Search PubMed⌕ Search

Biomedical subjects

L M Zhang

Publications and source records attributed to L M Zhang.

At least 37 records · Page 2Linked to original sources
PubMed1997

Response of cultured cerebral artery smooth muscle cells to the nitric oxide vasodilators, nitroglycerin and sodium nitroprusside.

We characterized the response of soluble guanylyl cyclase in smooth muscle cells cultured from cerebral vessels to the nitric oxide (NO)-producing vasodilators, nitroglycerin (NTG) and sodium nitroprusside (SNP) and determined the ability of these agents to induce tolerance. Smooth muscle cells were isolated from porcine basilar, anterior and middle cerebral, and internal carotid arteries. Following an initial series of experiments using NTG at various concentrations and times of exposure to determine conditions, concentration-response curves of intracellular guanosine 3',5'-cyclic monophosphate (cGMP) to NTG and SNP were determined in cells pretreated for 1 h with 100 mumol NTG to induce tolerance and compared with response curves in control cells. Basal cGMP levels were 2.1 +/- 0.4 pmol/mg cell protein (n = 16). Both NTG and SNP increased cGMP in nontolerant cells, and SNP was more effective. Maximum concentrations of SNP (1 mmol/L) increased cGMP to 163 +/- 5.9 pmol/mg versus 21 +/- 2.4 pmol/mg for 1 mmol/L NTG (p < 0.01). Cells made tolerant to NTG were unresponsive to NTG up to 1 mmol/L but remained responsive to SNP. However, the response curve to SNP was significantly depressed by approximately 25%. Following washout of NTG in tolerant cells, the response of cGMP to SNP returned to control within 12 h, while response to NTG required 36 h. Similar experiments were conducted in cells initially made tolerant to SNP. These results indicate that cerebral artery smooth muscle cells in culture express a functioning soluble guanylyl cyclase and the enzymes that are necessary to metabolize NTG to NO. Prolonged exposure of the cells to NTG induced tolerance as well as cross-tolerance to SNP.

Animals↗
PubMed1997

Melatonin decreases production of hydroxyl radical during cerebral ischemia-reperfusion.

AIM: To study the effect of melatonin on hydroxyl radical (.OH) contents during cerebral ischemia-reperfusion in rats. METHODS: Ischemia was induced by occluding left lateral middle cerebral artery for 30 min following reperfusion. The salicylate trapping method coupled with ipsilateral striatal microdialysis for measurement of hydroxyl radicals generated during ischemia and reperfusion. RESULTS: The contents of dihydroxybenzoic acid (DHBA) were increased at 15 min after ischemia and remained high for 30 min after reperfusion. Melatonin (4 mg.kg-1, sc, 30 min before ischemia) decreased the production of DHBA during ischemia for 16-30 min and reperfusion for 1-30 min. CONCLUSION: Melatonin inhibits the production of hydroxyl radicals in rat brain during ischemia and reperfusion.

Animals↗
PubMed1997

The psychophysiological assessment method for pilot's professional reliability.

BACKGROUND: Previous research has shown that a pilot's professional reliability depends on two relative factors: the pilot's functional state and the demands of task workload. The Psychophysiological Reserve Capacity (PRC) is defined as a pilot's ability to accomplish additive tasks without reducing the performance of the primary task (flight task). HYPOTHESIS: We hypothesized that the PRC was a mirror of the pilot's functional state. The purpose of this study was to probe the psychophysiological method for evaluating a pilot's professional reliability on a simulator. METHODS: The PRC Comprehensive Evaluating System (PRCCES) which was used in the experiment included four subsystems: a) quantitative evaluation system for pilot's performance on simulator; b) secondary task display and quantitative estimating system; c) multiphysiological data monitoring and statistical system; and d) comprehensive evaluation system for pilot PRC. Two studies were performed. In study one, 63 healthy and 13 hospitalized pilots participated. Each pilot performed a double 180 degrees circuit flight program with and without secondary task (three digit operation). The operator performance, score of secondary task and cost of physiological effort were measured and compared by PRCCES in the two conditions. Then, each pilot's flight skill in training was subjectively scored by instructor pilot ratings. In study two, 7 healthy pilots volunteered to take part in the experiment on the effects of sleep deprivation on pilot's PRC. Each participant had PRC tested pre- and post-8 h sleep deprivation. RESULTS: The results show that the PRC values of a healthy pilot was positively correlated with abilities of flexibility, operating and correcting deviation, attention distribution, and accuracy of instrument flight in the air (r = 0.27-0.40, p < 0.05), and negatively correlated with emotional anxiety in flight (r = -0.40, p < 0.05). The values of PRC in healthy pilots (0.61 +/- 0.17) were significantly higher than that of hospitalized pilots (0.43 +/- 0.15) (p < 0.05). The PRC value after 8 h sleep loss (0.50 +/- 0.17) was significantly lower than those before sleep loss (0.70 +/- 0.15) (p < 0.05). CONCLUSION: We conclude that a pilot's PRC, which was closely related to flight ability and functional state, could partly represent the pilot's professional reliability. It is worthwhile to further research using a pilot's PRC as a predictor of mental workload in aircraft design.

