Inclusive prompt photon production in hadronic final states of e+e- annihilation.
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Journal Article↗
Biomedical subjects
X Guo
Publications and source records attributed to X Guo.
Two-stage global search designs for linkage analysis using pairs of affected relatives.
We investigate the two-stage procedure proposed by Elston [(1992) Proceedings of the XVIth International Biometric Conference, Hamilton, New Zealand, December 7-11, 1992, pp 39-51, and (1994) "Genetic Approaches to Mental Disorders." Washington, DC: American Psychiatric Press, pp 3-21] for performing a global search of the genome to locate disease genes by linkage analysis using affected relative pairs. The optimal design depends on the type of pairs studied, the effect of the disease locus, the relative costs of recruiting affected persons and typing markers, how informative the markers are, and the amount of genetic heterogeneity. It is specified by the initial number of markers to use, the number of affected relative pairs to study, the initial significance level alpha* to use at the first stage, and the number of flanking markers to use at the second stage around markers significant at the first stage. Asymptotically, the optimal design does not depend separately on either the desired final significance level or power, but rather on a function of the two. Both as the effect of the disease locus increases and as the relative cost of recruiting a subject increases, the optimal number of initial markers increases and the optimal number of pairs decreases. The expected cost of the study decreases as the effect of the disease locus increases, but increases as the relative cost of recruiting a subject increases. The optimal initial number of markers decreases but the number of pairs increases when there is genetic heterogeneity present; conversely, the optimal initial number of markers increases when markers are less than fully informative. Compared to a one-stage procedure, a two-stage procedure typically halves the cost of a study.
Epidemiologic Methods↗
The effects of extracellular matrix and osteogenic protein-1 on the morphological differentiation of rat sympathetic neurons.
The growth patterns of axons and dendrites differ with respect to their number, length, branching, and spatial orientation; therefore, it is likely that these processes differ in their growth requirements. To examine this hypothesis, we have been analyzing the responses of cultured rat sympathetic neurons to three types of stimuli: large structural proteins of the extracellular matrix, matrix-associated growth factors, and neurotrophins. Purified structural proteins such as laminin and collagen IV have been found to promote only axonal growth; whereas the matrix associated growth factor, osteogenic protein-1, selectively stimulates dendritic growth. In contrast, nerve growth factor modulates the growth of both types of processes. These data suggest that process-specific interactions with the extracellular environment may be critical determinants of cell shape in neurons. Perinatal rat sympathetic neurons grown in culture in the absence of serum or glial cells extend a single process which is axonal in nature. Exposure to osteogenic protein-1 causes the formation of additional processes which express the morphological, cytoskeletal, and ultrastructural characteristics of dendrites. Consistent with observations on the regulation of dendritic growth in sympathetic neurons in situ, the dendrite-promoting activity of osteogenic protein-1 is independent of synaptic or electrical activity, but is modulated by nerve growth factor. In the presence of optimal concentrations of osteogenic protein-1 and nerve growth factor, the size of the dendritic arbor extended by cultured sympathetic neurons approximates that seen in situ at comparable developmental stages. Osteogenic protein-1 does not promote dendritic growth in cultured neurons obtained from embryonic ciliary, dorsal root, trigeminal or nodose ganglia, suggesting that its morphogenetic effects are cell selective. Since mRNA for osteogenic protein-1 is expressed in mature as well as embryonic target tissues of the sympathetic nervous system, we also examined the effects of osteogenic protein-1 on cultures of sympathetic neurons derived from adult rats. Consistent with results obtained with perinatal neurons, osteogenic protein-1 selectively promoted dendritic growth in adult neurons. These data suggest that this matrix-associated growth factor could play a role not only in the morphogenesis of the developing nervous system, but also in the maintenance and remodeling of dendritic structures in the mature animal.
Animals↗
The influence of buffer species and strength on diltiazem HCl release from beads coated with the aqueous cationic polymer dispersions, Eudragit RS, RL 30D.
