Resonance measurement of nonlocal spin torque in a three-terminal magnetic device.

A pure spin current generated within a nonlocal spin valve can exert a spin-transfer torque on a nanomagnet. This nonlocal torque enables new design schemes for magnetic memory devices that do not require the application of large voltages across tunnel barriers that can suffer electrical breakdown. Here we report a quantitative measurement of this nonlocal spin torque using spin-torque-driven ferromagnetic resonance. Our measurement agrees well with the prediction of an effective circuit model for spin transport. Based on this model, we suggest strategies for optimizing the strength of nonlocal torque.

Room-temperature ferromagnetic nanotubes controlled by electron or hole doping.

Nanotubes and nanowires with both elemental (carbon or silicon) and multi-element compositions (such as compound semiconductors or oxides), and exhibiting electronic properties ranging from metallic to semiconducting, are being extensively investigated for use in device structures designed to control electron charge. However, another important degree of freedom--electron spin, the control of which underlies the operation of 'spintronic' devices--has been much less explored. This is probably due to the relative paucity of nanometre-scale ferromagnetic building blocks (in which electron spins are naturally aligned) from which spin-polarized electrons can be injected. Here we describe nanotubes of vanadium oxide (VO(x)), formed by controllable self-assembly, that are ferromagnetic at room temperature. The as-formed nanotubes are transformed from spin-frustrated semiconductors to ferromagnets by doping with either electrons or holes, potentially offering a route to spin control in nanotube-based heterostructures.

Comparison of changes in markers of muscle damage induced by eccentric exercise and ischemia/reperfusion.

To examine the effects of eccentric exercise (EE) and ischemia/reperfusion (I/R) on the markers of muscle damage, 72 rats were randomly assigned to the EE group, I/R group and control group (C), respectively. The rats in EE ran downhill on a treadmill with a 16 ° inclination at a constant speed for 90 min, and the rats in the I/R group underwent 90 min of four-limb ischemia, followed by 24, 48 and 72 h of reperfusion. Blood and tissue samples were collected immediately, 24, 48 and 72 h after exercise or reperfusion. Quantitative analyses showed that the I/R group had a significantly larger mitochondrial volume at 24 h after reperfusion compared with the C, and there were more disrupted Z-lines in the EE group and more disrupted mitochondria in the I/R group at 24 h after exercise or reperfusion. When compared with the C, a significantly lower total antioxidant capacity and higher interleukin-6 value were observed after exercise or reperfusion. Our data suggest that although EE and I/R result in some similar changes in the muscle damage markers, there are still some differences. The EE- and I/R-induced muscle damage may be due to different mechanisms.

Mercury-Based Cuprate High-Transition Temperature Grain-Boundary Junctions and SQUIDs Operating Above 110 Kelvin.

The superconducting transport characteristics of HgBa(2) CaCu(2)O(6+delta) (Hg-1212) films and grain-boundary junctions grown on (100)-oriented SrTiO(3) bicrystal substrates have been investigated. The films exhibit a zero-resistance temperature of approximately 120 kelvin and sustain large critical current densities, with values as high as 10(6) amperes per square centimeter at around 100 kelvin. On the other hand, the grain boundaries behave as weak links, with substantially lower critical currents, as is observed for other cuprate superconductors. A reduction of three orders of magnitude in critical current was observed for transport across a 36.8 degrees grain boundary. The current-voltage characteristics of bridges across such a grain boundary show weak-link behavior qualitatively resembling that of a resistively shunted junction. Single-level direct-current superconducting quantum interference devices (SQUIDs) have been fabricated with such bicrystal junctions. These SQUIDs show clear periodic voltage modulations when subjected to applied magnetic fields. The SQUIDs operate at temperatures as high as 111.8 kelvin, which makes them attractive for operation in portable sensors and devices that utilize nonconventional cooling methods.

Elimination of current dissipation in high transition temperature superconductors.

