. Genotypically, 2 of the 4 cases examined in the first cutaneous group, 3 of the 4 cases examined in the second cutaneous group, and only 1 of the 11 nasal cases showed rearrangement of the TcRCbeta gene by the Southern blot method. Only 2 cutaneous cases with panniculitis and all 11 nasal cases showed a positive nuclear signal for EBV-encoded RNA (EBERs) by in situ hybridization. Thus, two types of cutaneous CD56-positive lymphoma were found, each having a unique cell characteristic, genotype, and EBV infection pattern that differed from that of nasal-type lymphoma.

Adult↗

PubMed1999

Free radical production in endothelial cells as a pathogenetic factor for vascular dysfunction in the insulin resistance state.

Impairment of nitric oxide-dependent vascular relaxation is a characteristic feature of the insulin-resistant state. To understand those mechanisms, we examined imbalance of O2-/NO production in aortic endothelial cells obtained from high fructose-fed, exogenous hyperinsulinemic, and control rats. Aortic segments from both high fructose-fed and insulin-treated rats produced a 4-fold more O2- than control rats evaluated by a chemiluminescence method. The O2- production in the aortas of both high fructose-fed and insulin-treated rats was mediated through activation of NADH/NADPH oxidase. In isometric tension studies, high fructose vessels with endothelium elicited impaired relaxation in response to acetylcholine or a calcium ionophore A23187 when compared with control rats, whereas these impaired vascular responses were not found in insulin-treated rats. Furthermore, endothelial constitutive NO synthase activity was increased in vessels from insulin-treated rats, but decreased in vessels from high fructose-fed rats. These results indicate that relative excess of O2- production through activation of NADH/NADPH oxidase over NO generation in endothelial cells may contribute to impaired endothelial-dependent relaxation in insulin-resistant state.

Acetylcholine↗

PubMed1999

Effects of endothelial impairment by saponin on the responses to vasodilators and nitrergic nerve stimulation in isolated canine corpus cavernosum.

1. Responsiveness to EDRF-releasing substances and inhibitory nerve stimulation of canine isolated penile corpus cavernosum with and without saponin treatment were investigated. 2. Histological studies demonstrated that saponin did not detach endothelial cells from underlying tissues, but induced degenerative changes in the endothelial cells selectively. 3. In the cavernous strips contracted with phenylephrine, addition of acetylcholine, sodium nitroprusside, ATP and Ca2+ ionophore A23187 induced relaxations, but substance P and bradykinin did not change the muscle tone. 4. Acetylcholine-induced relaxation was significantly attenuated but not abolished by NG-nitro-L-arginine (L-NOARG). L-arginine restored the response inhibited by L-NOARG. The L-NOARG resistant relaxation was not influenced by 1H[1,2,4]oxadiazole[4,3-a]quinoxalin-1-one (ODQ) but was suppressed in the strips contracted with K+. Treatment with saponin abolished the relaxation elicited by acetylcholine and A23187 but did not influence the response to nitroprusside and ATP. The ATP-induced relaxation was attenuated by aminophylline. 5. Transmural electrical stimulation at 2-20 Hz produced endothelium-independent relaxations which were abolished by tetrodotoxin and L-NOARG but unaffected by treatment with saponin. In saponin-treated cavernous strips, the neurogenic relaxation was not affected by acetylcholine, physostigmine, atropine and vasoactive intestinal peptide (VIP) but was abolished by ODQ. 6. It is concluded that acetylcholine-induced relaxations are endothelium-dependent and mediated partly by NO and also by other substances from the endothelium. The endothelium-independent relaxation to ATP is likely to be mediated by P1 purinoceptors. The function of nitrergic nerve does not seem to be prejunctionally modulated by acetylcholine and VIP.

Acetylcholine↗

PubMed1999

Involvement of CYP3A-derived arachidonic acid metabolite(s) in responses to endothelium-derived K+ channel opening substance in monkey lingual artery.

