Biomedical subjects

T Yong

Publications and source records attributed to T Yong.

13 recordsLinked to original sources

PubMed1997

Nicotine induces leukocyte rolling and adhesion in the cerebral microcirculation of the mouse.

Nicotine and several related metabolites were examined for their ability to induce leukocyte rolling and adhesion in the cerebral microcirculation of the mouse. A cranial window was surgically prepared for the visualization of the pial microcirculation using an intra-vital microscopy imaging system. Using this technique rhodamine-labeled leukocytes could be visualized and video-recorded as they traveled within the microvessels, and the quantitation of their rolling and adhesion along the pial venule walls was assessed during an off-line video playback analysis. Nicotine was found to produce significant dose-related increases in leukocyte rolling and adhesion. Cotinine, a major nicotine metabolite, did not induce the same degree of leukocyte rolling and adhesion. Mecamylamine, a nicotine antagonist, was found to inhibit the nicotine-induced leukocyte rolling and adhesion. Anti-P-selectin antibody blocked nicotine-induced leukocyte rolling, while anti-CD18 antibody effectively inhibited leukocyte adhesion, but not rolling in similar experiments. Nicotine-induced leukocyte rolling and adhesion were also inhibited by superoxide dismutase and catalase. These data suggest that nicotine, the principle pharmacological agent in cigarette smoke and related tobacco products, acts via a ganglionic-type nicotinic receptor to enhance leukocyte rolling via P-selectin and reactive oxygen radical-dependent mechanisms in cerebral microcirculation of the mouse.

Administration, Topical↗

PubMed1997

Local histamine release increases leukocyte rolling in the cerebral microcirculation of the mouse.

Histamine-mediated induction of leukocyte rolling and adhesion in the cerebral microcirculation was examined in two inbred strains of mice (SJL/J and BALB/c). A cranial window was surgically prepared for the visualization of the cerebral microcirculation using intra-vital microscopy. Leukocyte rolling and adhesion to pial venular walls were assessed during off-line video playback analyses. The surgical preparation of the cranial windows was found to trigger 'spontaneous' leukocyte rolling, and this was attributed to disruption of dural mast cells and localized release of vasoactive histamine. This spontaneous leukocyte rolling was observed only in the SJL/J strain of mice, and could be prevented by presurgical treatment with the mast cell stabilizer sodium cromoglycate. BALB/c mice did not show 'spontaneous' leukocyte rolling or adhesion; this strain is known to have low numbers of CNS-associated mast cells. Exogenous histamine, applied topically to the cerebral microcirculation via the cranial window in mice pretreated with sodium cromoglycate, produced significant dose-dependent increases in leukocyte rolling and adhesion to pial venules in SJL/J mice, but not in BALB/c mice. Diphenhydramine (H1 receptor antagonist), but not cimetidine (H2 receptor antagonist), abolished both 'spontaneous' and histamine-induced leukocyte rolling. Anti-P-selectin antibody was found efficiently to block both spontaneous and histamine-induced increases in leukocyte rolling, but not leukocyte adhesion.

Animals↗

PubMed1996

Hypothesis: a possible role for mast cells and their inflammatory mediators in the pathogenesis of autoimmune encephalomyelitis.

Mast cells and their potent chemical mediators are known to initiate and modulate a number of important inflammatory cascades. With respect to the central nervous system, the role of mast cells as participants in the promotion and resolution of inflammation has been widely underestimated. Mast cell-derived histamine, serotonin, kallikreins, and tumor necrosis factor-alpha (TNF-alpha) can enhance microvascular permeability, leukocyte rolling, adhesion, and extravasation of inflammatory cells into the brain and spinal cord. Mast cell mediators may play an important role in autoimmune encephalomyelitis and multiple sclerosis by promoting the entry of autoreactive T cells and the recruitment of nonspecific monocytes across the blood:brain barrier.

Animals↗

PubMed1996

Microvascular leakage in mouse pial venules induced by bradykinin.