The relaxation of the shielding current-induced magnetic moment in YBa(2)Cu(3)O(7) thin films, which were grown in situ, is studied as a function of temperature. Although typical relaxations cause a large amount of decay in the magnetic shielding current (on the order of 10 to 20 percent for the first 1000 seconds), it is shown that this is not necessarily a serious problem for applications such as magnets operating in persistent-current modes. This is because the decay of the magnetic shielding current depends sensitively on how far away the operating current density is from the critical current density J(c). By using a quenching process the shielding current is reduced slightly below J(c) and the relaxation is dramatically reduced. A general relation between the relaxation rate at J(c) and the reduction of the relaxation rate upon lowering of the operating current is obtained and is shown to be consistent with experimental data.

Modulation of immune response with cytotoxic T-lymphocyte-associated antigen 4 immunoglobulin-induced anergic T cells in chronic idiopathic thrombocytopenic purpura.

BACKGROUND: Platelet glycoprotein (GP)-reactive CD4+ T cells are essential for the stimulation and maintenance of antiplatelet autoantibody production in chronic idiopathic thrombocytopenic purpura (ITP). Blocking costimulatory signals could result in platelet-specific T-cell anergy. METHODS: GP-specific CD4+ T cells from patients with ITP were made anergic using cytotoxic T-lymphocyte-associated antigen 4 immunoglobulin (CTLA4-Ig). The CTLA4-Ig-induced GP-specific anergic T cells were investigated for their inhibitory function on GP-reactive T-cell proliferation and antibody production with in vitro culture systems. To further analyze their tolerizing mechanisms, we cocultured GP-anergic T cells with dendritic cells (DCs) from patients with ITP. RESULTS: Our studies demonstrated that the anergized GP-specific T cells have profound effects on both GP-specific T-cell proliferation and antibody production. These anergic T cells exerted their suppressive effects mainly in a cell contact-dependent manner, and they were not constitutively suppressive but required specific antigen stimulation to make DCs tolerogenic. The anergic T-cell-modulated DCs could induce the autoreactive T cells to be tolerant, and this effect was not restricted to T cells of the same specificity. CONCLUSION: Our studies demonstrate the efficacy of CTLA4-Ig in suppressing the pathologic autoimmune responses in ITP. These findings provide new insights into the underlying mechanisms of anergy induction in chronic ITP.

Assessing the genetic relatedness of higher ozone sensitivity of modern wheat to its wild and cultivated progenitors/relatives.

Modern wheat (Triticum aestivum L.) is one of the most ozone (O(3))-sensitive crops. However, little is known about its genetic background of O(3) sensitivity, which is fundamental for breeding O(3)-resistant cultivars. Wild and cultivated species of winter wheat including donors of the A, B and D genomes of T. aestivum were exposed to 100 ppb O(3) or charcoal-filtered air in open top chambers for 21 d. Responses to O(3) were assessed by visible O(3) injury, gas exchange, chlorophyll fluorescence, relative growth rate, and biomass accumulation. Ozone significantly decreased light-saturated net photosynthetic rate (-37%) and instantaneous transpiration efficiency (-42%), but increased stomatal conductance (+11%) and intercellular CO(2) concentration (+11%). Elevated O(3) depressed ground fluorescence (-8%), maximum fluorescence (-26%), variable fluorescence (-31%), and maximum photochemical efficiency (-7%). Ozone also decreased relative growth rate and the allometric coefficient, which finally reduced total biomass accumulation (-54%), but to a greater extent in roots (-77%) than in the shoot (-44%). Winter wheat exhibited significant interspecies variation in the impacts of elevated O(3) on photosynthesis and growth. Primitive cultivated wheat demonstrated the highest relative O(3) tolerance followed by modern wheat and wild wheat showed the lowest. Among the genome donors of modern wheat, Aegilops tauschii (DD) behaved as the most O(3)-sensitive followed by T. monococcum (AA) and Triticum turgidum ssp. durum (AABB) appeared to be the most O(3)-tolerant. It was concluded that the higher O(3) sensitivity of modern wheat was attributed to the increased O(3) sensitivity of Aegilops tauschii (DD), but not to Triticum turgidum ssp. durum (AABB) during speciation.

