Biomedical subjects

K Yin

Publications and source records attributed to K Yin.

44 records · Page 3Linked to original sources

PubMed1990

Effect of fish oil feeding on blood pressure and vascular reactivity in spontaneously hypertensive rats.

1. To examine possible antihypertensive mechanisms of fish oil feeding, we have studied vascular reactivity of aortic rings and blood pressure of spontaneously hypertensive rats (SHR). 2. SHR were fed a synthetic diet supplemented with either (10% by weight) 'Max EPA' fish oil or hydrogenated coconut oil (saturated fat) for 4 weeks. 3. Mean systolic blood pressure of fish oil fed rats was 9 mmHg lower than saturated fat fed controls. 4. Aortic rings of control SHR had a biphasic response to acetylcholine (ACh), relaxing at lower concentrations but contracting at concentrations higher than 3 x 10(-7) mol/L. No such contractions were seen in tissues of fish oil fed rats. The contractions were abolished by indomethacin, suggesting that they were caused by a cyclo-oxygenase product. 5. Tissue analysis showed that both aortic and serum generation of thromboxane B2(TxB2) was approximately three times less in fish oil fed rats than in control tissues. 6. These results indicate that the lowering of blood pressure in fish oil fed SHR could in part be due to decrease in production of thromboxane (TxA2), a potent vasoconstrictor, hence influencing vascular tone and compliance of the aorta.

Acetylcholine↗

PubMed1990

Interaction between terbutaline and ethyl 2-(4'-carboxybenzamido)-4-propionamidobenzoate sodium salt in tracheal smooth muscle relaxation of guinea pig.

Ethyl 2-(4-carboxybenzamido)-4-propionamidobenzoate sodium salt (AM-682) is a new, orally active, antiallergic compound which has been reported to inhibit the release of histamine and leukotrienes from mast cells more than disodium cromoglycate (DSCG) or Tranilast. In the present study, the interaction between terbulatine, a beta 2-receptor agonist, and AM-682 or met-A, AM-682's main metabolite in humans, in guinea pig tracheal smooth muscle was investigated by measuring the isometric tension in vitro. Combinations of terbutaline and AM-682 or met-A produced more than additive relaxant effects. Comparing the combined effects with the calculated algebraic sums of single drug effects, the differences were statistically significant for terbutaline 10(-9) mol/l and AM-682 3 X 10(-6) mol/l, 10(-5) mol/l and 3 X 10(-5) mol/l (p less than 0.01) or met-A 3 X 10(-6) mol/l, 10(-5) mol/l (p less than 0.05) on the spontaneous tone of tracheal smooth muscle, and for terbutaline 10(-9) mol/l and AM-682 10(-5) mol/l (p less than 0.01), 3 X 10(-5) mol/l (p less than 0.05) on the tension of tracheal smooth muscle induced by 5.4 X 10(-7) mol/l carbachol. Thus the tracheal smooth muscle relaxant effects of AM-682 and the beta 2-receptor agonist terbutaline were synergistic. It is suggested that the combination of AM-682 and a beta 2-receptor agonist, rather than administration of each drug separately, may provide the therapeutic advantage in the treatment of bronchial asthma.

Aminobenzoates↗

PubMed1988

Effect of pure eicosapentaenoic acid feeding on blood pressure and vascular reactivity in spontaneously hypertensive rats.

1. This study examined the effects of eicosapentaenoic acid (EPA) treatment on vascular reactivity and blood pressure in spontaneously hypertensive rats (SHR). 2. Twenty SHR were given pure EPA as the methyl ester (280 mg/kg) by gavage for 10 days. An equal number of control rats received vehicle alone. EPA treatment had no effect on blood pressure compared with control rats. 3. Aortic rings from EPA-treated rats, precontracted with PGF2 alpha showed increased endothelium-dependent relaxations to acetylcholine. Endothelium-independent relaxations to sodium nitroprusside were not altered. Rings from rats fed pure EPA did not show any differences in vasoconstrictor responses to noradrenaline or serotonin. 4. Serum thromboxane B2 (TXB2) levels fell 17% in animals given pure EPA, but prostacyclin production was not affected. These responses are less than those seen following Max EPA fish oil. 5. Thus, pure EPA treatment did not lower blood pressure, but may have a direct effect on aortic endothelia and cause increased endothelium-dependent relaxations in response to acetylcholine in SHR.