Adult↗
PubMed1997

[Effect of intestinal lymph on blood pressure of rat].

The effect of intestinal lymph on blood pressure in rats was observed by the methods of lymph drainage and lymph infusion. The results obtained are as follows: (1) After 150 min of the lymph drained through the cannula of intestinal lymph duct, the blood pressure was significantly lower than that of the sham group (P < 0.05). (2) Equivalent albumin or intralipid infusion was not able to prevent the decrease in blood pressure when the lymph was lost. But in jugular-intestinal lymph duct shunt group, no significant blood pressure decrease could be seen during the drainage procedure for 4 h. (3) The blood pressure of rat with serious hemorrhagic shock could be increased significantly with a little amount of intestinal lymph infusion, and the rats survived longer than those of the control group (P < 0.05-0.01). The above results suggest that the intestinal lymph may play an important role in maintenance of blood pressure, in addition to the known function of lymphatic system by returning tissue fluid to blood and maintaining circulating blood volume.

Animals↗
PubMed1996

Effect of rat mesenchymal stem cells on development of abdominal adhesions after surgery.

One of the common and most serious side effects of abdominal surgery is the formation of adhesions within the peritoneal cavity during healing. Efforts to prevent adhesion formation have concentrated on inhibiting the inflammatory response, inhibiting the formation or encouraging the lysis of fibrin, and protection of the damaged serosal surface. We are interested in regenerating the serosal surface by providing a source of mesothelial progenitor cells. Rats were divided into groups of 10 each. Abdominal adhesions were created by removing a circle of peritoneum and suturing it back into place. Two weeks later the rats were euthanized and the adhesions scored on a scale of 0-5. A population of mesenchymal stem cells (MSCs) isolated from the skeletal muscle of neonatal rats was tested. The cells were grown in primary culture to expand the population and then trypsinized and frozen at -80 degrees C. They are then thawed and grown in secondary culture before use. The control group were injected with saline i.p. immediately after surgery. The experimental groups received (1) 1.4 X 10(6) MSCs, (2) 5 X 10(6) MSCs, (3) 7.5 X 10(6) dead MSCs, (4) 5 X 10(6) rat smooth muscle cells immediately post-op, and (5) 5 X 10(6) MSCs 4-6 hours after surgery. Only live MSCs given immediately after surgery by i.p. injection significantly decreased the adhesion scores of the rats (mean score of 3.5 vs 0.9). MSCs injected i.p. 4-6 hours after surgery actually increased the adhesion scores (3.5 vs 4.7), and rat smooth muscle cells injected i.p. immediately after surgery had no effect on adhesions. The exact mechanism of action of the MSCs is unknown at this time. However, we postulate that the MSCs have the capacity to differentiate into mesothelial cells capable of repopulating the injured mesothelium.

Animals↗
PubMed1996

Human blood vessels release tumor necrosis factor-alpha from a smooth muscle cell source.