Lipid-rich carcinoma of the breast: a case report.

Lipid-rich carcinoma is a rare variant and accounts for < or = 2% of all breast cancer diagnoses. We report a case occurring in a 53-year-old female. The patient presented with a painless, right breast mass. Clinical examination and mammography suggested malignancy. Subsequent modified radical mastectomy revealed the diagnosis of lipid-rich carcinoma. The morphological features, differential diagnosis and treatment along with a brief review of the literature are discussed in this article. Lipid-rich carcinoma (L-RC) is a very rare variant of breast carcinomas with an aggressive clinical course and poor prognosis. It presents only 1% to 2% of all breast cases. It is classified as a specific variety of mammary carcinoma because the tumour cells possess abundant vacuolated cytoplasm which is strongly positive when stained for neutral fat. Aboumrad first described it in 1963 as lipid-secreting carcinoma. However, Ramos and Taylor renamed it as lipid-rich breast carcinoma. In China, the first case was reported in 1984. Herein, we report a case of lipid-rich carcinoma occurring in a 53-year-old female patient, and the literature is reviewed.

Recurrent ischemia in the canine heart causes recurrent bursts of free radical production that have a cumulative effect on contractile function. A pathophysiological basis for chronic myocardial "stunning".

Open-chest dogs (total number used, 117) underwent 10 5-min coronary occlusions (O) interspersed with 10 min of reperfusion (R). When systolic thickening fraction was measured 9 min after each R, the first O-R cycle was found to cause the largest decrement, with only a slight additional loss during the next four cycles and no further loss during the last five cycles (group IV), suggesting that the first few episodes of ischemia preconditioned the myocardium against the stunning induced by the last five episodes. However, different results were obtained when the total deficit of wall thickening during the final 4-h R interval was measured. The total deficit was similar after one and three 5-min O (groups V and VI, respectively), indicating that the first ischemic episode did precondition against the next two episodes; however, it was approximately 2.5-fold greater after 10 O (group IV) than after 3, indicating that the first 3 episodes failed to precondition against the next 7. Thus, at some point between the 4th and 10th O, the preconditioning effect was lost and recurrent ischemic episodes started to have a cumulative effect. Measurements of free radicals with alpha-phenyl N-tert-butyl nitrone (PBN) demonstrated a burst of free radical generation immediately after the 1st, 5th, and 10th R (group VIII). The total cumulative release of PBN adducts during the initial 5 min of reflow was 58% less after the 5th R than after the 1st (P < 0.05) but did not differ significantly between the 1st and 10th R. When administered throughout the 10 O-R cycles, the .OH scavenger mercaptopropionyl glycine significantly enhanced the recovery of function (group I) and markedly suppressed the formation of free radicals (group VII). However, the beneficial effects of mercaptopropionyl glycine were completely, or largely, lost if the drug was discontinued after the first five (group II) or eight (group III) O-R cycles, respectively, implying that (a) the oxidative stress associated with the last five, or even two, cycles was sufficient to cause severe postischemic dysfunction, and (b) the cumulative injury caused by repetitive ischemic episodes is mediated by recurrent oxidative stress. This study provides direct in vivo evidence that oxygen radicals play an important role in the pathogenesis of myocardial stunning after repetitive ischemia, and implicates .OH as a primary culprit. Taken together, the data indicate that recurrent brief ischemic episodes result in recurrent bouts of oxyradical-mediated injury that have a cumulative effect on contractility, a situation that could lead to protracted or even chronic myocardial stunning.

Late preconditioning against myocardial stunning. An endogenous protective mechanism that confers resistance to postischemic dysfunction 24 h after brief ischemia in conscious pigs.

