Endothelin(ET) is known as a family of potent hydrophobic, vasoactive peptide. We investigated the effect according to the concentrations of ET on intraocular pressure(IOP), aqueous outflow facility, pupillary diameter and light reflex and iris vessels. Twenty-four hours after injection of 2.5 microgram and 10 microgram of ET-1 into the anteriorvitreous of rabbit eyes, the IOP was reduced by 69% and 80%, respectively and did not return to the level of prefreatment until at least 14 days and 20 days, respectively. But the decrease of IOP was not due to the increased aqueous outflow. The pupillary diameter of ET-1 treated eyes was 1 to 2mm larger than the pretreatment. The time course of the pupillary effects generally ran paralled with the reduction of IOP. The iridial and conjunctival hyperemia was detectable during the pupillary dilatation. Endothelins are therefore potential participants in the local regulation of IOP, ocular blood vessel tone, and iris smooth muscle tone.
Blood Vessels ; Dilatation ; Endothelin-1* ; Endothelins ; Humans ; Hyperemia ; Intraocular Pressure ; Iris ; Muscle, Smooth ; Reflex

Animals ; Calcitonin Gene-Related Peptide ; blood ; Electric Stimulation ; Endothelin-1 ; blood ; Female ; Heart Arrest ; blood ; Male ; Rabbits ; Resuscitation ; methods

OBJECTIVETo investigate plasma endothelin-1 (ET-1) level in patients with prostate cancers and its clinical significance.

METHODSPlasma ET-1 level was measured by radioimmunoassay in 31 patients of prostate cancer (23 with non-HRPC, 8 with HRPC) and 26 patients of BPH.

RESULTSCompared with each other of the ET-1 level, there were no significant difference among the BPH group,non-HRPC group and HRPC group. No significant difference was found either between bone metastasis (BM) and non- BM, between high and middling differentiation prostate cancer group, as well as in different PSA level groups (P >0.05). But the ET-1 level in low differentiation prostate cancer was notably lower than those of the high and middle respectively (P < 0.05).

CONCLUSIONTo detect plasma endothelin-1 (ET-1) level is not a useful method to evaluate the development and the prognosis of prostate cancer.

Aged ; Aged, 80 and over ; Endothelin-1 ; blood ; Humans ; Male ; Prognosis ; Prostatic Hyperplasia ; blood ; Prostatic Neoplasms ; blood ; Radioimmunoassay

Carcinoma, Hepatocellular ; blood ; blood supply ; Endothelin-1 ; blood ; Female ; Humans ; Liver Neoplasms ; blood ; blood supply ; Male ; Neovascularization, Pathologic ; metabolism ; Nitric Oxide ; blood ; Vascular Endothelial Growth Factors ; blood

OBJECTIVETo investigate the relationship between endothelin-1 (ET-1) and tumor necrosis factor-alpha and myocardial microcircular dysfunction during coronary microembolization (CME).

METHODSCME was induced in 10 miniswine by selective infusion of microspheres (45 microm) into left anterior descending artery (LAD). We measured (1) coronary sinus level of ET-1, TNF-alpha using radioimmunoassay; (2) CFR, a measure of microvascular integrity, using Doppler flow wire in LAD at baseline and different doses of microspheres.

RESULTSCFR decrease significantly with different doses of microspheres (vs. baseline, P < 0.05). Level of ET-1, TNF-alpha increased significantly with doses of 5 x 10(4) and peaked with 10 x 10(4). Interestingly, ET-1 progressively decrease while TNF-alpha persistently elevated from doses of 12 x 10(4) to 15 x 10(4). There are reverse correlations between ET-1 and CFR (r = -0.31, P < 0.05).

CONCLUSIONSThe extent of microvascular injury wasn't linearly related to the extent of ME, where, it closely associated with myocardial ET-1.

Animals ; Coronary Thrombosis ; physiopathology ; Disease Models, Animal ; Endothelin-1 ; blood ; Microcirculation ; physiopathology ; Swine ; Swine, Miniature ; Tumor Necrosis Factor-alpha ; blood

OBJECTIVETo investigate the effect of coronary microemboliation (CME) on coronary microvascular injury and myocardial endothelin-1 (ET-1) level.

METHODSCME was induced in 10 miniswines by selective infusion of microspheres (45 microm) into left anterior descending artery (LAD). The ET-1 level in coronary sinus was measured with radioimmunoassay. The microvascular integrity indicator CFR was measured by Doppler flow wire in LAD at baseline and after infusion of microspheres.

RESULTCompared to the baseline, CFR decreased significantly with different doses of microspheres. ET-1 level increased significantly with doses of 5 x 10(4) and peaked with 10 x 10(4), and progressively decreased from doses of 12 x 10(4) to 15 x 10(4) microspheres. There was negative correlation between ET-1 and CFR (r=-0.31, P=0.02).