OBJECTIVES: In septic shock, the principal source of increased plasma concentrations of tumor necrosis factor alpha (TNF) is considered to be the macrophage. Release from the macrophage is stimulated by bacterial lipopolysaccharide (endotoxin). We tested the hypothesis that vascular tissue also responds to endotoxin by releasing TNF. DESIGN: Prospective repeated measures analysis of timed-release curves. SETTING: Anesthesia research laboratory in an academic medical center. SUBJECTS: With Institutional Review Board approval and patient consent, segments of internal mammary artery and saphenous vein were obtained during coronary artery bypass surgery. INTERVENTIONS: None MEASUREMENTS AND MAIN RESULTS: Segments of saphenous veins were incubated for 24 hrs in the presence or absence of bacterial lipopolysaccharide. At 0.5, 1, 3, 6, and 24 hrs, medium was assayed for TNF. In other experiments, smooth muscle cells were cultured from saphenous veins, incubated with our without bacterial lipopolysaccharide, and a time-course of TNF release determined. Bacterial lipopolysaccharide (20 micrograms/mL) significantly stimulated release of TNF from venous tissue in a time-dependent manner. At 0.5 hrs, TNF was undetectable in untreated tissue and was 48 +/- 8 U/g wet tissue weight in the presence of bacterial lipopolysaccharide. At 3 hrs, TNF was 43 +/- 27 U/g wet tissue weight in untreated and 388 +/- 185 U/g wet tissue weight in treated (p < .01 vs. control) tissue. Segments of internal mammary artery responded in a similar manner. In smooth muscle cells cultured from saphenous vein and internal mammary artery, bacterial lipopolysaccharide triggered the release of TNF. At 3 hrs, the release of TNF in control cells was 0.2 +/- 0.15 U/mg cell protein and 17 +/- 2 U/mg in the presence of 20 micrograms/mL of bacterial lipopolysaccharide (p < .01 vs. control). CONCLUSIONS: Human blood vessels, both artery and vein, produce TNF potentially from a smooth muscle cell source in response to bacterial lipopolysaccharide.

Analysis of Variance↗
PubMed1996

Response of human artery, vein, and cultured smooth muscle cells to atrial and C-type natriuretic peptides.

OBJECTIVES: We determined the response of intracellular cyclic GMP in human arteries and veins and in smooth muscle cells cultured from these vessels to C-type natriuretic peptide in comparison with atrial natriuretic peptide. DESIGN: Repeated-measures analysis of concentration-response curves. SETTING: Anesthesia research laboratory. SUBJECTS: Vascular smooth muscle cells from human blood vessels obtained with Institutional Review Board approval and patient consent. MEASUREMENTS AND MAIN RESULTS: Segments of internal mammary artery and saphenous vein were obtained from patients undergoing coronary artery bypass surgery. Smooth muscle cells were cultured from these vessels. Concentration-response curves of intracellular cyclic GMP were determined and analyzed by two-way analysis of variance with repeated measures. In segments of intact saphenous vein, C-type natriuretic peptide was significantly more effective than atrial natriuretic peptide (16-fold increase in cyclic GMP in response to 1 microM of C-type natriuretic peptide vs. six-fold increase in cyclic GMP in response to 1 microM of atrial natriuretic peptide, p < .05). In rings of intact internal mammary artery, 1 microM of atrial natriuretic peptide (26-fold increase in cyclic GMP over basal value) was more effective than 1 microM of c-type natriuretic peptide (three-fold increase in cyclic GMP over basal value, p < .05). In cultured cells from these vessels, the pattern of response to C-type natriuretic peptide and atrial natriuretic peptide was the same as in the intact vessels. CONCLUSIONS: These results indicated that human smooth muscle cells in arteries and veins express both forms of natriuretic peptide receptors but that atrial natriuretic peptide acts primarily on the artery and C-type natriuretic peptide acts predominantly on the vein. Increased concentrations of C-type natriuretic peptide could contribute to venous pooling in septic shock.

Analysis of Variance↗
PubMed1996

[Study on promoting and increasing lactation in postpartum patients].

Several methods to promote the secretion of milk in 280 puerperants have been tested in this study. A multi-agent controlling method to promote the secretion of the milk was found. The effective control agents, such as the condition of breast, the stimulation of the secretion of milk, and the collagen soup with appropriate time and quantity, have been selected. According to the observation, the percentage of milk fed infants reached 98% in 24 hours post partum in the study group, while it only reached 5% in the control group (P < 0.01). Compared with the general regulation that the secretion of milk started on the third day post partum, and reached 200 ml on the 4 approximately 5th day, the multi-agent controlling method to promote the secretion of milk improved the time and quantity of the milk secretion. It would lay an excellent foundation for the infant growth.