Conscious pigs underwent a sequence of 10 2-min coronary occlusions, each separated by 2 min of reperfusion, for three consecutive days (days 1, 2, and 3 of stage I). The recovery of systolic wall thickening (WTh) after the 10th reperfusion was markedly improved on days 2 and 3 compared with day 1, indicating that the myocardium had become preconditioned against "stunning." 10 d after stage I, pigs underwent again a sequence of 10 2-min coronary occlusions for two consecutive days (days 1 and 2 of stage II). On day 1 of stage II, the recovery of WTh after the 10th reperfusion was similar to that noted on day 1 of stage I; on day 2 of stage II, however, the recovery of WTh was again markedly improved compared with day 1. Blockade of adenosine receptors with 8-p-sulfophenyl theophylline failed to prevent the development of preconditioning against stunning. Northern blot analysis demonstrated an increase in heat stress protein (HSP) 70 mRNA 2 h after the preconditioning ischemia; at this same time point, immunohistochemical analysis revealed a concentration of HSP70 in the nucleus and an overall increase in staining for HSP70. 24 h after the preconditioning ischemia, Western dot blot analysis demonstrated an increase in HSP70. This study indicates the existence of a new, previously unrecognized cardioprotective phenomenon. The results demonstrate that a brief ischemic stress induces a powerful, long-lasting (at least 48 h) adaptive response that renders the myocardium relatively resistant to stunning 24 h later (late preconditioning against stunning). This adaptive response disappears within 10 d after the last ischemic stress but can be reinduced by another ischemic stress. Unlike early and late preconditioning against infarction, late preconditioning against stunning is not blocked by adenosine receptor antagonists, and therefore appears to involve a mechanism different from that of other forms of preconditioning currently known. The increase in myocardial HSP70 is compatible with, but does not prove, a role of HSPs in the pathogenesis of this phenomenon.

Evidence for an essential role of reactive oxygen species in the genesis of late preconditioning against myocardial stunning in conscious pigs.

Conscious pigs underwent a sequence of 10 2-min coronary occlusions, each separated by 2 min of reperfusion, for three consecutive days (days 1, 2, and 3). On day 1, pigs received an i.v. infusion of a combination of antioxidants (superoxide dismutase, catalase, and N-2 mercaptopropionyl glycine; group II, n = 9), nisoldipine (group III, n = 6), or vehicle (group I [controls], n = 9). In the control group, systolic wall thickening (WTh) in the ischemic-reperfused region on day 1 remained significantly depressed for 4 h after the 10th reperfusion, indicating myocardial "stunning." On days 2 and 3, however, the recovery of WTh improved markedly, so that the total deficit of WTh decreased by 53% on day 2 and 56% on day 3 compared with day 1 (P < 0.01), indicating the development of a powerful cardioprotective response (late preconditioning against stunning). In the anti-oxidant-treated group, the total deficit of WTh on day 1 was 54% less than in the control group (P < 0.01). On day 2, the total deficit of WTh was 85% greater than that observed on day 1 and similar to that observed on day 1 in the control group. On day 3, the total deficit of WTh was 58% less than that noted on day 2 (P < 0.01). In the nisoldipine-treated group, the total deficit of WTh on day 1 was 53% less than that noted in controls (P < 0.01). On days 2 and 3, the total deficit of WTh was similar to the corresponding values in the control group. These results demonstrate that: (a) in the conscious pig, antioxidant therapy completely blocks the development of late preconditioning against stunning, indicating that the production of reactive oxygen species (ROS) on day 1 is the mechanism whereby ischemia induces the protective response observed on day 2; (b) antioxidant therapy markedly attenuates myocardial stunning on day 1, indicating that ROS play an important pathogenetic role in postischemic dysfunction in the porcine heart despite the lack of xanthine oxidase; (c) although the administration of a calcium-channel antagonist (nisoldipine) is as effective as antioxidant therapy in attenuating myocardial stunning on day 1, it has no effect on late preconditioning on day 2, indicating that the ability of antioxidants to block late preconditioning is not a nonspecific result of the mitigation of postischemic dysfunction on day 1. Generation of ROS during reperfusion is generally viewed as a deleterious process. Our finding that ROS contribute to the genesis of myocardial stunning but, at the same time, trigger the development of late preconditioning against stunning supports a complex pathophysiological paradigm, in which ROS play an immediate injurious role (as mediators of stunning) followed by a useful function (as mediators of subsequent preconditioning).

