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Biomedical subjects

Dong Sun

Publications and source records attributed to Dong Sun.

At least 37 records · Page 2Linked to original sources
PubMed2005

Effects of prostaglandin E1 on the progression of aristolochic acid nephropathy.

OBJECTIVE: To investigate the effects of prostaglandin E1 (PGE1) on the progression of aristolochic acid nephropathy (AAN). METHODS: Twenty-four patients diagnosed as AAN with serum creatinine (Scr) between 1.5 mg/dL and 4 mg/dL during September 2001 to August 2003 were randomly divided into 2 groups. All patients had ingested long dan xie gan wan containing aristolochic acid (0.219 mg/g) for at least 3 months. Twelve patients were injected with Alprostadil (10 microg/d for 10 days in one month, summing up to 6 months). Except for PGE1, the other therapy was same in both groups. Renal function was assessed using reciprocal serum creatinine levels (1/Scr). RESULTS: The level of Scr an d serum hemoglobin (Hgb) was similar in both groups prior to therapy. During follow-up, 1/Scr levels in PGE1 group were significantly higher than control group (P < 0.01), and Hgb levels in PGE1 group were significantly increased compared with control (P < 0.05). CONCLUSION: PGE1 can slow the progression of renal failure and increase Hgb level of AAN patient.

Adult↗
PubMed2005

[Effects of functional electric stimulation on shoulder subluxation and upper limb motor function recovery of patients with hemiplegia resulting from stroke].

OBJECTIVE: To observe the effects of functional electric stimulation (FES) on shoulder subluxation and motor function recovery of the upper extremities of patients with hemiplegia resulting from stroke. METHODS: Forty-eight hemiplegic patients were randomly divided into two groups for treatment with FES and shoulder pads, respectively. The recovery of the patient's shoulder subluxation and movement function of upper extremities were evaluated 6 weeks after treatment and the effects of two therapies were compared. RESULTS: The shoulder subluxation and movement function of the upper extremities were improved after treatment with both therapies (P<0.01, and FES showed better effect (P<0.01). CONCLUSIONS: FES can improve shoulder subluxation and motor function of the upper extremities affected by hemiplegia resulting from stroke.

Electric Stimulation Therapy↗
PubMed2004

Mechanical compression elicits NO-dependent increases in coronary flow.

Our previous studies have demonstrated that a decrease in arteriolar diameter that causes endothelial deformation elicits the release of nitric oxide (NO). Thus we hypothesized that cardiac contraction, via deformation of coronary vessels, elicits the release of NO and increases in coronary flow. Coronary flow was measured at a constant perfusion pressure of 80 mmHg in Langendorff preparations of rat hearts. Hearts were placed in a sealed chamber surrounded with perfusion solution. The chamber pressure could be increased from 0 to 80 mmHg to generate extracardiac compression. To minimize the impact of metabolic vasodilatation and rhythmic changes in shear stress, nonbeating hearts, by perfusing the hearts with a solution containing 20 mM KCl, were used. After extracardiac compression for 10 or 20 s, coronary flow increased significantly, concurrent with an increased release of nitrite into the coronary effluent and increased phosphorylation of endothelial NO synthase in the hearts. Inhibition of NO synthesis eliminated the compression-induced increases in coronary flow. Shear stress-induced dilation could not account for this increased coronary flow. Furthermore, in isolated coronary arterioles, without intraluminal flow, the release of vascular compression elicited a NO-dependent dilation. Thus this study reveals a new mechanism that, via coronary vascular deformation, elicited by cardiac contraction, stimulates the endothelium to release NO, leading to increased coronary perfusion.

Animals↗
PubMed2004

Response of tyrosine hydroxylase and GTP cyclohydrolase I gene expression to estrogen in brain catecholaminergic regions varies with mode of administration.