PURPOSE: Eudragit RL and RS 30D are pseudolatexes frequently used in the coating of solid dosage forms. They are based on cationic copolymers stabilized with quaternary ammonium groups (poly(ethylacrylate-methylmethacrylate-trimethylammonioethyl methacrylate chloride). A pH-independent drug release is expected because of the quaternary nature of the cationic groups. The objective was to explain a distinct "pH-dependent" drug release in various buffer media with coated diltiazem beads. METHODS: The diltiazem HCl release from and water uptake of Eudragit RS/RL-coated beads was determined in various buffers of different buffer species, pH or concentration. RESULTS: The drug release in the different buffer media was in the following order: pH 5.0 acetate > pH 3.5 formate > pH 7.4 phosphate buffer > 0.1M HCl). This "pH-dependent" drug release could be explained with an anion exchange process; the chloride counterions of the quaternary groups were exchanged with the anionic buffer species during the dissolution study. The water uptake of the coated beads correlated well with the drug release from the beads. Increasing the buffer strength (acetate buffer) first increased and then decreased the drug release, while increasing the ionic strength of different buffers with NaCl decreased the drug release and eliminated the observed buffer effects because of the excess of chloride ions. CONCLUSIONS: The anionic buffer species and not the pH had a significant effect on the hydration and hence on the drug release from beads coated with the cationic polymers, Eudragit RS and RL.
Acrylic Resins↗
Exocytosis coupled to mobilization of intracellular calcium by muscarine and caffeine in rat chromaffin cells.
We used cultured rat chromaffin cells to test the hypothesis that Ca2+ entry but not release from internal stores is utilized for exocytosis. Two protocols were used to identify internal versus external Ca2+ sources: (a) Ca2+ surrounding single cells was transiently displaced by applying agonist with or without Ca2+ from an ejection pipette. (b) Intracellular stores of Ca2+ were depleted by soaking cells in Ca2+ -free plus 1 mM EGTA solution before transient exposure to agonist plus Ca2+. Exocytosis from individual cells was measured by microelectrochemical detection, and the intracellular Ca2+ concentration ([Ca2+]i) was measured by indo-1 fluorescence. KCl (35 mM) and nicotine (10 microM) caused an immediate increase in [Ca2+]i and secretion in cells with or without internal Ca2+ stores, but only when applied with Ca2+ in the ejection pipette. Caffeine (10 mM) and muscarine (30 microM) evoked exocytosis whether or not Ca2+ was included in the pipette, but neither produced responses in cells depleted of internal Ca2+ stores. Pretreatment with ryanodine (0.1 microM) inhibited caffeine- but not muscarine-stimulated responses. Elevated [Ca2+]i and exocytosis exhibited long latency to onset after stimulation by caffeine (2.9 +/- 0.38 s) or muscarine (2.2 +/- 0.25 s). However, the duration of caffeine-evoked exocytosis (7.1 +/- 0.8 s) was significantly shorter than that evoked by muscarine (33.1 +/- 3.5 s). The duration of caffeine-evoked exocytosis was not affected by changing the application period between 0.5 and 30 s. An approximately 20-s refractory period was found between repeated caffeine-evoked exocytosis bursts even though [Ca2+]i continued to be elevated. However, muscarine or nicotine could evoke exocytosis during the caffeine refractory period. We conclude that muscarine and caffeine mobilize different internal Ca2+ stores and that both are coupled to exocytosis in rat chromaffin cells. The nicotinic component of acetylcholine action depends primarily on influx of external Ca2+. These results and conclusions are consistent with our original observations in the perfused adrenal gland.
Adrenal Glands↗
2'-deoxyadenosine induces apoptosis in rat chromaffin cells.
We show here that 2'-deoxyadenosine (2'-dAdo) but not adenosine was toxic to chromaffin cells of 3-4-week-old rat adrenal glands. More than 75% of the cells plated in culture gradually died over a 3-day period in the presence of 100 microM 2'-dAdo plus 3 microM deoxycoformycin (DCF). Morphological observations together with bisbenzimide staining and terminal deoxynucleotidyl transferase-mediated nick and labeling showed membrane blebbing, shrinkage of cell bodies, chromatin condensation, and DNA fragmentation, suggesting apoptosis-like cell death by 2'-dAdo. Lethal effects of 2'-dAdo were potentiated by DCF, a drug that inhibits adenosine deaminase. 2'-dAdo-prompted cell death was not prevented by inhibitors of nucleoside transporter (3 microM dilazep or 1 microM nitrobenzylthioinosine), precursors of pyrimidine nucleotide biosynthesis (300 microM uridine or 100 microM 2'-deoxycytidine), or 5 mM nicotinamide. Cells incubated with 2'-dAdo (100 and 300 microM) showed a three- and ninefold, respectively, increase in content of dATP, a product known to be an inhibitor of ribonucleotide reductase, an enzyme essential for DNA synthesis. Formation of dATP was completely prevented by iodotubercidin (ITu), a drug that inhibits phosphorylation of 2'-dAdo to dATP by nucleoside kinase. It is interesting that nanomolar concentrations of ITu also completely protected chromaffin cells from 2'-dAdo lethality. Our study demonstrates for the first time that mammalian adrenal chromaffin cells undergo apoptotic cell death by a natural nucleoside and suggests that this model could be used to study apoptosis and cell function.