CONCLUSIONThe extent of microvascular injury is not linearly related to the extent of microembolization, but it is closely associated with myocardial ET-1 level.

Animals ; Coronary Vessels ; pathology ; Disease Models, Animal ; Embolism ; Endothelin-1 ; blood ; Female ; Male ; Myocardial Infarction ; blood ; pathology ; Swine ; Swine, Miniature

Expression of endogenous ouabain in placenta and the concentrations of serum ET-1 and NO were examined in 30 patients with hypertensive disorder complicating pregnancy (HDCP) and 30 healthy pregnant women to investigate the effect of endogenous ouabain on HDCP. Compared with the healthy pregnant group, the expression of endogenous ouabain dramatically increased in the HDCP groups (P<0.01). There was a significantly positive correlation between the expression of endogenous ouabain with ET-1 (r=0.5567, P<0.01), while the correlation of endogenous ouabain and NO was significantly negative (r=-0.6895, P<0.01). As expected, the correlation between ET-1 and NO was negative (r=-0.7796, P<0.01). ET-1 concentrations of maternal and cord sera in HDCP groups were significantly higher in comparison with healthy pregnant group (P<0.01). On the contrast, NO concentrations were much lower in the maternal and cord sera of HDCP groups as compared with healthy pregnant group (P<0.01). Our data suggest that endogenous ouabain is directly involved in the nosogenesis of HDCP, with accompanying decreased NO and the elevated of ET-1.
Case-Control Studies ; Endothelin-1/*blood ; Hypertension, Pregnancy-Induced/*metabolism ; Nitric Oxide/*blood ; Ouabain/*metabolism ; Placenta/*metabolism

BACKGROUNDSome studies have shown that serum resistin levels increase in hypertensive patients. Whether the increase of resistin is related to inflammatory or vascular endothelial function is still unknown. We investigated the relationship of increased resistin levels to inflammatory factors and circulating biomarkers of vascular endothelial function in hypertensive patients.

METHODSOne hundred and forty-four nondiabetic patients with new onset, hypertension were recruited. Blood pressure, blood glucose, insulin, resistin, tumour necrosis factor-α (TNF-α), interleukin-6 (IL-6), von Willebrand factor (vWF), endothelin-1 (ET-1) and nitric oxide (NO) were measured. The homeostasis model assessment, insulin resistance index (HOMA-IR) was calculated. Patients were divided into two groups according to the median level of resistin. Cytokine levels and indicators of vascular endothelial function were compared. Multiple linear regression was used to determine factors influencing resistin.

RESULTSSerum resistin ranged from 2.57 ng/ml to 20.18 ng/ml in hypertensive patients. High resistin group (> 8.36 ng/ml) had higher levels of TNF-α, IL-6, vWF and ET-1 but lower level of NO compared with low resistin group (P < 0.01). Resistin was positively correlated with body mass index, systolic blood pressure, HOMA-IR, low-density lipoprotein cholesterol, TNF-α and ET-1 but negatively correlated with NO (all P < 0.05). Multiple linear regression analysis revealed that HOMA-IR, TNF-α, NO and ET-1 are independent predictors of resistin with standardized regression coefficients of 0.625, 0.368, -0.260 and 0.222, respectively (all P < 0.01).

CONCLUSIONSWe conclude that higher resistin levels are associated with inflammatory activation and endothelial dysfunction, because patients with essential hypertension have increased TNF-α, IL-6, vWF and ET-1 and decreased NO. Moreover, the statistical association of resistin with TNF-α, NO and ET-1 suggests involvement of resistin in the progression of hypertension by influencing inflammation and endothelial function.

Endothelin-1 ; blood ; Enzyme-Linked Immunosorbent Assay ; Humans ; Hypertension ; blood ; Inflammation ; blood ; Interleukin-6 ; blood ; Resistin ; blood ; Tumor Necrosis Factor-alpha ; blood

OBJECTIVETo observe the protective effect of Shenmai Injection (SMI) on acute lung injury (ALI) induced by cardiac pulmonary bypass (CPB).

METHODSThirty patients, scheduled to receive cardiac valve replacement by CPB for the first time, were equally randomized into 2 groups, the treated group and the control group. Cardiac valve replacement was performed under extracorporeal circulation after general anaesthesia. SMI 0.6 mL/kg was given to the treated group by adding in 250 mL physiological saline for intravenous dripping at the time between intubation under anaesthesia and CPB, while 250 mL physiological saline was given to the control group alone. Blood-gas analysis was performed with blood withdrawal from the radial artery to record PaO2, PaCO2, fraction of inspired oxygen (FiO2), by them the alveolar-arterial difference of partial oxygen pressure [P(A-a) DO2] was calculated, and the respiratory index (RI), the blood concentrations of soluble intercellular adhesion molelue-1 (sICAM-1), endothelin-1 (ET-1) and nitric oxide (NO) were measured at various time points, i.e. before anesthesia induction, 0.5 h, 2 h, 6 h and 24 h after ending CPB.