Collagen↗
PubMed1995

C-natriuretic peptide but not atrial natriuretic peptide increases cyclic GMP in cerebral arterial smooth muscle cells.

A-type natriuretic peptide (ANP) is found primarily in the heart and is released into the circulation. C-type (CNP) is found principally in the brain and has also been detected in the systemic circulation. When injected, both peptides produce vasodilatation most likely by elevation of guanosine 3'5'-cyclic monophosphate (cGMP) in smooth muscle cells via two distinct receptors, NPR-A and NPR-B. In this present study, we determined the effects of these two peptides on intracellular cGMP in smooth muscle cells cultured from pig cerebral and peripheral arteries. In smooth muscle cells cultured from the left anterior descending coronary artery, ANP and CNP increased cGMP with equal potency and efficacy (EC50 for ANP and CNP, 3.6 +/- 0.2 x 10(-8) M and 6.7 +/- 0.8 x 10(-8) M, respectively). In contrast, in smooth muscle cells from cerebral arteries, ANP was without effect while CNP increased cGMP in a concentration dependent manner (EC50: 9.6 +/- 1.7 x 10(-8) M). Stimulation of the soluble guanylyl cyclase with either nitroglycerin or nitroprusside was equivalent in the two cell types. The pattern of response of intracellular cGMP to CNP and ANP in isolated intact arteries from brain and heart was similar to that found in the cultured cells. These results suggest that smooth muscle cells in cerebral arteries express only NPR-B while cells from peripheral arteries can express both NPR-A and NPR-B.

Animals↗
PubMed1995

Tolerance to nitroglycerin in vascular smooth muscle cells is not affected by the level of intracellular glutathione or L-cysteine.

A major hypothesis for the mechanism of tolerance to nitroglycerin (NTG) is that continued use causes a decrease in thiol donors within the vascular smooth muscle cell that are essential for the effect of NTG. We tested this idea directly in the target cell. NTG tolerance, measured as reduced formation of intracellular cyclic guanosine monophosphate (cGMP), was induced in pig coronary smooth muscle cells. The consequence of altering intracellular levels of the thiol donors, glutathione (GSH) and L-cysteine (L-cys), was determined. Incubating cells with 100 microM NTG for 1 h caused an 83% reduction in cGMP formation in response to acute readministration of 200 microM NTG for 2 min but was not associated with a reduction in intracellular GSH or L-cys. This result was not altered when intracellular GSH levels were increased three-fold by including 1 mM GSH in the incubation buffer. Also, recovery from tolerance was not affected by supplementation with GSH. Further, the response of cGMP to NTG was not altered by inhibiting the synthesis of GSH and lowering intracellular levels of GSH by 77%. Similar findings were made with supplemental L-cys or N-acetyl-L-cysteine. These results do not support the hypothesis that tolerance to NTG is the result of a reduction of the thiol donors GSH and L-cys within vascular smooth muscle cells.

Acetylcysteine↗
PubMed1995

Protamine does not affect the formation of cGMP or cAMP in pig vascular smooth muscle cells in response to vasodilators.