6-Ketoprostaglandin F1 alpha↗

PubMedDate not supplied

Growth and behavioral changes in mice prenatally exposed to methylmercury and heat.

Postnatal and behavioral changes in mice exposed prenatally to methylmercury and heat were investigated. Pregnant ICR mice were immersed in water at 37 degrees C or 42 degrees C for 10 min once or twice daily from day 12 through day 15 of gestation. Two hours after the heat exposure on day 12 of age, mice were injected s.c. with 5 mg Hg/kg of methylmercury (MeHg, as chloride) or saline. Prenatal exposure to heat significantly induced inactivity in an open field test (OPF) in males and retarded walking ability in both males and females. Prenatal exposure to MeHg caused significant inactivity in the OPF in females. Although heat did not enhance the effect of MeHg on physical growth or the behavior of pups and vice versa, there were some interactions between the effects of these two agents. Thus, the difference in walking ability in both sexes caused by heat was more distinctive in the saline-treated groups than in the MeHg-treated groups; the difference in locomotion in OPF caused by MeHg in females was more distinctive in the normothermic group than among the hyperthermic groups. The mechanisms underlying these behavioral changes need to be further examined.

Analysis of Variance↗

PubMedDate not supplied

In utero exposure to methylmercury and Se deficiency converge on the neurobehavioral outcome in mice.

Pregnant female ICR mice, maintained on torula-based diets containing various amounts of Se (0.02, 0.05, or 0.4 mg/kg diet), were given methyl-mercury (MeHg; 0, 5, or 9 mg Hg/kg in total) on the 12-14th days of gestation. The neurobehavioral function of the offspring born to these dams was evaluated with respect to reflex and motor development, thermal preference, and open-field activity. Se deficiency per se as well as exposure to MeHg exerted additive or synergistic effects on the neurobehavioral functions examined. The group of mice most affected was the group given the lowest amount of Se and the highest dose of MeHg. Thus, the neurobehavioral outcome of in utero MeHg exposure and Se deficiency converged. Although the dietary level of Se did not affect the Hg concentration in the fetal brain, the Se concentration and the activity of glutathione peroxidase, a selenoenzyme, were severely depressed by MeHg in the neural tissue. The possibility that functional Se deficiency by MeHg exposure partly accounts for the neurobehavioral toxicity of MeHg is discussed.

Animals↗

PubMedDate not supplied

Heterogenous and compartment-specific activation of nonlymphocytic, mononuclear cells in intraabdominal sepsis.

Although sepsis is associated with increased production of cellular pro- and anti-inflammatory mediators by monocyte/macrophages, the compartmentalization and nature of such activation has not been clearly defined. The authors examined the activation of nonlymphocytic mononuclear cells in different compartments in the cecal ligation and puncture (CLP) model of septic peritonitis. Control and CLP rat mononuclear cells from the peritoneal cavity, bronchoalveolar, as well as the lung vascular compartment were isolated 24 and 48 hours post surgery and release of nitric oxide (NO), interleukin (IL)-12, and monocyte chemoattractant protein-1 (MCP-1) was measured from culture media. Peritoneal macrophages (PMs) from CLP rats increased release of all three mediators compared to controls. Cells from the lung vascular compartment after CLP increased release of NO, but MCP-1 release was unchanged. Levels of IL-12 were not detectable. Similarly, bronchoalveolar macrophages (BMs) of CLP rats had increased release of NO, whereas IL-12 was not detectable. Release of MCP-1 increased 48 hours after CLP. Almost all PMs and BMs possessed innate phagocytic ability that was not altered during sepsis. The percentage of cells in the lung vascular compartment that had phagocytic ability, increased 48 hours post CLP, versus controls. The authors also evaluated lung injury at 24 hours after surgery by measurement of bronchoalveolar lavage protein and LDH activity. There was an increase in both these parameters 24 hours after CLP as compared to controls. Thus, there was heterogenous and compartment-specific activation of mononuclear cells in sepsis. There was nonspecific inflammatory activation in the primary site of injury. In a remote organ (lung), the authors show for the first time that there was selective activation of NO without increased release of the proinflammatory cytokine, IL-12. Phagocytic activity was maintained in the bronchoalveolar compartment whereas in the lung vascular compartment, the percentage of phagocytic cells increased.