The effect of different dose, mode and duration of estradiol administration was examined in the different brain catecholaminergic areas in ovariectomized (OVX) female rats. We determined changes in mRNA levels of tyrosine hydroxylase (TH), rate-limiting enzyme in catecholamine (CA) biosynthesis of GTP cyclohydrolase I (GTPCH), rate-limiting enzyme in biosynthesis as well as of tetrahydrobiopterin (BH4), and concentration of BH4, which is an essential cofactor for TH, tryptophan hydroxylase and nitric oxide synthase. Short-term administration of estradiol benzoate (EB) by five injections of 15 or 40 microg/kg 12 h apart led to increase in TH and GTPCH mRNA levels in dopaminergic and noradrenergic cell bodies of the ventral tegmental area (VTA), substantia nigra (SN), locus coeruleus (LC) and the nucleus of solitary tract (NTS) depending on dose of administration. Estrogen-elicited alterations in BH4 concentrations were mostly correlated with changes in GTPCH mRNA levels, except in SN. Long-term administration of estradiol by injections (EB: 25 microg/kg, 16 injections 26 h apart; 50 microg/kg, 16 injections 48 h apart) or pellets (0.1 mg 17 beta-estradiol, 14 days) were not very effective in modulating mRNA levels for both genes in most locations except the NTS. Long-term injections of EB elevated GTPCH mRNA levels throughout the NTS and in microvessels. Administration of estradiol by pellets led to decline of TH mRNA in rostral-medial and elevation in caudal parts of the NTS. Thus, estradiol has a complex and differential effect on TH and GTPCH gene expression in a tissue specific manner and depends on the mode of administration.

Analysis of Variance↗
PubMed2004

Epidermal growth factor-induced cell proliferation in the adult rat striatum.

Current strategies for repairing the adult CNS following injury include cell transplantation and/or the use of viral vectors to deliver therapeutic agents. Although promising, both techniques are limited in their usefulness due to the immunological response triggered in the brain as a result of the introduction of foreign antigens. An alternative method to repair the damaged CNS is to stimulate endogenous cells within the brain to divide thereby replacing cells lost to injury. Since it has been shown that growth factors such as epidermal growth factor (EGF) are potent mitogens to CNS cells in vitro, we sought to assess the mitogenic effect of an in vivo application of EGF to the adult mammalian brain. Accordingly, varying doses of human recombinant EGF were administered to the striatum of adult rats, followed 48 h later by intraperitoneal injections of 5-bromodeoxyuridine (BrdU), a marker for cell proliferation. Of four doses assessed, 0.05 ng of EGF induced the highest levels of cell proliferation. To determine the cellular identity of these proliferating cells, animals were injected with (3)H-thymidine 48 h following EGF administration to label dividing cells. Sections were subsequently immunostained for markers to astrocytes, microglia, oligodendrocytes, neural precursors, and mature neurons. Compared to controls, a significant proportion of the newly generated cells resulting from EGF administration were identified as immature and mature astrocytes. Collectively, these results provide valuable information for utilizing a growth factor administration approach to mobilize the proliferative response of endogenous cells to replace those lost to injury or disease.

Animals↗
PubMed2004

Reduced release of nitric oxide to shear stress in mesenteric arteries of aged rats.

We hypothesized that aging is characterized by a reduced release of nitric oxide (NO) in response to shear stress in resistance vessels. Mesenteric arterioles and arteries of young (6 mo) and aged (24 mo) male Fischer 344 rats were isolated and cannulated. Shear stress (15 dyn/cm(2))-induced dilation was significantly reduced and shear stress (1, 5, 10, and 15 dyn/cm(2))-induced increases in perfusate nitrite were significantly smaller at all shear stress levels in vessels of aged rats. Inhibition of NO synthesis abolished shear stress-induced release of nitrite. Furthermore, shear stress (15 dyn/cm(2))-induced release of nitrate was significantly higher and total nitrite (nitrite plus nitrate) was significantly lower in vessels of aged rats. Tiron or SOD significantly increased nitrite released from vessels of aged rats, but this was still significantly less than that in young rats. Superoxide production was increased and the activity of SOD was decreased in vessels of aged rats. There were no differences in endothelial NO synthase (eNOS) protein and basal activity or in Cu/Zn-SOD and Mn-SOD proteins in vessels of the two groups, but extracellular SOD was significantly reduced in vessels of aged rats. Maximal release of NO induced by shear stress plus ACh (10(-5) M) was comparable in the two groups, but phospho-eNOS in response to shear stress (15 dyn/cm(2)) was significantly reduced in vessels of aged rats. These data suggest that an increased production of superoxide, a reduced activity of SOD, and an impaired shear stress-induced activation of eNOS are the causes of the decreased shear stress-induced release of NO in vessels of aged rats.