The actions of bradykinin on pial venule leaky site formation were measured intra-vitally in two inbred strains of mice (BALB/c and SJL/J). Pial venules were visualized using an open cranial window microscopy technique and the microvascular leaky site formation was assessed visually using a fluorescein-dextran (70 kDa) INDICATOR. The SJL/J strain was found to be very sensitive to bradykinin-induced microvascular leakage. Pial venule leaky site formation was observed after exposure to 10 pM of bradykinin. In contrast, the BALB/c strain was found to be refractory to bradykinin-induced leakage. Pial arterioles were dilated in response to bradykinin in both strains of mice. These results support the concept that genetically controlled differences in vascular sensitivity and localization of inflammatory peptides play important roles in the generation of vasogenic oedema and inflammation in CNS trauma and disease.

Animals↗

PubMed1995

[Quantitative study of a SEM image processing system on the absorptive mesothelium of the diaphragmatic peritoneum].

SEM and a medical image processing system attached to SEM were used to study the peritoneal mesothelium on mice diaphragm. The absorptive mesothelium was first reported owing to its function and morphology. The absorptivity of diaphragmatic peritoneum was surveyed by the measurement of the area of the absorptive mesothelium. The arrangement of the absorptive mesothelium on diaphragmatic peritoneum was block-like with abnormal distribution, and the maximum and minimum areas of the block were 1153 microns 2 and 66 microns 2. But the absorptive mesothelium on left and right half diaphragm were normally distributed. The average areas of the absorptive mesothelium on all diaphragm, left half diaphragm and right half diaphragm were 432.6 microns 2, 270.5 microns 2 and 512.0 microns 2 respectively. The distributive law of the absorptive mesothelium was costal portion > sternum portion > vertebral column portion. The average absorptivity of all diaphragmatic peritoneum was 29.2%, but that of left and right half diaphragmatic peritoneum were 17.4% and 32.9% respectively.

Absorption↗

PubMed1994

Histamine-induced microvascular leakage in pial venules: differences between the SJL/J and BALB/c inbred strains of mice.

The actions of histamine on pial venule leaky site formation were measured intravitally in two inbred strains of mice (BALB/c and SJL/J). Pial venules were visualized using a cranial window microscopy technique, and microvascular leaky site formation was assessed visually using a fluorescein-dextran indicator. SJL/J mice were found to be sensitive to histamine-induced leakage, whereas the BALB/c strain was refractory. Exposure to pertussis toxin enhanced the sensitivity to histamine in the SJL/J strain, but little effect was observed for BALB/c mice. However, the employment of a polymerase chain reaction (PCR) technique for the detection of mRNA for histamine H1 receptor identified receptor-specific message in isolated cerebrovascular endothelium from both strains of mice. The lack of pial responsiveness in the BALB/c mice remains unexplained. Mast cells in the dura mater were found to be more numerous in SJL/J mice than in BALB/c mice. This observation supports previous observations of strain-specific differences in CNS inflammation. The results support the concept that genetically controlled differences in vascular sensitivity and localization of CNS-associated mast cells may play important roles in the generation of vasogenic edema and inflammation in CNS trauma and disease.

Animals↗

PubMed1994

[Study on the pelvic stomata and computer image processing].

A medical image processing system attached to electron microscope was used to study the pelvic stomata of fetuses quantitatively. Two kinds of the mesothelial cells were found on the pelvic peritoneum of fetuses and mice, i.e. flattened and cuboidal cells. The pelvic stomata, arranged in clusters, only were located among the cuboidal cells with skewed distribution. Discrete scale of the pelvic stomata area varied greatly. The average area of a stoma was 10.00 +/- 9.44 microns2. Coefficient of variation was 94.40. Standard deviation and standard error were 9.44 and 0.98, respectively. Most of the pelvic stomata present were 1.34 microns2 to 32.11 microns2, and the maximum and the minimum areas of stomata were 43.4 microns2 and 0.8 micron2. The average percentage of the pelvic stomata was 7.2%.