Adenosine↗
Sample sizes for experiments with multivariate repeated measures.
Procedures for determining sample size in multivariate repeated measures experiments are discussed. The focus is on designs with either one group or two independent groups of subjects, the point of departure being multivariate repeated measures. Determination of the minimum sample size required is based on power considerations associated with Hotelling's T2 and the F-test. We first consider procedures for determining sample size assuming an arbitrary covariance matrix. The special case where we assume that the transformed data have a multivariate spherical covariance matrix is also considered. Tables of the minimum sample sizes required for several hypotheses from multivariate analysis are presented.
Mathematical Computing↗
Effect of cyclic GMP reduction on regional myocardial mechanics and metabolism in experimental left ventricular hypertrophy.
We tested the hypotheses that decreased myocardial cyclic GMP levels produced by intracoronary injection of methylene blue would increase local myocardial work and O2 consumption while decreasing intracellular cyclic GMP and that the relation between work, O2 consumption, and cyclic GMP may be altered in left ventricular hypertrophy (LVH) produced by aortic valve plication. In 8 control and 8 LVH open-chest anesthetized dogs, 1 mg/kg/min methylene blue was infused into the left anterior descending coronary artery (LAD); the circumflex region (CFX) served as control area. Regional work was calculated as the integrated product of force (miniature transducer) and segment shortening (sonomicrometry). Regional myocardial O2 consumption was calculated from flow measurements (radioactive microspheres), and regional O2 saturations (microspectrophotometry). A radioimmunoassay was used to determine intracellular level of cyclic GMP in the myocardium. Global hemodynamics and blood gases were unchanged by methylene blue in both control and LVH animals. Intracoronary methylene blue increased regional work from 762 +/- 129 to 1,451 +/- 307 g center dot mm/min in controls and from 912 +/- 173 to 1581 +/- 253 g center dot mm/min in the LVH groups. No significant changes in CFX regional work were observed. Regional blood flow, O2 extraction, and O2 consumption remained unchanged after injection of methylene blue in both control and LVH animals. The basal levels of cyclic GMP in the LVH group were fivefold higher than that in controls. In both groups, cyclic GMP levels were significantly decreased by methylene blue and to a greater extent in the LVH animals (from 6.16 +/- 1.2 to 3.34 +/- 0.44 pmol/g) than in the control animals (from 1.32 +/- 0.20 to 1.09 +/- 0.19 pmol/g). Therefore, intracoronary methylene blue increased regional myocardial work equally in control and LVH hearts without affecting regional metabolism (i.e., increased efficiency). For the same increased mechanical function, the hypertrophic myocardium exhibited a greater reduction in cyclic GMP pool size.
Animals↗
Nuclear dependence in direct photon production.
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Journal Article↗
Recruitment of purinergically stimulated Cl- channels from granule membrane to plasma membrane.
HT29-Cl.16E and HT29-Cl.19A are two different subcloned cell lines derived from the human adenocarcinoma cell line HT-29. They are similar in their ability to grow and differentiate to polarized epithelial cells but differ in that HT29-Cl.16E is goblet cell-like with many mucin granules, whereas HT29-Cl.19A lacks mucin granules. Extracellular ATP stimulates Cl- secretion in both cell lines through luminal purinergic P20 receptors and, in HT29-Cl.16E, also mucin secretion release. To evaluate whether fusion of mucin granules is associated with an increase in Cl- conductance of the plasma membrane, the effects of two fusion inhibitors on luminal Cl- conductance were measured. Blockage of actin depolymerization with phalloidin (1 microM) inhibited purinergically stimulated but not adenosine 3',5'-cyclic monophosphate (cAMP)-stimulated luminal Cl- efflux by 50% in HT29-Cl.16E. The same treatment was without effect in HT29-Cl.19A. The fungal metabolite wortmannin, which is an inhibitor of regulated exocytosis in leukocytes, at 100 nM inhibited Cl- secretion by 70% in HT29-Cl.16E. This inhibition was not a direct effect on purinergically stimulated Cl- channels because wortmannin concentrations of up to 1 microM did not affect the secretory response in HT29-Cl.19A. The wortmannin inhibition of Cl- secretion is associated with an inhibition of granule fusion as judged by electron microscopy. The differential inhibition of Cl- secretion in the related HT-29 clones that differ with respect to the presence of mucin granules indicates that 1) the granule fusion inhibitors, phalloidin and wortmannin, have no direct inhibitory effects on purinergically and cAMP-activated Cl- channels, 2) a major portion of purinergically but not cAMP-activated Cl- channels is associated with granule fusion in HT29-Cl.16E, and 3) the signaling pathways for Cl- secretion and granule fusion are not completely identical.
