Biomedical subjects

Xiao-Ping Yang

Publications and source records attributed to Xiao-Ping Yang.

At least 37 records · Page 2Linked to original sources

PubMed2004

Reduction of cardiac fibrosis decreases systolic performance without affecting diastolic function in hypertensive rats.

Pressure-overload left ventricular hypertrophy (LVH) is characterized by an increase in myocyte size and fibrosis. However, it is not clear how each of these components affects hypertensive heart disease (HHD). We have shown in 2 different rat models of hypertension that cardiac fibrosis can be reduced with N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP), an antifibrotic peptide normally present in mammals. To assess how inhibition of fibrosis affects HHD, spontaneously hypertensive rats (SHR) and normotensive controls (WKY) were treated with Ac-SDKP or vehicle. Cardiac systolic and diastolic function were assessed using in vivo pressure-volume (PV) analysis. Left ventricle passive compliance was also determined ex vivo. We found that in SHR, Ac-SDKP normalized left ventricle total collagen content and interstitial collagen fraction without changing myocyte diameter or left ventricle mass. In WKY, collagen did not change significantly after treatment. Ac-SDKP did not affect left ventricle diastolic function, determined in vivo and ex vivo in SHR and WKY, whereas systolic function was significantly decreased in SHR treated with Ac-SDKP and unchanged in treated WKY. We concluded that in adult SHR, reducing left ventricle collagen deposition with Ac-SDKP does not improve diastolic function, whereas it decreases systolic performance. These findings suggest that total left ventricle collagen reduction per se does not necessarily benefit cardiac function. In HHD, other factors besides collagen quantity, such as myocyte hypertrophy and/or collagen type or cross-link, might be targeted to improve cardiac function.

Animals↗

PubMed2004

Temporal changes in matrix metalloproteinase expression and inflammatory response associated with cardiac rupture after myocardial infarction in mice.

We previously found that male mice with myocardial infarction (MI) had a high rate of cardiac rupture, which generally occurred at 3 to 5 days after MI. Since matrix metalloproteinases (MMPs) play an important role in infarct healing, tissue repair and extracellular matrix (ECM) remodeling post-MI, we studied the temporal relationship of MMP expression and inflammatory response to cardiac rupture after acute MI. Male C57BL/6J mice were subjected to MI (induced by ligating the left anterior descending coronary artery) and killed 1, 2, 4, 7 or 14 days after MI. MMP-2 and MMP-9 activity in the heart were measured by zymography. Collagen content was measured by hydroxyproline assay. We found that after MI, MMP-9 activity increased as early as 1 day and reached a maximum by 2-4 days, associated with a similar increase in neutrophil and macrophage infiltration in the infarct area. MMP-2 started to increase rapidly within 4 days, reaching a maximum by 7 days and remaining high even at 14 days. Intense macrophage infiltration appeared by 4 days after MI and then gradually decreased within 7 to 14 days. Collagen content was unchanged until 4 days after MI, at which point it increased and remained high thereafter. Our data suggest that in mice, overexpression of MMP-2 and MMP-9 (possibly expressed mainly by neutrophils and macrophages) may lead to excessive ECM degradation in the early phase of MI, impairing infarct healing and aggravating early remodeling which in turn causes cardiac rupture.

Animals↗

PubMed2004

Role of a selective aldosterone blocker in mice with chronic heart failure.

BACKGROUND: Spironolactone, a nonselective aldosterone blocker, has a cardioprotective effect; however, significant endocrine side effects limit its use. Eplerenone is a new selective aldosterone blocker. We investigated whether eplerenone attenuates cardiac remodeling and improves function in a mouse model of heart failure and whether coadministration of eplerenone and an angiotensin-converting enzyme inhibitor (ACEi) provides better cardioprotection than either agent alone. METHODS AND RESULTS: C57BL/6J mice were subjected to myocardial infarction (MI) by ligating the left anterior descending coronary artery. Two weeks later, the mice were either left untreated or treated with (1) eplerenone, (2) ACEi, or (3) eplerenone plus ACEi for 12 weeks. Systolic blood pressure (SBP) was measured and echocardiography performed before MI and weekly thereafter. At the end of the study, interstitial collagen fraction (ICF) and myocyte cross-sectional area (MCSA) were examined histologically. We found that (1) eplerenone significantly improved ejection fraction and cardiac output and decreased left ventricular (LV) systolic area, LV weight, ICF, and MCSA independently of changes in SBP compared with untreated animals; (2) ACEi had similar beneficial effects, accompanied by a significant reduction in SBP; and (3) combined treatment offered limited additional benefit beyond monotherapy. CONCLUSIONS: In mice with MI, eplerenone attenuates progression of heart failure comparably to ACEi, and its effect is independent of BP lowering.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed2004

Two new cytotoxic tetracyclic tetraterpenoids from the soft coral Sarcophyton tortuosum.