RESULTSAll indices wer not significantly different between the two groups before operation (P > 0.05). After CPB, P(A-a) DO2 and RI were gradually elevated and reached the peak at 2 h after ending CPB, the increment in the treated group was lower than that in the control group (P < 0.05 or P < 0.01). Compared with the P(A-a) DO2 before anesthesia induction, P (A-a) DO2 at 0.5-24 h was statistically different (P < 0.05 or P < 0.01). Compared with the RI before anesthesia induction, RI at 2-24 h was statistically different (P < 0.05 or P < 0.01). Blood concentrations of sICAM-1 gradually raised after CPB, and reached the peak at 2 h after ending CPB, showed a higher level at 0.5-6 h after ending CPB as compared with that before anesthesia induction (P < 0.05 or P < 0.01). Blood ET-1 showed a figure of increasing as sICAM did (P < 0.05 or P < 0.01), and with a lower degree at 0.5-2 h after ending CPB in the treated group (P < 0. 01). Blood NO obviously reduced after CPB, it was lower at 0.5-24 h after ending CPB than at that before anesthesia induction (P < 0.01), and the decrement was lesser in the treated group (P < 0.05 or P < 0.01).

CONCLUSIONSMI can attenuate the acute lung injury after CPB by way of inhibiting vascular endothelial cell adhesion with inflammatory cells, antagonizing lipid peroxidation, and improving the ventilation and oxygenation function of lung.

Anesthesia ; Cardiopulmonary Bypass ; adverse effects ; Drug Combinations ; Drugs, Chinese Herbal ; therapeutic use ; Endothelin-1 ; blood ; Humans ; Intercellular Adhesion Molecule-1 ; blood ; Lung Injury ; drug therapy ; Nitric Oxide ; blood

OBJECTIVE: To investigate the effect of plasminogen activator inhibitor-1 (PAI-1), tissue type plasminogen activator (t-PA), and endothelin-1 (ET-1) on the atherosclerosis progress in the maintenance hemodialysis patients. METHODS: We enrolled 19 patients with maintenance hemodialysis (MHD) and 11 healthy people as control. Patients were divided into 2 groups according to their age above or below 40 years old (11 and 8 in each, respectively), whereas the subjects in control group were below 40 years old. All the clinical information of the research subjects was collected: including age, gender, time of hemodialysis, blood pressure, blood urea nitrogen (BUN), and serum creatinine (SCr). Immunohistochemistry and pathological image analysis were used to investigate the pathological changes, calcification and the expression of PAI-1, t-PA, and ET-1 on the blood vessel. RESULTS: Compared with the age-matched healthy control group, there were higher blood vascular media thickness, blood vascular media thickness/diagmeter ratio, blood vascular media thickness area/vascular inter-wall area ratio (P<0.05) and more calcification (P<0.05) in the the internal iliac artery in the chronic renal failure MHD patients. All the results were similar when compared the above 40 years old group with the below 40 years old one in the chronic renal failure MHD patients. There were positive correlation of blood vascular media thickness with age and blood pressure (P<0.05). Expression of PAI-1, ET-1, t-PA on the internal iliac artery vessel was elevated in the chronic renal failure MHD patients compared with the health control (P<0.05). The level of PAI-1 or ET-1 was much higher in the above 40 years old group than the below 40 years old one in the chronic renal failure MHD patients, whereas there was no significant difference in the t-PA expression between the 2 groups (P<0.05). There were positive correlation of PAI-1 or ET-1 expression with age and blood pressure (P<0.05). There were positive correlation of PAI-1 or ET-1 expression with blood vascular media thickness and calcification (P<0.05 or P<0.01). There was no correlation of hemodialysis time with blood vascular media thickness, calcification, PAI-1, t-PA, or ET-1 expressions. CONCLUSION MHD patients accompany with atherosclerosis which is severer in the patients above 40 years old than the patients below 40 years old. The higher of the blood pressure, the severer of the atherosclerosis. Abnormal expression of PAI-1 plays an important role in the progress of the atherosclerosis in the chronic renal failure MHD patients, whereas t-PA has no function in this process. The level of PAI-1 and ET-1 would be helpful to evaluating the degree of atherosclerosis in the chronic renal failure MHD patients. Hemodialysis time may not be a potential accelerator for atherosclerosis progression.
Adult ; Atherosclerosis ; blood ; etiology ; Endothelin-1 ; blood ; Female ; Humans ; Kidney Failure, Chronic ; therapy ; Male ; Middle Aged ; Plasminogen Activator Inhibitor 1 ; blood ; Renal Dialysis