Difference in resting-state fractional amplitude of low-frequency fluctuation between bipolar depression and unipolar depression patients.

OBJECTIVE: To investigate the difference in fractional amplitude of low-frequency fluctuation (fALFF) of localized brain activities in the resting-state between bipolar depression and unipolar depression patients and to find biological markers that differentiate the two groups of patients. PATIENTS AND METHODS: Thirteen patients with bipolar depression, 15 patients with unipolar depression, and 16 healthy control subjects that were matched in age and years of education were subjected to 3.0 T resting-state functional magnetic resonance scans. The values of whole brain fALFF were calculated and statistical analysis was performed. RESULTS: The fALFF-values of the right inferior temporal gyrus, left cerebellar posterior lobe, right middle temporal gyrus, left inferior frontal gyrus/insula, right inferior frontal gyrus/insula, left lingual gyrus and right middle temporal gyrus of the three groups showed significant differences (p < 0.05). Compared with the healthy control (HC) group, the fALFF-values of the unipolar depression (UD) patient group significantly increased in the right superior temporal gyrus, left insula, left inferior frontal gyrus, right inferior frontal gyrus, right supramarginal gyrus and right medial frontal gyrus but significantly decreased in the right medial occipital gyrus, left frontal lobe, right superior parietal lobule; the fALFF-values of the bipolar depression (BD) patient group significantly decreased in the left cerebellum posterior lobe, right lingual gyrus, left lingual gyrus, right middle temporal gyrus, left middle temporal gyrus, and left superior frontal gyrus and significantly increased in the right inferior frontal gyrus and left insula compared to those of the HC group; compared with those of the UD group, the fALFF-values of the BD group significantly decreased in the left middle occipital gyrus, right middle temporal gyrus, left middle frontal gyrus, and left medial frontal gyrus. CONCLUSIONS: The brain activities of BD and UD patients in the resting-state exhibit abnormalities, which differ between the two groups of patients.

Simplified techniques in rat heterotopic small bowel transplantation.

AIM: Establish a simplified heterotopic small bowel transplantation (SBT) in the rat. METHODS: Ninety pairs of male Wistar rats were used as donors and recipients. The whole small intestine with a vascular pedicle composed of superior mesenteric artery (SMA) and portal vein (PV) was harvested as the graft. Revascularization was accomplished by end-to-side anastomosis between donor SMA and recipient infrarenal aorta and cuffed end-to-end anastomosis between donor PV and left renal vein of recipient. The distal end of graft was exteriorized to form an enterostoma. RESULTS: Average time of an operation was 130 minutes and the mean warm ischemia time of grafts was 30 minutes. The technical success rate of this model was 100% and 7-day survival was 95.6% (86/90). CONCLUSION: This simplified technique was effective and practical to improve the outcome of rat heterotopic SBT.

Amelioration of graft ischemia-reperfusion injury by breviscapine in rat small bowel transplantation.