Two new cytotoxic tetracyclic tetraterpenoids, methyl tortuoate A (1) and methyl tortuoate B (2), along with the known methyl sartortuoate (3) were isolated from the soft coral Sarcophyton tortuosum. The structures of 1 and 2 were established by spectroscopic methods, mainly on the basis of 2D NMR techniques, and were confirmed by single-crystal X-ray diffraction analysis. The cytotoxic activities of these compounds were carried out in vitro on human nasophyringeal carcinoma (CNE-2) and murine lymphocytic leukemia (P-388) tumor cell lines.

Animals↗

PubMed2004

The Chinese Visible Human (CVH) datasets incorporate technical and imaging advances on earlier digital humans.

We report the availability of a digitized Chinese male and a digitzed Chinese female typical of the population and with no obvious abnormalities. The embalming and milling procedures incorporate three technical improvements over earlier digitized cadavers. Vascular perfusion with coloured gelatin was performed to facilitate blood vessel identification. Embalmed cadavers were embedded in gelatin and cryosectioned whole so as to avoid section loss resulting from cutting the body into smaller pieces. Milling performed at -25 degrees C prevented small structures (e.g. teeth, concha nasalis and articular cartilage) from falling off from the milling surface. The male image set (.tiff images each of 36 Mb) has a section resolution of 3072 x 2048 pixels ( approximately 170 micro m, the accompanying magnetic resonance imaging and computer tomography data have a resolution of 512 x 512, i.e. approximately 440 micro m). The Chinese Visible Human male and female datasets are available at http://www.chinesevisiblehuman.com. (The male is 90.65 Gb and female 131.04 Gb). MPEG videos of direct records of real-time volume rendering are at: http://www.cse.cuhk.edu.hk/~crc

Adult↗

PubMed2004

Modification of transmitter release from periarterial nerve terminals by dipyridamole in canine isolated splenic artery.

1. The aim of the present study was to determine the modulatory effects of dipyridamole on purinergic and adrenergic transmission in the canine isolated, perfused splenic artery. 2. Periarterial nerve electrical stimulation readily induced a double-peaked vasoconstriction consisting of an initial transient, predominantly P2X receptor-mediated constriction followed by a prolonged, mainly alpha1-adrenoceptor-mediated response. 3. Exposure of tissues to dipyridamole (0.1-1 micro mol/L) dose-dependently inhibited both the first and second peaks of the vasoconstrictor response at a low frequency of stimulation (1 Hz), whereas at an intermediate frequency of stimulation (4 Hz), the first peak of the response was depressed without any significant effect being observed on the second peak of constriction. 4. At a higher dose (1 micro mol/L) dipyridamole potentiated vasoconstrictor responses to noradrenaline (0.03-1 nmol). At any doses used, dipyridamole had no effect on the vasoconstrictor responses to ATP (0.03-1 micro mol). 5. Tyramine (0.01-0.3 micro mol) induced vasoconstriction in a dose-dependent manner. The dose-response curves for tyramine were shifted to the right following treatment with dipyridamole (0.1-1 micro mol/L). 6. The present results indicate that dipyridamole may inhibit purinergic and adrenergic transmission presynaptically, whereas postsynaptically dipyridamole may potentiate the adrenergic vascular constriction by inhibition of transmitter uptake.

Adenosine Triphosphate↗

PubMed2004

Dual inhibition of ACE and NEP provides greater cardioprotection in mice with heart failure.