Animals↗

PubMed1993

Enhancement of histamine-induced vascular leakage by pertussis toxin in SJL/J mice but not BALB/c mice.

Pertussis toxin (PTX) from Bordetella pertussis is known to enhance inflammatory responses which involve histamine and serotonin, including cell-mediated delayed-type hypersensitivity reactions. In this study we examined the effects of PTX on histamine-modulated microvascular responses. The actions of histamine on arteriole diameter and post-capillary leaky site formation in the cremaster muscle were measured intra-vitally in two inbred strains of mice (viz. BALB/c and SLJ). In SJL mice the rate and extent of histamine-induced leaky site formation were greatly enhanced (from 8.3 to 21.0 leaky sites per 0.1 cm2) by pre-exposure to PTX. In sharp contrast, PTX did not alter histamine-induced leaky site formation in BALB/c mice. Histamine-mediated dilation in arterioles in both strains of mice were not enhanced by PTX. PTX may enhance the development of inflammatory responses by enhancing histamine-induced leaky site formation of the microvasculature.

Animals↗

PubMed1992

Effect of prostaglandin E1 on leukotriene C4-induced increases in vascular permeability of hamster cheek pouch.

Our goal was to determine whether there is a synergistic effect of prostaglandin E1 (PGE1) on leukotriene C4 (LTC4)-induced increases in vascular permeability of the hamster cheek pouch in vivo. Changes in permeability were quantified by counting venular leaky sites (LS) and calculating clearance (CLR) of fluorescein isothiocyanate (FITC)-dextran 70kDa, during suffusion of the cheek pouch with LTC4 in the absence or presence of PGE1. LTC4 produced a dose-related increase in LS and CLR, and PGE1 (0.01 microM) significantly potentiated the effect of LTC4. During suffusion with LTC4 (15.0 nM) in the absence of PGE1, LS increased from 0 to 19 +/- 3/0.11 cm2 and CLR increased from 0.3 +/- 0.1 to 1.0 +/- 0.2 x 10(-6) ml/sec. During superfusion with LTC4 (15.0 nM) in the presence of PGE1, LS increased from 0 to 40 +/- 3/0.11 cm2, and CLR increased from 0.4 +/- 0.1 to 2.1 +/- 0.5 x 10(-6) ml/sec. To determine whether the effect of PGE1 on LTC4-induced increases in vascular permeability was related to the vasodilatory effect of PGE1, we examined the effect of isoproterenol (ISO). In contrast to that observed with PGE1, ISO decreased LTC4-induced increases in LS and CLR. Our data suggest that there is a synergistic effect of PGE1 on LTC4-induced increases in venular permeability that is not mediated by a vasodilatory action of PGE1.

Alprostadil↗

PubMed1992

Role of peptidases in bradykinin-induced increase in vascular permeability in vivo.

The purpose of this study was to examine whether neutral endopeptidase and angiotensin I-converting enzyme, two membrane-bound metalloenzymes that are widely distributed in the microcirculation, play a role in bradykinin-induced increase in vascular permeability in the hamster cheek pouch. Changes in vascular permeability were quantified by counting the number of leaky sites and by calculating the clearance of fluorescein isothiocyanate (FITC)-dextran (molecular mass, 70,000 d) during suffusion of the cheek pouch with bradykinin. Bradykinin produced a concentration- and time-dependent increase in the number of leaky sites and clearance of FITC-dextran. The selective, active site-directed neutral endopeptidase inhibitors phosphoramidon (1.0 microM) and thiorphan (10.0 microM) and the selective angiotensin I-converting enzyme inhibitor captopril (10.0 microM) each shifted the concentration-response curve to bradykinin significantly to the left. During suffusion with bradykinin (1.0 microM) and phosphoramidon, the number of leaky sites increased significantly from 17 +/- 2 to 27 +/- 4 sites per 0.11 cm2 (mean +/- SEM, p less than 0.05), and FITC-dextran clearance increased significantly from 1.0 +/- 0.2 to 2.1 +/- 0.3 ml/sex x 10(-6).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1992

In vivo responses of allografted cerebral parenchymal arterioles to ethanol and angiotensin II: effect of calcium channel blockade.