Actins↗
Cyclic ADP-ribose does not regulate sarcoplasmic reticulum Ca2+ release in intact cardiac myocytes.
Cyclic ADP-ribose (cADPR), an intracellular second messenger known to mobilize Ca2+ in sea urchin eggs, has been implicated in modulating Ca2+ release in a variety of mammalian tissues. On the basis of studies of isolated cardiac sarcoplasmic reticulum (SR) vesicles and single SR Ca2+ release channels, cADPR has also been proposed to be a modulator of SR Ca2+ release in heart. In the present study, we directly examined the ability of cADPR to trigger SR Ca2+ release and to modulate Ca(2+)-induced Ca2+ release (CICR) in intact rat ventricular myocytes. Voltage-clamped myocytes were dialyzed with up to 100 mumol/L caged cADPR and 0.6 mumol/L calmodulin along with the Ca(2+)-sensitive dye fluo 3. A step increase in the cADPR concentration induced by flash photolysis of caged cADPR neither directly triggered SR Ca2+ release nor modulated CICR in intact myocytes. In contrast, under similar conditions, extracellular application of caffeine (1 to 2.5 mmol/L) onto myocytes produced both effects. Under equivalent conditions, flash photolysis of caged cADPR-loaded sea urchin eggs resulted in large Ca2+ transients. Further, the sustained presence of high cytosolic concentrations of either cADPR or its antagonist, 8-amino-cADPR, was ineffective in altering normal CICR in myocytes. These findings indicate that cADPR does not regulate SR Ca2+ release in intact cardiac myocytes.
Adenosine Diphosphate Ribose↗
Genetic studies of a new mutant strain showing shivering in the mouse.
A new mutant with shivering, Hula dance Sendai (tentatively named hus gene), was found in the IVCE strain. A congenic strain, C57BL/6JJcl-hus, was established by the cross-intercross method using IVCE-hus as the donor strain and C57BL/6JJcl as the recipient. No significant differences were observed in the age of the onset of shivering and life span between B6-hus and IVCE-hus mice. Genetic analyses demonstrated that this mutation is governed by an autosomal recessive gene (Mbphus) and is an allele of the Mbpshi gene (Chr. 18).
Aging↗
Inhibitory effect of BQ-123 on endothelin-1-stimulated mitogen-activated protein kinase and cell growth of rat vascular smooth muscle cells.
Studies have suggested that endothelin-1 (ET-1) activates cellular contraction and proliferation in rat vascular smooth muscle cells (VSMC). We examined whether an ET(A) receptor antagonist, BQ-123, inhibits the following cellular actions of ET-1 in rat VSMC: cytosolic free calcium ([Ca2+]i) mobilization, cellular contraction, mitogen-activated protein (MAP) kinase activation, [3H]thymidine incorporation, and MTT reduction. [Ca2+]i was measured by the fluorescent method. MAP kinase activity was measured by the phosphorylation of a synthetic peptide of a specific substrate for MAP kinase. The specificity of BQ-123 for ET-1-activated MAP kinase was checked by Western blotting analysis. [3H]thymidine incorporation and MTT reduction studies were performed using the cells incubated for 12 h with serum-free medium containing effectors. BQ-123 inhibited ET-1 receptor binding and blocked [Ca2+]i mobilization, cellular contraction, MAP kinase activation, [3H]thymidine incorporation, and MTT reduction in response to ET-1. BQ-123 did not affect the arginine vasopressin (AVP)- and angiotensin II (Ang II)-induced increases in [Ca2+]i mobilization or in MAP kinase activity. Preincubation with BQ-123 did not enhance its inhibitory effects but these effects of BQ-123 were diminished by washing after preincubation. Receptor studies revealed that the washing procedure decreased the inhibitory effect of BQ-123 on ET-1 binding to receptors. These results indicate that BQ-123 is a potent and specific ET(A) receptor antagonist that blocks the ET-1-induced cellular contraction and proliferation in rat VSMC.