OBJECTIVES: Protamine has recently been shown to have a direct vasodilator action in isolated vascular tissue. As one possible mechanism for this action, it has been hypothesized that protamine might increase the response of vascular smooth muscle to the endothelium-derived relaxing factor, nitric oxide. In this study, we tested this hypothesis and examined the effect of protamine on other guanosine 3'5'-cyclic monophosphate (cGMP)- and adenosine 3'5'-cyclic monophosphate (cAMP)-dependent processes. DESIGN: Prospective, repeated measures analysis of concentration-response curves. SETTING: Anesthesia research laboratory in an academic medical center. SUBJECTS: Cultured coronary artery smooth muscle cells from pig heart. INTERVENTIONS: Sodium nitroprusside was used to mimic the action of the endothelium-derived relaxing factor by stimulating the soluble guanylyl cyclase and increasing intracellular cGMP. Atrial natriuretic peptide was used to stimulate the particulate guanylyl cyclase. Isoproterenol and forskolin were used to increase intracellular cAMP. The responses to these agents were determined in the presence and absence of protamine. MEASUREMENTS AND MAIN RESULTS: In cultured vascular smooth muscle cells, sodium nitroprusside increased cGMP, the second messenger for endothelium-derived relaxing factor, in a concentration-dependent manner. In cells treated with protamine (32 to 250 micrograms/mL), we could detect no effect of protamine on basal intracellular levels of cGMP until a concentration of 250 micrograms/mL of protamine was used. At this concentration, protamine increased basal cGMP concentrations from 4.2 +/- 0.3 to 9.0 +/- 0.6 pmol/mg protein (p < .001). The response of intracellular cGMP to sodium nitroprusside in cells treated with 250 micrograms/mL or other concentrations of protamine was not different from control. Likewise, we could detect no effect of protamine on intracellular cGMP stimulated with the atrial natriuretic peptide or on cAMP stimulated with the beta-adrenergic receptor agonist, isoproterenol, or with forskolin. CONCLUSIONS: These experiments show that protamine does not alter the responses of the intracellular second messengers, cGMP and cAMP, to the vasodilators sodium nitroprusside, atrial natriuretic peptide, isoproterenol, and forskolin. These results do not support the hypothesis that protamine sensitizes vascular smooth muscle cells to the endothelium-derived relaxing factor, nitric oxide.

Analysis of Variance↗
PubMed1994

Run-down of calcium current is related to intracellular sodium.

Run-down of Ca2+ current was studied in isolated guinea pig ventricular cells and it was found to be attenuated by intracellular sodium. Calcium currents were recorded after activation of Na+ channels by a step pulse. The "run-down" in 30 min was significantly reduced compared with control cells. When NaCl (0.1-10 mM) diffused from the micropipette into the cells, run-down of Ca2+ current was also significantly attenuated. However, the resulted increase of intracellular Na+ did not affect voltage dependent activation of Ca2+ current, but the duration of the action potential was shortened slightly.

Action Potentials↗
PubMed1994

Thromboxane A2/prostaglandin H2-stimulated mitogenesis of coronary artery smooth muscle cells involves activation of mitogen-activated protein kinase and S6 kinase.

Prostaglandin H2 (PGH2) and thromboxane A2 (TXA2) are potent activators of platelets and vascular smooth muscle whose responses are mediated through a common G-protein coupled receptor (TXA2/PGH2 receptor). Despite the many studies describing their ability to aggregate platelets and contract vascular smooth muscle, little is known concerning the potential mitogenic capabilities of these autocoids. Mitogen-activated protein kinases (MAP kinases) and ribosomal S6 kinases are well characterized intracellular mediators involved in proliferation of cells. The present study was designed to examine the activation of MAP kinase and S6 kinase in guinea pig coronary artery smooth muscle cells (CASMC) in response to stimulation by a TXA2/PGH2 mimetic, I-BOP ([1S-(1 alpha,2 beta(5Z),3 alpha(1E,3R*),4 alpha)]-7-[3-(3-hydroxy-4-(4'- iodophenoxy)-1-butenyl)-7-oxabicyclo-[2.2.1]heptan-2-yl]-5-h eptenoic acid). Equilibrium radioligand binding assays using [125I]BOP defined a single class of high affinity TXA2/PGH2 receptors on monolayers of guinea pig CASMC (Kd = 0.18 +/- 0.03 nM; 26,476 +/- 3,600 sites/cell; 0.08 +/- 0.01 pmol/mg of protein; n = 12). I-BOP produced a concentration-dependent increase in [3H]thymidine incorporation in these cells (EC50 = 0.3 nM) which was inhibited by a series of TXA2/PGH2 receptor antagonists as well as by verapamil and staurosporine. I-BOP also produced a time-dependent increase in the activation of kinases phosphorylating myelin basic protein (MBP; a substrate for MAP kinase) and RRLSSLRA (S6 peptide; a substrate for pp85rsk kinase), reaching a peak activation between 5 and 10 min. Stimulated MBP kinases were identified as ERK1 and ERK2. The activation of these kinases by I-BOP was inhibited by the TXA2/PGH2 receptor antagonist SQ29548 and also by staurosporine. These results indicate that I-BOP, a TXA2/PGH2 mimetic, produces growth of coronary artery vascular smooth muscle cells, which is preceded by activation of MAP kinase and S6 kinase.

Animals↗