The goals of these studies were to determine: 1) the effect of ethanol and angiotensin II on the diameter of allografted cerebral parenchymal arterioles in vivo, and 2) the effect of the calcium antagonist, verapamil, in modulating the responses of allografted cerebral parenchymal arterioles to ethanol and angiotensin II. Using a chamber technique, neonatal (< 24 hours old) cortical tissue was transplanted onto the cheek pouch of adult hamsters. Eight to thirteen days after allografting, hamsters were anesthetized with sodium pentobarbital (6.0 mg/100 grams i.p.), and allografted cerebral parenchymal arterioles were viewed using intravital microscopy. Diameter of allografted cerebral parenchymal arterioles was measured before (control), during and after topical application of ethanol (0.1%, 0.25%, 0.5%, 1.0%, and 2.0%) and angiotensin II (0.1 and 1.0 ng/ml). Application of ethanol and angiotensin II was repeated after changing the suffusion fluid to one containing verapamil (50 mg/L). We found that ethanol and angiotensin II produced dose-related constriction of allografted cerebral parenchymal arterioles. In addition, verapamil significantly attenuated vasoconstriction produced by ethanol and angiotensin II. Thus, our findings suggest that ethanol and angiotensin II cause constriction of allografted cerebral parenchymal arterioles through a calcium-dependent mechanism.

Angiotensin II↗

PubMed1991

Cigarette smoke extract attenuates endothelium-dependent arteriolar dilatation in vivo.

The purpose of this study was to examine the effects of cigarette smoke extract on endothelium-dependent and endothelium-independent dilatation of arterioles in vivo. Using intravital microscopy, we measured diameter of arterioles contained within the microcirculation of the hamster cheek pouch during suffusion with acetylcholine and nitroglycerin, before and after treatment with cigarette smoke extract. Under control conditions, acetylcholine and nitroglycerin produced dose-related dilatation of cheek pouch arterioles. Superfusion of cigarette smoke extract (1.0%) did not alter baseline diameter of arterioles or vasodilatation in response to nitroglycerin but impaired dilatation of arterioles in response to acetylcholine. Next, we examined the possibility that impaired dilatation of cheek pouch arterioles in response to acetylcholine after exposure to cigarette smoke extract may be related to the release of substances produced via the cyclooxygenase pathway. In indomethacin-pretreated hamsters, acetylcholine produced similar vasodilatation before and after exposure to cigarette smoke extract. Thus these findings suggest that cigarette smoke extract impairs endothelium-dependent responses of cheek pouch arterioles. The mechanism of impaired responses of cheek pouch arterioles after exposure to cigarette smoke extract appears to be related to the release of substances produced via the cyclooxygenase pathway.

Acetylcholine↗

PubMed1989

Volume expansion attenuates baroreflex sensitivity in the conscious nonhuman primate.

We examined the effect of intravascular volume expansion (VE) on the arterial baroreflex control of pulse rate (PR) in conscious, chronically instrumented monkeys tethered in their cages. A total of five monkeys was studied after surgical implantation of catheters in the descending aorta, the left atrium, and the internal jugular vein. Mean arterial blood pressure (MABP)-PR stimulus response curves were constructed by decreasing and increasing blood pressure with nitroprusside and phenylephrine, respectively. The data were analyzed with a regression analysis that generated a sigmoid curve and the maximum sensitivity (slope) of the curve. The data were obtained before and after VE with an isotonic isoncotic dextran solution equal to 20% of the estimated blood volume. After VE, the MABP-PR curve shifted to the right at the high blood pressures, and there was a significant decrease in the maximum sensitivity from 5.65 +/- 1.44 for control to 2.14 +/- 0.63 after VE (P less than 0.05). We concluded that VE attenuates the baroreflex control of heart rate in the conscious nonhuman primate.

Animals↗