Angiotensin II↗
Complete interference and nonrandom distribution of meiotic crossover in a mollusc, Mulinia lateralis (Say).
In gene mapping, the genetic distance between two genes is measured by the frequency of meiotic crossovers occurring between them. It is generally assumed that there is more than one crossover per chromosome, and the distribution of crossovers along chromosomes is random and follows a Poisson distribution (no interference), or that interference is inversely correlated with distance. Although those assumptions may be correct for some organisms, we report here a novel exception in the marine mollusc Mulinia lateralis Say. Using segregation analysis of gynogenetic diploids, we found surprisingly high gene-centromere recombinant frequencies for most of the 13 allozyme loci studied. For at least six loci, there was always one and only one crossover occurring between the gene and its centromere, suggesting complete interference where the occurrence of one crossover completely suppressed the occurrence of another. The complete interference was confirmed by the cytogenetic observation that there was only one chiasma for all bivalents. Further, sites of the single crossover seem not to be randomly distributed along chromosomes, but preferentially located in a recombination hot-region proximal to the centromere. The restricted distribution of a single crossover per chromosome provides one explanation for the unique phenomenon of heterozygote deficiency in M. lateralis and other molluscs.
Animals↗
Activities of novel nonglycosidic epipodophyllotoxins in etoposide-sensitive and -resistant variants of human KB cells, P-388 cells, and in vivo multidrug-resistant murine leukemia cells.
Previous structure-activity studies of the antitumor compound etoposide (VP-16) have suggested that replacement of the glycoside moiety could afford therapeutically active analogues with different biochemical determinants for cellular accumulation and drug resistance. In the present report, 10 analogues of VP-16 in which the glycosidyl moiety was replaced with alkyl or arylamino substituents exhibited 5-10-fold better binding affinity for topoisomerase II/DNA complex in human KB cells. A similar increase in the binding affinity was observed in an isolated-nuclei model. The analogues displayed greater or comparable potency to VP-16 in cell growth-inhibition studies and were less affected by cell membrane-associated drug resistance mechanisms, as exemplified by overexpressions of P-glycoprotein multidrug-resistance gene or multidrug resistance-associated protein. Interestingly, in animal studies, analogues least affected by the membrane transport-deficiency phenotypes exhibited low therapeutic index values, thus suggesting that highly efficient modulation of cellular membrane transport defects could perturb the selectivity of antitumor agents for cancer cells. This report also suggests a new method of quantifying drug-induced protein-linked DNA breaks by graphically determining the apparent dissociation-inhibition constant (Kdi) for the inhibitors.
ATP Binding Cassette Transporter, Subfamily B, Mem↗
Action of acetylcholine on regional myocardial work and metabolism in vivo: association with cyclic GMP.
This study was designed to test the hypothesis that in the in vivo dog heart, increases in cyclic (c) GMP and also decreases in cAMP induced by intracoronary administration of acetylcholine are associated with depressed myocardial function. In 10 open-chest anesthetized dogs, 0.5 microgram.kg-1.min-1 of acetylcholine was infused into the left anterior descending coronary artery. The intracoronary infusion of acetylcholine was continued simultaneously with 0.1 microgram.kg-1.min-1 of isoproterenol. Regional segment work was calculated as the integrated product of force (auxotonic force transducer) and segment shortening (sonomicrometry). Regional myocardial O2 consumption was calculated from blood flow measurements and regional O2 saturations. Competitive radioligand binding assays were used to determine the intracellular level of cAMP and cGMP in the myocardium. Local intracoronary infusion of acetylcholine significantly reduced regional segment work (from 36.7 +/- 6.5 to 19.1 +/- 3.7 x 10(-3) J/min) and O2 consumption (from 6.4 +/- 0.8 to 3.8 +/- 0.7 mL O2.min-1.100 g-1). This was related to a decrease in cAMP levels (from 364 +/- 25 to 262 +/- 17 pmol/100 g) and an increase in cGMP levels (from 1.34 +/- 0.06 to 1.78 +/- 0.15 pmol/100 g). When isoproterenol (0.1 microgram.kg-1.min-1) was added to the acetylcholine infusion line, cAMP levels tripled to 769 +/- 84 pmol/100 g, while O2 consumption rose to 6.6 +/- 1.4 mL O2.min-1.100 g-1. However, regional work was only partially restored (25.7 +/- 4.8 x 10(-3) J/min). Thus, both cAMP decrements and cGMP elevation occurred together with the negative inotropic effect of acetylcholine, and increased cAMP alone (produced by isoproterenol) did not fully overcome the acetylcholine effect. This was associated with elevated intracellular levels of cGMP.