1. In monkey lingual artery strips partially contracted with prostaglandin F2alpha, acetylcholine-induced, concentration-related relaxations were abolished by removal of the endothelium. The response was not significantly influenced by indomethacin but attenuated by NG-nitro-L-arginine (L-NOARG); the effect of the nitric oxide (NO) synthase inhibitor was reversed by L-arginine. 2. The response to acetylcholine resistant to L-NOARG was suppressed in the strips exposed to high K+ media. Charybdotoxin partially inhibited the relaxation, and the remaining relaxation was abolished by additional treatment with apamin, whereas glibenclamide, iberiotoxin or apamin alone was without effect. Relaxations induced by sodium nitroprusside were not influenced by charybdotoxin. 3. The L-NOARG-resistant acetylcholine-induced relaxation was inhibited by metyrapone, proadifen and 17-octadecynoic acid, non-selective cytochrome P450 mono-oxygenase (CYP) inhibitors, and progesterone and ketoconazole, inhibitors selective to CYP3A. The inhibitors did not affect the nitroprusside-induced relaxation. Selective inhibitors of other CYP isoforms, such as debrisoquine and lauric acid, did not reduce the response to acetylcholine. 4. Reaction mixture containing human liver microsome rich in CYPs, arachidonic acid and NADPH incubated at 37 degrees C and filtrated relaxed endothelium-denuded monkey lingual artery strips, used as bioassay tissues. This response was abolished in the strips exposed to high K+ media. The response was also suppressed by combined treatment of the assay tissue with charybdotoxin plus apamin, but was not affected by treatment with iberiotoxin. The reaction mixture co-incubated with ketoconazole failed to relax the strips. 5. It is concluded that the monkey lingual arterial relaxation dependent on the endothelium is mediated by NO and also by a charybdotoxin plus apamin-sensitive but iberiotoxin-insensitive Ca2+-activated K+ channel opening substance(s) that may be a CYP3A-derived arachidonic acid metabolite(s).

Animals↗

PubMed1999

Frequent chromosome arm 13q deletion in aggressive non-Hodgkin's lymphoma.

To clarify the role of allelic loss on chromosome arm 13q in lymphomagenesis, we performed fluorescence in situ hybridization (FISH) analysis of a total of 43 primary lymphomas, including both indolent and aggressive non-Hodgkin's lymphoma (NHL) and Hodgkin's disease (HD), using the specific probes at RB1 and D13S319 loci on the centromeric portion of chromosome arm 13q. Monosomy at either or both RB1 and D13S319 loci was detected in 15 of 43 (35%) lymphomas (14 of 43 cases at RB1 locus and seven of 43 cases at D13S319 locus); the 13q deletion was frequently detected in the aggressive NHLs (40%; 12 of 30 cases) compared with that in indolent NHL (17%; one of six cases) and a subset of HD (29%; two of seven cases). There are only six cases of 43 which have total monosomy 13q14, all aggressive NHL, 14% of total or 20% of this subgroup. In addition, we analyzed the loss of heterozygosity in 15 of the 43 primary lymphoma samples for several polymorphic microsatellite loci (D13S168, RB1 and D13S272) on the chromosome arm 13q, and confirmed the 13q deletion in four of five cases that were positive on FISH analysis. The subchromosomal region frequently altered in lymphoma on 13q14 is the region around RB1 locus and centromeric to D13S319 locus, which is an overlapped region frequently deleted in chronic lymphocytic leukemia. Together, our data indicate that the 13q alterations are present in a variety of types of lymphoma and occur in a significant proportion of aggressive NHLs, suggesting the possible presence of common candidate gene(s) on the 13q14 region, whose alteration may play an important role in the formation or development of a wide variety of mature lymphoid malignancies.

Adult↗

PubMed1999

Multiple autoimmune haemopoietic disorders and insidious clonal proliferation of large granular lymphocytes.

We report a patient with clonal proliferation of CD3+8+TCRalphabeta+ large granular lymphocytes (LGL) presenting multiple episodes of autoimmune cytopenia, including autoimmune neutropenia, idiopathic thrombocytopenic purpura, autoimmune haemolytic anaemia, and pure red cell aplasia. Each disorder appeared separately or as a combination during an 11-year clinical course. The increase of blood CD3+8+TCRalphabeta+ LGL was detected 6 years after the initial diagnosis of cytopenia, but the absolute number of LGL cells was always < 1.0 x 109/l. LGL cells were of monoclonal origin and had a chromosomal abnormality. LGL cells transiently responded to cyclosporine A therapy, which was also effective on all of these autoimmune cytopenias. Accordingly, an undetectable level of proliferation of a clonal LGL population could cause various autoimmune haemopoietic disorders.

Adolescent↗

PubMed1999

Mechanisms underlying arginine vasopressin-induced relaxation in monkey isolated coronary arteries.