Aging↗
PubMed2004

Perfluorocarbon emulsion improves cerebral oxygenation and mitochondrial function after fluid percussion brain injury in rats.

OBJECTIVE: Cerebral ischemia is a common secondary sequela of traumatic brain injury (TBI). Experimental models of stroke have demonstrated reductions in ischemia after perfluorocarbon (PFC) administration; however, there are no published reports of PFC efficacy after TBI. The current study analyzed the effect of the PFC emulsion Oxygent (AF0144; Alliance Pharmaceutical Corp., San Diego, CA) on cerebral oxygenation, mitochondrial redox potential, and free radical formation after lateral fluid percussion injury. METHODS: After fluid percussion injury, five 2.25 ml/kg doses of PFC or saline were administered to rats breathing 100% O(2), and oxygen tension was recorded. In a second experiment, a single bolus (11.25 ml/kg) of PFC or saline was given after injury, and redox potential and free radical formation were measured at 1 or 4 hours with Alamar blue dye and dihydrorhodamine 123, respectively. RESULTS: Cerebral oxygen tension was significantly increased in both injured and sham animals treated with 11.25 ml/kg of PFC as compared with saline (P < 0.05). Likewise, PFC significantly increased mitochondrial redox potential as compared with saline at 4 hours after injury (P < 0.01). Mitochondrial peroxynitrite and peroxide production also increased with the administration of PFC (P < 0.05). CONCLUSION: The current study demonstrates that a PFC emulsion can significantly increase cerebral oxygenation after TBI and enhance mitochondrial function at 4 hours after injury as compared with saline. This study demonstrates a new therapeutic potential for PFC to enhance cerebral oxygenation and aerobic metabolism after TBI. However, the increased free radical formation with high-dose PFCs suggests the need for further studies combining PFCs with free radical scavengers.

Animals↗
PubMed2004

Effects of hyperbaric oxygen therapy on cerebral oxygenation and mitochondrial function following moderate lateral fluid-percussion injury in rats.

OBJECT: In the current study, the authors examined the effects of hyperbaric O2 (HBO) following fluid-percussion brain injury and its implications on brain tissue oxygenation (PO2) and O2 consumption (VO2) and mitochondrial function (redox potential). METHODS: Cerebral tissue PO2 was measured following induction of a lateral fluid-percussion brain injury in rats. Hyperbaric O2 treatment (100% O2 at 1.5 ata) significantly increased brain tissue PO2 in both injured and sham-injured animals. For VO2 and redox potential experiments, animals were treated using 30% O2 or HBO therapy for 1 or 4 hours (that is, 4 hours 30% O2 or 1 hour HBO and 3 hours 100% O2). Microrespirometer measurements of VO2 demonstrated significant increases following HBO treatment in both injured and sham-injured animals when compared with animals that underwent 30% O2 treatment. Mitochondrial redox potential, as measured by Alamar blue fluorescence, demonstrated injury-induced reductions at 1 hour postinjury. These reductions were partially reversed at 4 hours postinjury in animals treated with 30% O2 and completely reversed at 4 hours postinjury in animals on HBO therapy when compared with animals treated for only 1 hour. CONCLUSIONS: Analysis of data in the current study demonstrates that HBO significantly increases brain tissue PO2 after injury. Nonetheless, treatment with HBO was insufficient to overcome injury-induced reductions in mitochondrial redox potential at 1 hour postinjury but was able to restore redox potential by 4 hours postinjury. Furthermore, HBO induced an increase in VO2 in both injured and sham-injured animals. Taken together, these data demonstrate that mitochondrial function is depressed by injury and that the recovery of aerobic metabolic function may be enhanced by treatment with HBO.

Animals↗
PubMed2003

Estrogen elicits cytochrome P450--mediated flow-induced dilation of arterioles in NO deficiency: role of PI3K-Akt phosphorylation in genomic regulation.