BACKGROUND: Vasopeptidase inhibitors (VPi) may provide a new means of treating hypertension and congestive heart failure, because they simultaneously block angiotensin-converting enzyme (ACE) and neutral endopeptidase-24.11 (NEP-24.11), thereby inhibiting the renin-angiotensin system and enhancing vasodilator and natriuretic substances such as kinins and natriuretic peptides. METHODS: Using B(2) kinin receptor gene knockout mice (B(2)-/-), we tested the hypotheses that (1) VPi may provide better cardioprotection than ACE or NEP inhibitors alone (ACEi and NEPi) and (2) the effects of these inhibitors are partially mediated by kinins. Four weeks after myocardial infarction, B(2)-/- mice and B(2)+/+ mice were started on vehicle, ACEi (ramipril, 2.5 mg/kg/d), NEPi (candoxatril, 20 mg/kg/d) or VPi (omapatrilat, 50 mg/kg/d), which was continued for 20 weeks. Systolic blood pressure was measured weekly and cardiac function evaluated monthly by echocardiography. Myocyte cross-sectional area and interstitial collagen fraction were measured histopathologically. RESULTS: We found that ACEi or NEPi improved cardiac function and remodeling and that these effects were more obvious in mice receiving VPi. Furthermore, the beneficial cardiac effects of ACEi, NEPi, and VPi were significantly attenuated in B(2)-/- mice. We concluded that dual inhibition of ACE and NEP with VPi provides better cardioprotection than ACEi or NEPi alone in mice with congestive heart failure induced by myocardial infarction, and these effects are mediated at least in part via kinins.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed2004

[Enhancement of FG020326 on sensitivity of MCF-7/ADR cells to taxotere via enhancing activation of caspase-8 and caspase-3].

BACKGROUND & OBJECTIVE: Multidrug resistance (MDR) is often characterized by over-expression of P-glycoprotein (P-gp) as drug efflux protein. Recent researches showed P-gp can inhibit caspase-dependent apoptosis, and protect MDR cells from apoptosis. This study was designed to investigate reversal effect of FG020326, a potent MDR modulator,on drug-resistance of MCF-7/ADR cells towards taxotere,and its mechanism. METHODS: Drug-resistant MCF-7/ADR cells, over-expressed P-gp, were cultured with FG020326 and taxotere. The reversal effect of FG020326 was assayed by MTT method. Apoptotic morphology of MCF-7/ADR cells was observed under fluorescent microscope after Hoechst33258 staining, cell apoptosis was measured by flow cytometry (FCM). Activation of caspase-8 and caspase-3 was measured by Western blot and colorimetric assay. RESULTS: FG020326 enhanced sensitivity of MCF-7/ADR cells to taxotere, and gave a 24-fold reversal of apoptosis-resistance with concentration of 10 micromol/L. Under effect of 10 micromol/L FG020326,chromatin condensation, apoptotic bodies, and sub-G1 peak were observed in MCF-7/ADR cells. Sensitivities of caspase-8 and caspase-3 were enhanced by demostrating cleavage of caspase-8, caspase-3,and PARP in MCF-7/ADR cells. Activities of caspase-3 and caspase-8 in MCF-7/ADR cells cultured with 10 micromol/L FG020326 and 0.1 micromol/L taxotere were increased in a time-dependent manner,and reached peak values at 48 h, which were significantly higher than those in cells cultured with taxotere alone. CONCLUSION: FG020326 may reverse drug-resistance of MCF-7/ADR cells towards taxotere through enhancing activation of caspase-8 and caspase-3 induced by taxotere.

Antineoplastic Agents, Phytogenic↗

PubMed2003

Ac-SDKP reverses inflammation and fibrosis in rats with heart failure after myocardial infarction.

