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Biomedical subjects

T Supaporn

Publications and source records attributed to T Supaporn.

5 recordsLinked to original sources

PubMed2004

Role of patient-support groups in the Thailand transplant program.

Thailand started kidney transplantation in 1972 when vascular and nonvascular transplant programs were first established. Presently, we have 27 kidney, 6 liver, and 6 intrathoracic private or governmental transplantation centers, all approved and members of the Organ Donation Centres Thai Red Cross Society (ODC). They also provide organ procurement teams to the ODC. The Thai Medical Council has issued and supervised the criterion of brain death and ethical rules of transplantation to all practicing physicians since 1989. All recipients must register at these selected transplantation centers and at the ODC. When the potential donor arrives from any hospital in Thailand, the donor hospital notifies the ODC and organ procurement teams are sent out to harvest organs and transfer them to the recipient transplantation centers. The ODC computerizes and shares organs according to ABO, HLA typing, and crossmatching results. After transplantation all patients register with the Thai Transplantation Society (TTS) and the ODC. The TTS, the Thai Transplant Coordinator Society, and the ODC are responsible for the education of surgeons, physicians, nurses, patients, the public, and mass media to improve our transplant program. Bone marrow transplantation has separate regulations. Pooled, nonrelated bone marrow donors are registered at the blood-bank of the Thai Red Cross Society to provide donors for bone marrow transplantation. Financially, government support recipients only if they are state enterprise workers or civil servants. Public fund support through the ODC for organ procurement and the Kidney Foundation of Thailand is available for kidney transplantation. The ODC and the transplantation centers are the main patient-support groups for transplant programs in Thailand.

Education, Continuing↗

PubMed2000

Simple and sensitive high-performance liquid chromatographic.

A rapid, selective, sensitive, and reproducible reversed-phase HPLC procedure for the quantitative determination of mycophenolic acid (MPA)--an active plasma metabolite of the immunosuppressant mycophenolate mofetil (MMF) in plasma is described. The procedure involves one-step extraction of MPA and the internal standard, standard [RS-60461-000: (E)-6-[1,3-dihydro-4-(4-carboxy-butoxy)-6-methoxy-7-methyl-3-oxo-5-is obenzo-furanyl-4-methyl-4-hexenoic acid] with dichloromethane-dichloroethane (1:1, v/v) at acidic pH. Chromatographic separation consisted of the mobile phase [acetonitrile-0.05% phosphate buffer, pH 3.4 (45:55, v/v)] running through the column (Techopak-10 C18) at flow-rate of 0.8 ml/min. Detection was at UV wavelength of 254 nm. The mean recoveries of MPA and the internal standard at concentrations of 0.1 and 20 microg/ml were 89-98%, and 90-96%, respectively. The within-day coefficients of variation for MPA were 0.3-7.8% and the day-to-day coefficients of variation were 1.1-2.0%. The minimum detectable concentrations for both MPA and the internal standard in plasma were 0.005 microg/ml. The method was found to be suitable for use in clinical pharmacokinetic study.

Chromatography, High Pressure Liquid↗

PubMed1998

Cardiovascular actions of ET-B activation in vivo and modulation by receptor antagonism.

The endothelin (ET)-B receptor subtype is expressed on vascular endothelial and smooth muscle cells and participates in vasodilatation and vasoconstriction. Controversy exists regarding the role of the ET-B receptor as a mediator of systemic, pulmonary, and renal vasoconstriction in states of marked ET-1 activation. Moreover, the potential activation of endogenous ET-1 with secondary stimulation of the ET-A receptor in response to sarafotoxin S6c (S6c) remains unclear. This study was designed to assess the cardiovascular actions of ET-B activation with S6c in the presence and absence of selective ET-A antagonism with FR-139317 and dual ET-A/ET-B antagonism with SB-209670 in the anesthetized dog. Compared with time control (n = 5), S6c increased from baseline systemic vascular resistance (SVR) [28 +/- 7 vs. 14 +/- 3 resistance units (RU), P < 0.05] and pulmonary vascular resistance (PVR) (3.2 +/- 0.7 vs. 0.9 +/- 0.3 RU, P < 0.05) and decreased cardiac output (CO) (-1.7 +/- 0.3 vs. -0.5 +/- 0.1 l/min, P < 0.05), with no differences in renal vascular resistance in association with increases in plasma ET-1. S6c also decreased mixed venous oxygen saturation (SVO2) (56 +/- 6 vs. 76 +/- 5%, P < 0.05). Selective ET-A receptor antagonism did not affect the actions of S6c, with the exception that ET-A receptor antagonism blocked the increase in SVR to high-dose S6c. Dual ET-A/ET-B receptor antagonism attenuated the increase from baseline in SVR (7 +/- 1 vs. 28 +/- 7 RU, P < 0.05) and PVR (0.7 +/- 0.2 vs. 3.2 +/- 0.7 RU, P < 0.05) and decrease from baseline in CO (-0.9 +/- 0.1 vs. -1.7 +/- 0.3 l/min, P < 0.05) and SVO2 (-7 +/- 3 vs. -20 +/- 3%, P < 0.05) observed with S6c alone. In summary, this study demonstrates an important role of ET-B receptor activation in vivo, which results in increases in plasma ET-1 and systemic and pulmonary vasoconstriction and reductions in CO and SVO2. This study also supports a modest role for the ET-A receptor in mediating the systemic vasoconstrictor response to high-dose S6c.