OBJECTIVE: We sought to evaluate the effects of breviscapine to ameliorate graft ischemia-reperfusion (I/R) injury in a rat small bowel transplantation model. METHODS: Thirty-six recipients were randomly divided into three groups (n = 12): operative controls, in which grafts were implanted immediately after harvesting; an I/R control group with grafts preserved in cold lactated Ringer's solution at 4 degrees C for 4 hours before transplantation; and a breviscapine group wherein the graft was treated in the same way as the I/R control group but breviscapine (25 mg/kg/d) was injected intraperitoneally into both the donors and the recipients for 3 days before the operation of and into the recipients after transplantation. We compared the pathological scores for I/R injury, apoptosis index, and content of malondialdehyde (MDA) in the graft. RESULTS: Breviscapine diminished the pathological change caused by I/R injury (breviscapine vs I/R control on 24 hours after operation, 1.50 +/- 0.55 vs 2.17 +/- 0.75; P < .05), decreased the apoptotic index (breviscapine vs I/R control at 24 hours after operation, 27.33 +/- 0.167 vs 73.83 +/- 0.077; P < .05), and reduced the graft tissue content of MDA (breviscapine vs I/R control on 24 hours after operation, 1.717 +/- 0.131 vs 3.167 +/- 0.196; P < .05). CONCLUSIONS: Breviscapine may protect the transplanted small intestine against I/R injury during transplantation in rats.

Effects of ulinastatin on postoperative systemic inflammatory response of recipients of rat small bowel transplantation.

AIM: We sought to evaluate the effects of ulinastatin on postoperative systemic inflammatory responses of recipients of rat small bowel transplantations (SBT). METHODS: Twenty-four recipients of rat heterotopic SBT were randomly divided into a control group and a treated group. Ulinastatin (50,000 U/kg(-1)/d(-1)) was injected intravenously 30 minutes before graft revascularization. Measured variables included plasma concentrations of tumor necrosis factor (TNF), interleukin (IL)-6, and C-reactive protein (CRP) on postoperative days 1 and 3. RESULTS: Administration of ulinastatin attenuated the postoperative increases in plasma concentrations of TNF, IL-6, and CRP. CONCLUSION: Ulinastatin attenuated the postoperative systemic inflammatory response of rat recipients of SBT.

Intratumoral administration of endostatin plasmid inhibits vascular growth and perfusion in MCa-4 murine mammary carcinomas.

Endostatin, a fragment of the COOH-terminal domain of mouse collagen XVIII is a recently demonstrated endogenous inhibitor of tumor angiogenesis and endothelial cell growth. Antiangiogenic therapy with endostatin in animals requires multiple and prolonged administration of the protein. Gene therapy could provide an alternative approach to continuous local delivery of this antiangiogenic factor in vivo. Established MCa-4 murine mammary carcinomas, grown in immunodeficient mice, were treated with intratumoral injection of endostatin plasmid at 7-day intervals. At the time of sacrifice, 14 days after the first injection, endostatin-treated tumor weights were 51% of controls (P < 0.01). Tumor growth inhibition was accompanied by a marked reduction in total vascular density. Specifically, computerized image analysis showed a 18-21% increase in the median distances between tumor cells and both the nearest anatomical (CD31-stained) vessel [48.1 +/- 3.8 versus 38.3 +/- 1.6 microm (P < 0.05)] and the nearest tumor-specific (CD105-stained) vessel [48.5 +/- 1.5 versus 39.8 +/- 1.5 microm (P < 0.01)]. An increased apoptotic index of tumor cells in endostatin-treated tumors [3.2 +/- 0.5% versus 1.9 +/- 0.3% (P < 0.05)] was observed in conjunction with a significant decrease in tumor perfused vessels (DiOC7 staining), and an increase in tumor cell hypoxia (EF5 staining). Hypoxia resulting from endostatin therapy most likely caused a compensatory increase of in situ vascular endothelial growth factor (VEGF) and VEGF receptor mRNA expression. Increased immunoreactivity of endostatin staining in endostatin-treated tumors was also associated with an increased thrombospondin-1 staining [1.12 +/- 0.16 versus 2.44 +/- 0.35]. Our data suggest that intratumoral delivery of the endostatin gene efficiently suppresses murine mammary carcinoma growth and support the potential utility of the endostatin gene for cancer therapy.

Microsurgical techniques in rat heterotopic small bowel transplantation: analysis of 450 cases.