Inflammation may play an important role in the pathogenesis of cardiac fibrosis in heart failure (HF) after myocardial infarction (MI). N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) is a naturally occurring antifibrotic peptide whose plasma concentration is increased 4- to 5-fold by angiotensin-converting enzyme inhibitors. We tested the hypothesis that in rats with HF after MI, Ac-SDKP acts as an anti-inflammatory cytokine, preventing and also reversing cardiac fibrosis in the noninfarcted area (reactive fibrosis), and thus affording functional improvement. We found that Ac-SDKP significantly decreased total collagen content in the prevention group from 23.7+/-0.9 to 15.0+/-0.7 microg/mg and in the reversal group from 22.6+/-2.2 to 14.4+/-1.6 (P<0.01). Interstitial collagen volume fraction and perivascular collagen were likewise significantly reduced. We also found that infiltrating macrophages were reduced from 264.7+/-8.1 to 170.2+/-9.2/mm2, P<0.001 (prevention), and from 257.5+/-9.1 to 153.1+/-8.5 mm2, P<0.001 (reversal), while transforming growth factor (TGF)-beta-positive cells were decreased from 195.6+/-8.4 to 129.6+/-5.7/mm2, P<0.01 (prevention), and from 195.6+/-8.4 to 130.7+/-10.8/mm2, P<0.01 (reversal). Ac-SDKP did not alter either blood pressure or left ventricular hypertrophy (LVH); however, it depressed systolic cardiac function in the prevention study while having no significant effect in the reversal group. We concluded that Ac-SDKP has an anti-inflammatory effect in HF that may contribute to its antifibrotic effect; however, this decrease in fibrosis without changes in LVH was not accompanied by an improvement in cardiac function.

Animals↗

PubMed2003

Inhibition of cyclooxygenase-2 improves cardiac function after myocardial infarction in the mouse.

Cyclooxygenase (COX)-2 is expressed in the heart in animal models of ischemic injury. Recent studies have suggested that COX-2 products are involved in inflammatory cell infiltration and fibroblast proliferation in the heart. Using a mouse model, we questioned whether 1). myocardial infarction (MI) in vivo induces COX-2 expression chronically, and 2). COX-2 inhibition reduces collagen content and improves cardiac function in mice with MI. MI was produced by ligation of the left anterior descending coronary artery in mice. Two days later, mice were treated with 3 mg/kg NS-398, a selective COX-2 inhibitor, or vehicle in drinking water for 2 wk. After the treatment period, mice were subjected to two-dimensional M-mode echocardiography to determine cardiac function. Hearts were then analyzed for determination of infarct size, interstitial collagen content, brain natriuretic peptide (BNP) mRNA, myocyte cross-sectional area, and immunohistochemical staining for transforming growth factor (TGF)-beta and COX-2. COX-2 protein, detected by immunohistochemistry, was increased in MI versus sham hearts. MI resulted in increased left ventricular systolic and diastolic dimension and decreased ejection fraction, fractional shortening, and cardiac output. NS-398 treatment partly reversed these detrimental changes. Myocyte cross-sectional area, a measure of hypertrophy, was decreased by 30% in the NS-398 versus vehicle group, but there was no effect on BNP mRNA. The interstitial collagen fraction increased from 5.4 +/- 0.4% in sham hearts to 10.4 +/- 0.9% in MI hearts and was decreased to 7.9 +/- 0.6% in NS-398-treated hearts. A second COX-2 inhibitor, rofecoxib (MK-0966), also decreased myocyte cross-sectional area and interstitial collagen fraction. TGF-beta, a key regulator of collagen synthesis, was increased in MI hearts. NS-398 treatment reduced TGF-beta immunostaining by 40%. NS-398 treatment had no effect on infarct size. These results suggest that COX-2 products contribute to cardiac remodeling and functional deficits after MI. Thus selected inhibition of COX-2 may be a therapeutic target for reducing myocyte damage after MI.

Animals↗

PubMed2003

Interaction between neuropeptide Y Y1 receptors and alpha1B-adrenoceptors in the neurovascular junction of canine splenic arteries.

Previous study has demonstrated that periarterial electrical nerve stimulation (30-s trains of pulses at a frequency of 1 or 4 Hz) induces a double-peaked vasoconstriction consisting of an initial transient, predominantly P2X-receptor-mediated constriction followed by a prolonged, mainly alpha(1)-adrenoceptor-mediated response in the isolated canine splenic artery. Treatment with 8-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-8-azaspiro[4.5]decane-7,9-dione (BMY 7378, 0.1 micromol/l), a selective alpha(1D)-adrenoceptor antagonist, produced a slight but significant inhibition of the second peaked responses. A marked inhibition of second peaked responses was obtained by exposure of the tissues to chloroethylclonidine (60 micromol/l), an alpha(1B)- and alpha(1D)-adrenoeptor antagonist. Neither BMY 7378 nor chloroethylclonidine affected the first peaked vasoconstrictor responses. [Leu(31),Pro(34)]Neuropeptide Y (10-30 nmol/l), a selective neuropeptide Y Y(1) receptor agonist, enhanced the second peaked responses in the presence of BMY 7378 but failed to enhance the responses in the presence of chloroethylclonidine. The results indicate that the postjunctional alpha(1B)-adrenoceptor subtype is likely coupled to neuropeptide Y Y(1) receptors responsible for the cooperation of the sympathetic adrenergic and neuropeptide Yergic transmission in the canine splenic artery.