This study investigated the mechanisms responsible for the estrogen-dependent, cytochrome P450 (CYP)-mediated dilator responses to shear stress in arterioles of NO-deficient female rats and mice. Flow-induced dilation (FID) was assessed in isolated arterioles from N(G)-nitro-L-arginine methyl ester (L-NAME)-treated male and ovariectomized female rats before and after overnight incubation with 17beta-estradiol (17beta-E2, 10(-9) mol/L). In control conditions, prostaglandins (PGs) mediated FID, because indomethacin (INDO) abolished the responses. After incubation of the vessels with 17beta-E2, the basal tone of arterioles was significantly reduced and FID was augmented. INDO did not affect the dilation of the vessels incubated with 17beta-E2. Dilations of these vessels, however, were eliminated by PPOH and miconazole, inhibitors of CYP/epoxygenase. Simultaneous incubation of the vessels with 17beta-E2 plus ICI, 182,780, an estrogen receptor antagonist, or wortmannin, an inhibitor of phosphatidylinositol 3-kinase (PI3K) phosphorylation or the transcriptional inhibitor DRB, prevented the reduced arteriolar tone and the enhanced CYP-mediated FID caused by incubation of vessels with 17beta-E2. Western blot analysis indicated a significantly increased phospho-Akt level in arterioles incubated with 17beta-E2 compared with those without 17beta-E2. The enhanced phospho-Akt in response to 17beta-E2 was localized, by immunohistochemistry, to arteriolar endothelial cells. Moreover, GC-MS analysis indicated a significantly increased production of epoxyeicosatrienoic acids, vasodilator metabolites of CYP/epoxygenase, in arterioles incubated with 17beta-E2, a response that was prevented by ICI 182780 and wortmannin, respectively. Thus, estrogen, via a receptor-dependent, PI3K/Akt-mediated pathway, transcriptionally upregulates CYP activity, leading to an enhanced arteriolar response to shear stress.

Androstadienes↗
PubMed2003

Hypoxia in paranasal sinuses of patients with chronic sinusitis with or without the complication of nasal allergy.

OBJECTIVE: In order to elucidate the pathogenesis of the radiologic opacity of the sinuses frequently observed in patients with allergic rhinitis, the mechanisms underlying their sinus mucosal swelling were studied clinically. MATERIAL AND METHODS: We confirmed the presence of hypoxia in inflamed sinuses and obstruction of the sinus ostium in operated patients with chronic sinusitis by digitally monitoring the oxygen tension. The possibility of radiologic sinus shadow was also investigated after transient obstruction of the natural ostium. RESULTS: The oxygen tension was significantly lower in inflamed than non-inflamed sinuses (p < 0.01), irrespective of the presence or absence of allergic rhinitis. In 54.5% of patients without sinusitis, transient obstruction of the middle meatus by gauze packing resulted in the appearance of a pathologic sinus shadow on radiograms obtained after septoplasty and turbinotomy. In both allergic and non-allergic rhinitis, thick opacity was the most frequently encountered pattern (p < 0.01). CONCLUSION: Our study revealed that in the absence of a primary allergic reaction in the sinus mucosa, blocking of the middle meatus and ostium by allergic swelling of the nasal mucosa may induce hypoxia and secondary mucosal swelling in the sinuses.

Adult↗
PubMed2003

Tempol, a novel stable nitroxide, reduces brain damage and free radical production, after acute subdural hematoma in the rat.

Recent studies have shown that there is increased production of deleterious free radicals following acute subdural hematoma (ASDH). Scavenging them may therefore be of therapeutic benefit. Nitroxides are new, low molecular weight, cell permeable superoxide dismutase mimics. This study investigated the neuroprotective effect of 4-hydroxy-2,2,6,6-tetramethylpiperidine-1-oxyl (Tempol) following ASDH in the rat. Twenty-one male Sprague-Dawley rats were used in two studies: (1) a volumetric study of ischemic brain damage (n = 10); and (2) a microdialysis study measuring free radical generation after ASDH (n = 11). Ten minutes after induction of hematoma, the animals received 10 mg/kg Tempol or vehicle intravenously. In the volumetric study, 4 h after treatment, the rats were perfused, the brain removed, cut into serial 12-microm coronal sections, and stained. Ischemic areas were measured in eight predetermined stereotactic planes. In the microdialysis study, free radical production was measured using the salicylate trapping technique by quantifying 2,3-dihydrobenzoic acid (2,3-DHBA) and 2,5-DHBA using HPLC. In the volumetric study, Tempol treatment significantly reduced infarct volumes; 100.2 +/- 15.7 mm3 in Tempol-treated animals compared with 171.5 +/- 13.6 mm3 in controls (42% reduction, p = 0.0005). The microdialysis study demonstrated an early twofold increase of free radical production at 30 min, and returning to the baseline levels in controls. However, in Tempol-treated animals, this early surge was attenuated, and all measured values remained around the baseline levels throughout the experiments. Tempol thus provides significant neuroprotective effect in a rat model of ASDH, related to attenuation of superoxide radical production. The use of these low molecular weight, cell-permeable agents, which readily cross the blood-brain barrier and enter cells, thus appears indicated for acute pathologies, ASDH.