BACKGROUND: We sought to review 450 rat small bowel transplantation (SBT) operations having a modified microsurgical technique to discuss the key steps for a successful operation. METHODS: Four hundred fifty rat heterotopic small bowel transplantations were performed in 3 stages: the first 80 cases were a training stage, the following 330 cases were for formal experiments, and, in the last stage, 40 cases were to analyze the relationship between the duration of cold preservation and recipient mortality. For all cases, revascularization of the graft was accomplished by an end-to-side anastomosis between the donor superior mesenteric artery or aorta and the recipient infra-renal aorta, and cuffed end-to-end anastomosis between the donor portal vein and the left renal vein of the recipient. The duration of each operation, graft warm ischemia time, and recipient survival rate were compared. RESULTS: In the first stage, the graft warm ischemia time was about 90 minutes where as it was only 35 minutes in the second stage. The longterm survival rates (>5 days) of recipients were 8.8% and 97.3%, respectively. In the 3rd stage, long cold preservation period significantly increased recipient mortality. CONCLUSIONS: Graft warm ischemia time was a key issue associated with recipient mortality; a well-trained, simplified microsurgical anastomosis between graft superior mesenteric artery and recipient aorta accomplished in a shorter time rendered intravenous transfusion not essential for the recipient.

Amelioration of ischemia-reperfusion injury of transplanted small intestine by ulinastatin: effects on accumulation and adhesion of neutrophil.

BACKGROUND: The graft protective effect of ulinastatin (UTI) against ischemia-reperfusion injury in small bowel transplantation (SBT) was verified with a rat SBT model. This study was carried out to investigate the effects of UTI on the accumulation and adhesion of neutrophils. METHODS: Twenty-four recipients of rat SBTs were randomly divided into a control group and a UTI group. UTI was injected intravenously into the donor (before harvest of the graft) and into the recipient (50,000 U/kg/d). Variables included graft pathological score; myeloperoxidase content (MPO); expression of intercellular adhesion molecule-1 (ICAM-1) in the graft and plasma concentration of tumor necrosis factor (TNF) in the recipient. RESULTS: The pathological changes of control group grafts were more significant than those of the UTI group. The content of MPO and expression of ICAM-1 in transplanted small intestines were lower among the UTI group as were plasma concentrations of TNF. CONCLUSIONS: UTI may ameliorate graft ischemia-reperfusion injury in SBT through decreasing accumulation and adhesion of neutrophils.

Effects of the spin trap alpha-phenyl N-tert-butyl nitrone on myocardial function and flow: a dose-response study in the open-chest dog and in the isolated rat heart.

Alpha-phenyl N-tert-butyl nitrone (PBN) is widely used in spin-trapping experiments, but its possible toxicity has not been systematically evaluated. The purpose of this study was to investigate the effects of different doses of PBN on cardiac function in vivo (open-chest dogs) and in vitro (isolated rat hearts). In open-chest dogs, PBN was infused intracoronarily to achieve coronary arterial concentrations ranging from 1.6 mM to 10.0 mM. At coronary arterial concentrations of 1.6 mM and 2.5 mM, PBN had no appreciable effect on regional myocardial function (assessed as systolic wall thickening). However, coronary arterial concentrations of PBN of 5.0 mM and 10.0 mM produced a marked reduction and, eventually, a complete loss of systolic wall thickening (53% of baseline values after 30 min at 5.0 mM and 14% after 30 min at 10.0 mM). Furthermore, PBN increased coronary blood flow by approximately 25% at 2.5 mM and by > 100% at 10.0 mM. In isolated rat hearts, perfusion with 2.5 and 5.0 mM PBN for 60 min did not significantly affect global myocardial function, assessed as developed pressure, rate-pressure product, and positive and negative dP/dt. At the 10.0 mM concentration, however, these variables were significantly decreased after 30 min (developed pressure: -77% vs. controls; rate-pressure product: -84%; +dP/dt: -60%; -dP/dt: -70%); two out of five hearts stopped beating within 30 min.(ABSTRACT TRUNCATED AT 250 WORDS)