Adrenergic alpha-1 Receptor Antagonists↗

PubMed2003

Assessment of sarcoplasmic reticulum Ca2+-uptake during the development of left ventricular hypertrophy.

Cardiac sarcoplasmic reticulum (SR) sequesters Ca(2+) and plays a crucial role in the regulation of intracellular Ca(2+). Its functional properties are central to the excitation-contraction cycle of cardiac muscle. In this study, we hypothesized that alterations in SR function occur during the development of left ventricular (LV) hypertrophy. LV hypertrophy was produced in Lewis rats by the one-kidney, one-clip (1K1C) procedure. LV tissues were obtained from 1K1C rats 1 week (mild, N=7), 4 weeks (moderate, N=7), and 8 weeks (severe, N=7) post-surgery and from the corresponding age-matched, sham-operated controls (N=7 at each stage). In all of these rats, the ratio of LV weight (g) to body weight (kg) was determined and considered as an index for LV hypertrophy. In addition, the ratio of lung weight (g) to body weight (kg) was determined and considered as an index for pulmonary congestion and heart failure. In each LV specimen, SR Ca(2+)-uptake and tissue Ca(2+)-ATPase (CAA) level were determined. In 1K1C rats, LV hypertrophy increased by 21, 40, and 90% at 1, 4, and 8 weeks post-surgery, respectively, compared to the age-matched, sham-operated rats, whereas pulmonary congestion did not occur at 1 and 4 weeks but increased significantly by about 21% at 8 weeks. Further, both SR Ca(2+)-uptake and immunodetectable CAA level did not change at 1 week, increased (54%) to the same extent at 4 weeks, and decreased (42%) by approximately the same extent at 8 weeks in 1K1C rats compared to the age-matched, sham-operated rats. In summary, as LV hypertrophy evolved, Ca(2+)-uptake and CAA expression did not change in the early, increased in the moderate, and then declined in the later stages of hypertrophy development. The increase in Ca(2+)-uptake and CAA expression suggests, at the cellular level, a compensatory response to LV hypertrophy, while the decline at later stages indicates the transition to heart failure.

Animals↗

PubMed2003

NAD(P)H oxidase mediates angiotensin II-induced vascular macrophage infiltration and medial hypertrophy.

OBJECTIVE: Our preliminary data suggested that angiotensin II (Ang II)-induced reactive oxygen species are involved in intercellular adhesion molecule-1 (ICAM-1) expression and leukocyte infiltration in the rat thoracic aorta. Other reports demonstrating reactive oxygen species-induced cell growth suggested a potential role of NAD(P)H oxidase in vascular hypertrophy. In the present study, we postulate that NAD(P)H oxidase is functionally involved in Ang II-induced ICAM-1 expression, macrophage infiltration, and vascular growth, and that oxidase inhibition attenuates these processes independently of a reduction in blood pressure. METHODS AND RESULTS: Rats were infused subcutaneously with vehicle or Ang II (750 microg/kg per day) for 1 week in the presence or absence of gp91 docking sequence (gp91ds)-tat peptide (1 mg/kg per day), a cell-permeant inhibitor of NAD(P)H oxidase. Immunohistochemical staining for ICAM-1 and ED1, a marker of monocytes and macrophages, showed that both were markedly increased with Ang II compared with vehicle and were reduced in rats receiving Ang II plus gp91ds-tat. This effect was accompanied by an Ang II-induced increase in medial hypertrophy that was attenuated by coinfusion of gp91ds-tat; however, gp91ds-tat had no effect on blood pressure. CONCLUSIONS: Ang II-enhanced NAD(P)H oxidase plays a role in the induction of ICAM-1 expression, leukocyte infiltration, and vascular hypertrophy, acting independently of changes in blood pressure.

Aldehydes↗

PubMed2003

Estrogen and testosterone have opposing effects on chronic cardiac remodeling and function in mice with myocardial infarction.