Acetylcholine↗
[Immunohistochemical double labelling studies on liver tissues superinfected with hepatitis C virus and hepatitis B virus].
OBJECTIVE: To explore the relatiship between hepatitis C virus (HCV) and hepatitis B virus (HBV) replication in liver tissue of patients superinfected with HCV and HBV. METHODS: The expresion and distribution of HCVAg and HBVAg in paraffin-embeded liver tissue from 25 autopsy cases were studied with immunohistochemical double labelling techniques using monoclonal anti-HCV NS3 and anti-HCV NS5 as well as polyclonal anti-HBs and anti-HBc. RESULTS: HBsAg and HCV NS3 or NS5 antigen were detected at the same section in 11 and 12 cases, and HBcAg and HCV NS3 or NS5 antigen in each 10 cases, respectively. Nearly all of the specimens with single labelling stained positive tissue for HC-VAg or HBVAg were also those positive with double labelling studies for HCVAg and HBVAg. The distribution of HCV and HBV infected hepatocytes was characterized as diffuse and single or cluster scattered in liver lobular. There were no differences in expression related to replication such as membranous, cytoplasmic type of HBsAg or cytoplasmic type of HBcAg and the cases positive for HCV NS3Ag or HCV NS5Ag between the group of HCV superinfected with HBV and the group infected with single HCV or HBV (chi 2 = 0.154 and 0.198, P > 0.05). CONCLUSION: The results suggested that there was no interference or suppression each other in liver tissues superinfected with HCV and HBV.
Hepacivirus↗
[The effects of cardioplegia and reperfusional blood containing captopril on myocardial ultrastructure alterations after cardiac arrest].
OBJECTIVE: To investigate the myocardial protective effect of captopril on the ischemia and reperfusion injury in the canine heart. METHODS: Twelve mongrel dogs were randomly divided into control and captopril groups. In the former, only modified St. Thomas cardioplegia was used, and in the latter, modified St. Thomas cardioplegia and reperfusional blood containing 4.6mumol/L captopril were used. Sixty minutes after reperfusion, myocardial renin activity (MRA), angiotensin II (AII) and melondyldialdehyde (MDA) content in myocardium were measured, and the subendocardial myocardium of the left ventricle was taken for electromicroscopy. RESULTS: The MRA in the Cp1 group was significantly higher than that in the control group (P < 0.01), while the AII and MDA content in the myocardium in the Cp1 group were significantly lower than those in the control group (P < 0.01). Electronmicroscopically, the damage of the myocardium including sarcomeres, mitochondria and microvascular endothelial cells were less obvious in the Cp1 group than that in the control. The mitochondrial average cross-section area and average volume (0.59 +/- 0.15 micron2 and 0.74 +/- 0.23 micron3) in the Cp1 group were significantly lower than those in the control (0.83 +/- 0.34 micron2, P < 0.01 and 1.1 +/- 0.4 micron3, P < 0.01). The numerical density (0.46 +/- 0.16 micron-3), specific surface of mitochondria (6.4 +/- 1.1 microns-1) and memberance density of mitochondrial cristae (21 +/- 10 microns-1) in the Cp1 group were significantly higher than those in the control (0.29 +/- 0.06 micron-3, P < 0.05, 4.8 +/- 0.8 micron-1, P < 0.01 and 15.3 +/- 2.0 microns-1, P < 0.01): CONCLUSION: Cardioplegia and reperfusional blood containing 4.6 mumol/L captopril could effectively protect the myocardial mitochondria and microvascular endothelial cells against ischemia and reperfusion injury.
Angiotensin-Converting Enzyme Inhibitors↗