Animals↗

PubMedDate not supplied

Computational blood flow modeling based on in vivo measurements.

Study of the relationship between hemodynamics and atherogenesis requires accurate three-dimensional descriptions of in vivo arterial geometries. Common methods for obtaining such geometries include in vivo medical imaging and postmortem preparations (vessel casts, pressure-fixed vessels). We sought to determine the relative accuracy of these methods. The aorto-iliac (A/I) region of six rabbits was imaged in vivo using contrast-enhanced magnetic resonance imaging (MRI). After sacrifice, the geometry of the A/I region was preserved via vascular casts in four animals, and ex situ pressure fixation (while preserving dimensions) in the remaining two animals. The MR images and postmortem preparations were used to build computer representations of the A/I bifurcations, which were then used as input for computational blood flow analyses. Substantial differences were seen between MRI-based models and postmortem preparations. Bifurcation angles were consistently larger in postmortem specimens, and vessel dimensions were consistently smaller in pressure-fixed specimens. In vivo MRI-based models underpredicted aortic dimensions immediately proximal to the bifurcation, causing appreciable variation in the aorto-iliac parent/child area ratio. This had an important effect on wall shear stress and separation patterns on the "hips" of the bifurcation, with mean wall shear stress differences ranging from 15% to 35%, depending on the model. The above results, as well as consideration of known and probable sources of error, suggests that in vivo MRI best replicates overall vessel geometry (vessel paths and bifurcation angle). However, vascular casting seems to better capture detailed vessel cross-sectional dimensions and shape. It is important to accurately characterize the local aorto-iliac area ratio when studying in vivo bifurcation hemodynamics.

Animals↗

PubMedDate not supplied

Role of nitric oxide in hepatic ischemia-reperfusion with endotoxemia.

Reactive oxygen species such as nitric oxide (NO) and/or superoxide have been proposed as mediators in the pathogenesis of reperfusion injury and acute endotoxemia. The purpose of this study was to examine the role of NO in a model of hepatic ischemia-reperfusion with endotoxemia (I/R + LPS). Rats subjected to 30 min of partial hepatic ischemia followed by reperfusion and LPS (Salmonella enteritidis, 1 mg/kg, i.v.,) administration, exhibited a marked, time-dependent increase in plasma alanine aminotransferase (ALT) levels compared to sham controls. An abrupt increase in liver nitrite/nitrate levels was also observed in I/R + LPS rats in association with the increases in plasma ALT. Although liver NO production in I/R + LPS rats increased with time, exacerbation of liver damage was not evident. Administration of L-NAME decreased NO production in plasma and liver but did not affect the liver damage in rats subjected to I/R + LPS. Superoxide levels in livers from I/R + LPS rats increased by threefold after 90 min reperfusion as compared to sham controls but dropped to control levels after 4 hr. There was a significant increase in neutrophils in liver lobes subjected to ischemia-reperfusion and LPS compared to sham controls and to non-ischemic lobes which received LPS. The number of neutrophils in the liver increased further in rats given L-NAME. These results suggest that the progressive injury seen in livers of I/R + LPS rats was possibly due to NO interaction with superoxide forming another reactive oxygen species such as peroxynitrite. However, inhibition of NO synthesis did not ameliorate liver damage, possibly because of an increase in tissue accumulation of activated polymorphonuclear leukocytes (PMN). Lung NO production increased in I/R + LPS rats after 4 hr reperfusion compared to sham controls. Prior administration of L-NAME did not prevent a significant rise in pulmonary NO generation (P < 0.05 at 90 min and 4 hr, compared to sham controls). This unexpected rise of pulmonary NO in the L-NAME treated group of rats was associated with a tendency for increased PMN accumulation (based on myeloperoxidase data) and superoxide generation. The results suggest that endogenous NO protected against excessive neutrophil infiltration in the lung in this model of hepatic ischemia-reperfusion and endotoxemia, and the use of L-NAME, a nonselective NOS inhibitor, may aggravate lung injury.

Alanine Transaminase↗