Premenopausal women are much less prone to develop cardiovascular disease than men of similar age, but this advantage no longer applies after menopause. We previously found that male mice have a significantly higher rate of cardiac rupture than females during the acute phase of myocardial infarction (MI); however, the effects of sexual hormones on chronic remodeling are unknown. We hypothesized that estrogen (E) may protect the heart from chronic remodeling and deterioration of function post-MI, whereas testosterone (T) may have adverse effects. Mice (4 wk old) of both genders were divided into four groups: female groups consisted of 1) sham ovariectomy (S-Ovx) + placebo (P) (S-Ovx + P), 2) S-Ovx + T, 3) Ovx + P, and 4) Ovx + T; and male groups consisted of 1) sham castration (S-Cas)+ P (S-Cas + P), 2) S-Cas + 17beta-estradiol (E), 3) Cas + P, and 4) Cas + E. MI was induced 6 wk later. Echocardiography was performed to assess cardiac function and left ventricular dimensions (LVD). Myocyte cross-sectional area (MCSA) was measured at the end of the study. In females, both testosterone and ovariectomy decreased ejection fraction (EF) and increased LVD, and when combined they aggravated cardiac function and remodeling further. Testosterone significantly increased MCSA. In males, castration or estrogen increased EF and reduced LVD, whereas castration significantly reduced MCSA. Our data suggest that estrogen prevents deterioration of cardiac function and remodeling after MI, but testosterone worsens cardiac dysfunction and remodeling and has a pronounced effect when estrogen levels are reduced.

Animals↗

PubMed2003

Syntheses, crystal structures, and luminescent properties of lanthanide complexes with tripodal ligands bearing benzimidazole and pyridine groups.

Two tripodal ligands, bis(2-benzimidazolylmethyl)(2-pyridylmethyl)amine (L(1)) and bis(2-pyridylmethyl)(2-benzimidazolylmethyl)amine (L(2)), were synthesized. With the third chromophoric ligand antipyrine (Antipy), three series of lanthanide(III) complexes were prepared: [LnL(1)(Antipy)(3)](ClO(4))(3) (series A), [LnL(1)(Antipy)Cl(H(2)O)(2)]Cl(2)(H(2)O)(2) (series B), and [LnL(2)(NO(3))(3)] (series C). The nitrate salt of the free ligand H(2)L(1).(NO(3))(2) and six complexes were structurally characterized: Pr(3+)A, Y(3+)A, Eu(3+)B, Eu(3+)C, Gd(3+)C and Tb(3+)C, in which the two A and three C complexes are isomorphous. Crystallographic studies showed that tripodal ligands L(1) and L(2) exhibited a tripodal coordination mode and formed 1:1 complexes with all lanthanide metal ions. The coordination numbers of the lanthanide metal ions for the A, B, and C complexes were 7, 8, and 10, respectively. Conductivity studies on the B and C complexes in methanol showed that, in the former, the coordinated Cl(-) dissociated to give 3:1 electrolytes and, in the latter, two coordinated NO(3)(-) ions dissociated to give 2:1 electrolytes. Detailed photophysical studies have been performed on the free ligands and their Gd(III), Eu(III), and Tb(III) complexes in several solvents. The results show a wide range in the emission properties of the complexes, which could be rationalized in terms of the coordination situation, the (3)LC level of the complexes, and the subtle variations in the steric properties of the ligands. In particular the Eu(3+)A and Tb(3+)A complexes, in which the central metal ions were wholly coordinated by chromophoric ligands of one L(1) and three antipyrine molecules, had relatively higher emission quantum yields than their corresponding B and C complexes.

Journal Article↗

PubMed2003

Creation of the Chinese visible human data set.

The United States Visible Human Project (VHP) created a digital image data set of complete human male (data acquisition finished in November 1994) and female (data acquisition finished in December 1995) cadavers in magnetic resonance imaging (MRI), computed tomography (CT), and anatomical (anatomic serial section) modes. VHP aroused worldwide enthusiasm for Visible Human Research (VHR), and the data set is being used in a variety of research and educational domains. The Visible Korean Human (VKH) male was produced in March 2001. To accelerate worldwide VHR and to promote virtual anatomy as a revolutionary break with conventional anatomy, more visible human data sets representative of different populations of the world are in demand. The Chinese Visible Human (CVH) male (created in October 2002) and female (created in February 2003) project achieved greater integrity of images, easier blood vessel identification, and were free of organic lesion (unlike the other visible human projects). We performed data acquisition, three-dimensional (3D) reconstruction, and visualization with improved technology to create CVH male and female. CVH is the first volumetric data representing a complete normal adult human male and female of an Asian population. This article presents the history of Chinese Visible Human cadavers and the methods and technology used to produce the data set.