Animals↗
PubMed2002

Norepinephrine elicits beta2-receptor-mediated dilation of isolated human coronary arterioles.

BACKGROUND: The exact role of adrenoceptors in norepinephrine (NE)-mediated regulation of the human coronary circulation has yet to be elucidated. Thus, the goals of this study were to characterize the adrenoceptors involved in the responses to NE in isolated human coronary arterioles and small arteries. METHODS AND RESULTS: Arterioles (n=39) and small arteries from the left ventricle of explanted human hearts were isolated and cannulated. Vessels from the hearts of 21 patients were studied: 15 males and 6 females, aged 0.5 to 63 years. Nineteen patients were considered to be New York Heart Association class 4. All hearts exhibited hypertrophy (190+/-20%). The passive diameter of arterioles was 167+/-8 microm (range 97 to 323 microm). NE (10(-7) to 3x10(- 7) mol/L) elicited concentration-dependent dilations (47+/-4 microm) that were unaffected by endothelium removal, N(omega)-nitro-L-arginine (10(- 4) mol/L, an NO synthase inhibitor), or practolol (10(-6) mol/L, a beta1-receptor blocker). However, administration of propranolol (10(-5) mol/L, a combined beta1- and beta2-blocker) or butoxamine (10(-6) mol/L, a beta2-receptor blocker) completely eliminated the NE-induced dilation. Constrictions to NE (2 of 39 vessels) were inhibited by prazosin (10(-6) mol/L, an alpha1-receptor blocker). Methoxamine (10(-9) to 10(-5) mol/L, an alpha1-agonist) had no effect, whereas U44619, a thromboxane mimetic, elicited dose-dependent constriction of vessels. CONCLUSIONS: Our data indicate that isolated human coronary arterioles and small arteries dilate to NE via beta2-receptors on smooth muscle. These findings are important to our understanding of the mechanisms action of NE in the human coronary circulation.

Adolescent↗
PubMed2002

Decreased arteriolar sensitivity to shear stress in adult rats is reversed by chronic exercise activity.

OBJECTIVE: We tested the hypothesis that the decline in endothelium-dependent arteriolar dilation in adult rats is reversed by chronic exercise activity. METHODS: Rats were divided into young (8-10 weeks)-sedentary (SED(Y)), adult (29-32 weeks)-sedentary (SED(A)), and adult-exercised (EX(A), treadmill exercise for 18-20 weeks) groups. Responses of isolated arterioles ( approximately 50 microm at 80 mm Hg) of gracilis muscle were assessed to increases in perfusate flow and vasoactive agents. RESULTS: With no differences in basal tone, maximal flow-induced dilations were not different between arterioles of SED(Y) and SED(A) rats (71 +/- 2 and 72 +/- 2% of passive diameter, respectively), yet the sensitivity of arterioles to shear stress (WSS(50)) was significantly less in SED(A) than in SED(Y) rats (35 +/- 4 vs. 23 +/- 3 dyne/cm(2), respectively). In vessels of EX(A) rats, maximal flow-induced dilation was significantly augmented (88 +/- 2% of passive diameter) and WSS(50) (15 +/- 1 dyn/cm(2)) was significantly reduced. Dilation to acetylcholine was enhanced in arterioles of EX(A), whereas dilation to sodium nitroprusside was not different in vessels of the three groups. CONCLUSION: Chronic exercise activity reverses age related reduction in sensitivity of arterioles to increases in wall shear stress.

Acetylcholine↗
PubMed2002

Quantifying porphobilinogen deaminase mRNA in microdissected nephron segments by a modified RT-PCR.