Animals↗

PubMed1996

Blunted cGMP response to agonists and enhanced glomerular cyclic 3',5'-nucleotide phosphodiesterase activities in experimental congestive heart failure.

The natriuretic peptide (NP) and nitric oxide (NO) systems are activated in congestive heart failure (CHF), resulting in increased synthesis of cGMP, which serves as a second messenger for both humoral systems. These two regulatory systems play functional roles in the preservation of glomerular filtration rate (GFR) and sodium excretion in both acute and chronic CHF. A progressive decline in glomerular responsiveness to atrial natriuretic peptide (ANP) characterizes the terminal stage of chronic CHF despite elevation of plasma ANP. Phosphodiesterase isozymes (PDEs) are integral factors in determining cellular content and accumulation of cGMP, and up-regulation of PDE activity could participate in the glomerular resistance to ANP in severe CHF. To date, characterization of possible alteration of glomerular PDE isozyme activities in CHF is unknown, as is the in vitro glomerular response to the nitric oxide-soluble guanylyl cyclase pathway. We, therefore, first determined cGMP generation in response to particulate and soluble guanylyl cyclase activation by ANP and sodium nitroprusside (SNP) in isolated glomeruli from normal (N = 6) and CHF dogs (N = 5) in which CHF was induced by rapid ventricular pacing for 18 to 28 days. Secondly, we explored the presence of major PDE isozymes in glomeruli isolated from the control and CHF dogs. When ANP or SNP (10(-10) to 10(-4) M) were incubated with the suspension of isolated glomeruli, cGMP accumulation was lower by -72 to -96% with ANP and -42 to -77% with SNP in all glomerular medias obtained from CHF compared to controls. PDE hydrolyzing activity of both cAMP and cGMP were higher in the glomerular homogenates obtained from the kidneys of the CHF group (N = 5) compared to those of the control group (N = 5). We conclude that in severe chronic experimental CHF, glomerular cGMP accumulation decreases in response to both ANP and SNP, and CHF is characterized by enhanced cGMP- and cGMP-PDE activities that may participate in glomerular maladaptation to this cardiovascular syndrome.

3',5'-Cyclic-AMP Phosphodiesterases↗

PubMed1996

Role for the endogenous natriuretic peptide system in the control of basal coronary vascular tone in dogs.

1. While the natriuretic peptides (atrial, brain and C-type) mediate potent endothelium-independent vasorelaxing actions in vitro, the role of the endogenous natriuretic peptide system in vascular regulation in vivo remains unclear. 2. HS-142-1 is a novel natriuretic peptide receptor antagonist derived from a fungus named Aureobasidium sp. which selectively blocks particulate guanylate cyclase-linked natriuretic peptide A and B receptors that bind atrial, brain and C-type natriuretic peptide, and thus attenuates the generation of cGMP. 3. To characterize the vascular actions of the endogenous natriuretic peptide system in the control of basal coronary and systemic haemodynamics, six normal male mongrel anaesthetized dogs were studied while a second group of five dogs served as a control. HS-142-1 was given as an intravenous bolus at 3 mg/kg and was studied over five 20 min periods. 4. No significant difference after HS-142-1 was observed in mean arterial pressure, heart rate, cardiac output, right atrial pressure, pulmonary capillary wedge pressure or systemic vascular resistance compared with control. In contrast, a significant increase in coronary vascular resistance and decrease in coronary blood flow were observed which were different from the baseline values and the responses of the control group. 5. These studies demonstrate that HS-142-1 produces vasoconstriction in the coronary circulation. We conclude that the endogenous natriuretic peptide system, which is of cardiac and endothelial cell origin, is an important regulator of basal coronary vascular tone.

Animals↗