Anatomy, Cross-Sectional↗

PubMed2003

Effects of reserpine on nerve stimulation-induced constrictions in canine isolated splenic artery.

1. Our previous studies have demonstrated that peri-arterial electrical nerve stimulation (PNS) of the canine splenic artery induces a double-peaked vasoconstriction consisting of an initial transient, dominantly P2X purinoceptor-mediated constriction, followed by a prolonged, mainly alpha1-adrenoceptor-induced response. In the present study, we examined the effects of reserpine on PNS-induced double-peaked responses. 2. The vasoconstrictor response to tyramine was abolished after reserpine treatment, but the responses to noradrenaline (NA) and ATP were not significantly modified. 3. The PNS-induced second peak vasoconstrictor responses were markedly reduced in reserpinized vessels, whereas the first peak vasoconstrictor responses were not so strongly influenced (i.e. they were not significantly affected at 1 Hz, but were significantly affected at 4 and 10 Hz). 4. All reserpine-resistant responses were unaffected by treatment with prazosin, but were abolished by subsequent application of alpha,beta-methylene ATP. The exposure of reserpine-treated tissues to NA almost completely restored tyramine-induced vasoconstriction and the second neurogenic peak vasoconstrictor response, but failed to affect the first neurogenic response. 5. The present results indicate that ATP and NA are cotransmitters responsible for the double-peaked vasoconstrictor responses of canine splenic artery. In addition, it is suggested that PNS causes NA release not only from intragranular NA storage sites, but also from tyramine-sensitive cytoplasmic sites.

Animals↗

PubMed2003

Purinergic and adrenergic cotransmission in canine isolated and perfused gastroepiploic arteries.

1. The vasoconstrictor responses of canine gastroepiploic artery to periarterial electrical nerve stimulation (PNS; 30 s trains of pulses at a frequency of 2, 4 or 8 Hz) were observed in a frequency dependent manner. The PNS-induced vasoconstrictions were abolished by tetrodotoxin (1 micromol/L) and mostly depressed but not completely by guanethidine (10 micromol/L). 2. Vasoconstrictor responses to administered noradrenaline were antagonized significantly by prazosin (0.1 micromol/L), an alpha1-adrenoceptor antagonist, but were not significantly affected by suramin (100 micromol/L), a P2 purinoceptor antagonist, or alpha,beta-methylene ATP (1 micromol/L), a P2X receptor desensitizing agent. Exogenous ATP-induced responses were clearly depressed by suramin or alpha,beta-methylene ATP, but were not significantly affected by prazosin. 3. The vasoconstrictor responses to PNS at a low frequency (2 and 4 Hz) of stimulation were markedly inhibited by suramin (100 micromol/L) and by alpha,beta-methylene ATP (1 micromol/L). The remaining responses after suramin or alpha,beta-methylene ATP were abolished by subsequent application of prazosin (0.1 micromol/L). At a high frequency (8 Hz) of stimulation, the vascular response was not significantly inhibited by suramin or alpha,beta-methylene ATP, but it was abolished by prazosin. 4. Injection of xylazine (0.3-30 nmol/L), an alpha2-adrenoceptor agonist, did not induce any clear vasoconstriction. The exposure of tissues to rauwolscine (0.1-0.3 micromol/L), an alpha2-adrenoceptor antagonist, dose-dependently increased PNS-induced vasoconstrictions at all frequencies tested. 5. The present results indicate that ATP acts as a cotransmitter with noradrenaline and is responsible for post-junctional vasoconstrictor responses at low frequencies of sitmulation, whereas the effect of noradrenaline is dominant at high-frequency stimulation in canine gastroepiploic artery. Prejunctional alpha2-adrenoceptor autoinhibition may modulate the release of either noradrenaline or ATP from sympathetic nerve terminals.

Adenosine Triphosphate↗