BACKGROUND: Quantifying mRNA levels by reverse transcription-polymerase chain reaction (RT-PCR), although widely exercised, is still difficult. METHODS: A modified quantitative RT-PCR in which genomic DNA was used as standard was developed. The quantity of mRNA was expressed as the ratio of the PCR product from cDNA and that from genomic DNA (CG ratio). Nephron distribution of porphobilinogen deaminase (PBGD) mRNA was examined in microdissected nephron segments using the method. The enzyme activity and mRNA quantity of PBGD also were measured in tissue homogenates. RESULTS: Tubular segments expressed substantially more PBGD mRNA than glomeruli (expressed as CG ratios, 1.04 +/- 0.10 in glomeruli, 4.53 +/- 0.32 in PCT, 5.71 +/- 0.25 in PST, 5.13 +/- 0.52 in mTAL, 5.29 +/- 0.20 in cTAL, 4.05 +/- 0.35 in DCT, 2.88 +/- 0.25 in CCD, and 4.90 +/- 0.24 in OMCD). PBGD mRNA level in liver homogenate (3.17 +/- 0.36) was much higher than glomeruli but lower than most of the tubular segments. The enzyme activity in tissue homogenates correlated well with mRNA levels. CONCLUSION: The method reported here is simple and reliable, and especially suitable for quantitating specific mRNA amounts in minute tissue samples such as microdissected nephron segments.

Actins↗
PubMed2002

Neuronal NOS-dependent dilation to flow in coronary arteries of male eNOS-KO mice.

Flow-induced dilation was examined in isolated coronary arteries of endothelial nitric oxide (NO) synthase knockout mice (eNOS-KO) and wild-type (WT) mice. The basal tone of arteries (percentage of passive diameter) was significantly greater in eNOS-KO than in WT mice; their flow-induced dilations, however, were similar. Endothelial removal eliminated the dilations in vessels of both strains of mice. In arteries of WT mice, N(omega)-nitro-L-arginine methyl ester (L-NAME) (10(-4) M) or indomethacin (10(-5) M) alone, inhibited flow-induced dilation by approximately 50%, whereas their simultaneous administration abolished the responses. In arteries of eNOS-KO mice, flow-induced dilation was inhibited by approximately 40% with L-NAME. The residual portion (60%) of the response was eliminated by the additional administration of indomethacin. 7-Nitroindazole (10(-4) M) attenuated flow-induced dilation by approximately 40% in arteries of eNOS-KO mice, but did not affect responses in those of WT mice. 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (3 x 10(-5) M) inhibited the L-NAME/7-nitroindazole-sensitive portion of the responses in arteries of eNOS-KO mice. Immunohistochemical evidence confirms the presence of neuronal NOS (nNOS) in the arterial endothelium of eNOS-KO mice. In conclusion, nNOS-derived NO, via activation of cGMP, together with prostaglandins, maintains flow-induced dilation in coronary arteries of male eNOS-KO mice.

Animals↗
PubMed2002

[Changes of inflammatory factors in patients with coronary artery disease during perioperation].

OBJECTIVE: To investigate the proinflammatory cytocine factors in patients with coronary artery disease by different treatments during perioperation. METHODS: TNF-alpha, IL-6, c-reactive protein (CRP) were measured in 37 patients with coronary artery disease (CAD) and 10 patients with mitral valve replacement (MVR, control group) before operation and aortic clamping or before coronary artery bypass grafting (CABG) in the patients with cardiopulmonary bypass, or before transmyocardial laser reperfusion (TMLR), when aortic declamping and 3, 6, 24 hours after operation. RESULTS: The level of proinflammatory factors increased more significantly after operation than before operation. TNF-alpha increased more significantly in the patients with CPB than in those without CPB after operation [(4.10 +/- 0.71) pg/ml vs. (1.34 +/- 0.29) pg/ml, P < 0.05)]. IL-6 was not the different among all groups after operation. CRP was higher in the CAD patients with CPB than in the control group after operation [(12.89 +/- 0.29) pg/ml vs. (12.00 +/- 0.31) pg/ml, P < 0.05]. CONCLUSION: Inflammatory response can be seen after operation in all CAD patients. In patients undergoing CABG without CPB or undergoing TMLR, the changes in flammatory response are milder than those in patients with CPB. Thus patients should undergo CABG without CPB if they are indicated.

Aged↗