OBJECTIVE: The present study was undertaken to examine whether arginine vasopressin (AVP) relaxes primate coronary artery and to analyse the mechanisms of its action in reference to endothelial nitric oxide and AVP receptor subtype. METHODS: Isometrical tension responses to AVP and desmopressin were recorded in isolated monkey coronary arteries. RESULTS: AVP (10(-9) to 10(-7) mol/l) induced a concentration-related relaxation; endothelium-denudation abolished the response. Treatment with N(G)-nitro-L-arginine, but not the D-enantiomer, abolished the endothelium-dependent relaxation, which was restored by L-arginine. Treatment with SR49059 and [Pmp1,Tyr(Me)2]-Arg8-vasopressin, selective inhibitors of V1 receptor subtype, attenuated the relaxant response to AVP, whereas the relaxation induced by sodium nitroprusside was not affected by SR49059. Desmopressin, a V2 receptor agonist, up to 10(-8) mol/l did not elicit relaxation. CONCLUSIONS: It is concluded that AVP-induced monkey coronary arterial relaxation is mediated via nitric oxide synthesized from L-arginine in association with stimulation of V1 receptor subtypes in the endothelium.

Animals↗

PubMed1999

Neurogenic vasodilation mediated by nitric oxide in porcine cerebral arteries.

Mechanisms of neurogenic vasodilatation and its modification by superoxide, acetylcholine, and vasoactive intestinal peptide (VIP) in porcine cerebral arteries were investigated. Relaxant responses to transmural electrical stimulation and nicotine of cerebral artery strips without endothelium were abolished by tetrodotoxin and hexamethonium, respectively. N(G)-nitro-L-arginine, a nitric oxide (NO) synthase inhibitor, abolished or markedly reduced the neurogenic response but did not affect the relaxation by exogenous NO. The inhibitory effect was reversed by L-arginine. Duroquinone, a superoxide-generating agent, did not alter the relaxations induced by electrical stimulation and nicotine. However, in the strips treated with diethyldithiocarbamate, an inhibitor of copper/zinc superoxide dismutase (SOD), the responses were significantly inhibited by duroquinone. The inhibition was partially reversed by SOD. Physostigmine inhibited, but atropine potentiated, the neurogenic response. The relaxation was attenuated by acetylcholine but not by VIP. There were nerve fibers and bundles containing NADPH diaphorase in the adventitia of cerebral arteries. It appears that porcine cerebral arteries are innervated by NO synthase-containing nerves that liberate NO on excitation as a neurotransmitter to produce muscular relaxation, and the nerve function is protected by endogenous SOD from degradation of NO by superoxide anions. The neurogenic relaxation is inhibited by acetylcholine released from cholinergic nerves, possibly because of an impaired production or release of NO.

Acetylcholine↗

PubMed1999

Calpain inhibitor-1 reduces infarct size and DNA fragmentation of myocardium in ischemic/reperfused rat heart.

Myocardial ischemia/reperfusion activates a calcium-dependent protease, calpain, in the ischemic myocytes. It is not known whether calpain is involved in the mechanism of ischemia/reperfusion injury in hearts. Thus the purpose of this study was to clarify the effect of a selective calpain inhibitor (CAI) on infarct size and the extent of DNA damage in ischemic/reperfused rat hearts. Rats were divided in four groups (n = 7 each). In saline group, 0.3 ml of saline was administered (i.v.) 10 min before 30-min coronary occlusion followed by 6-h reperfusion. In vehicle group, 0.3 ml of 10% dimethyl sulfoxide (DMSO) was administered 10 min before the 30-min ischemia. CAI (0.5 mg/kg) was administered 10 min before the 30-min ischemia (CAI-A group) and 10 min before the 6-h reperfusion period (CAI-B group). Infarct size was detected with triphenyl tetrazolium chloride, and DNA fragmentation was detected by agarose gel electrophoresis and by in situ nick end labeling (ISEL). Infarct size was significantly smaller in the CAI-A group compared with the vehicle group (13+/-9% vs. 48+/-12%; p < 0.01), and the incidence of ISEL-positive myocyte nuclei in the subendocardial region was significantly reduced in the CAI-A group compared with the vehicle group (26+/-3% vs. 59+/-6%; p < 0.01). However, the effects of CAI in CAI-B group were not significant. Activation of calpain is involved in the mechanism of ischemia/reperfusion injury, and the preischemic administration of CAI was effective in reducing myocardial infarct size and the DNA damage of the myocytes in ischemic/reperfused rat heart.

Animals↗