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Biomedical subjects

T Li

Publications and source records attributed to T Li.

At least 559 records · Page 31Linked to original sources
PubMed1989

[Hyperamylasemia in acute exacerbation in patients with chronic respiratory failure].

Serum amylase level was examined in 129 cases (225 episodes) of chronic respiratory failure at acute exacerbation, and in 59 cases (62 episodes) of pneumonia without respiratory failure as a control. Cases accompanying diseases, such as acute pancreatitis, parotiditis, ileus, and renal dysfunction, which were expected to develop hyperamylasemia were excluded. The 225 episodes were divided according to the cause of acute exacerbation into 4 groups: pneumonia, bronchitis, right heart failure without infection, and others (e.g. hemoptysis). Hyperamylasemia (greater than 400 S-U) was observed in groups of pneumonia (15/40 = 35.5%) and of bronchitis (12/95 = 12.6%) respectively, but not in those of right heart failure without infection (0/73 = 0%) and others (0/17 = 0%). As a result, hyperamylasemia was found only under conditions of inflammation of lung parenchyma and bronchi with acute exacerbation of respiratory failure. On the other hand no hyperamylasemia was observed in 62 episodes of only pneumonia without respiratory failure. It was concluded that both respiratory tract infection and acute respiratory failure are necessary factors for development of hyperamylasemia originating from lung or bronchi.

Aged↗
PubMed1989

[The pharmacokinetic study of 3H-alpha-2-butylhydroxybenzyl alcohol in rabbits].

A derivative of Gastrodigenin, alpha-2-butylhydroxybenzyl alcohol, has shown a high distribution in the mice brain and stronger pharmacologic effects than its parent compounds. With 3H-alpha-2-butylhydroxybenzyl alcohol as radioactive tracer, pharmacokinetic data were obtained after the intravenous administration of a single dose alpha-2-butylhydroxybenzyl alcohol to rabbits, according to a cross-over design. Then, serial plasma samples were taken from 1 min to 480 min and measured by liquid scintillation counter. The data were analyzed by IBMPC computer for the estimation of pharmacokinetic parameters and the judgement of compartment model with a program recently developed by ourselves. The results suggested that the pharmacokinetics of alpha-2-butylhydroxybenzyl alcohol accords with the two compartment open model based on either the comparison of the calculated theoretic value with measured concentration or F test for the model judgement, and that the process of distribution was quite rapid, and the elimination half-life (T1/2 beta) was 12 h, indicating a slow elimination process.

Animals↗
PubMed1988

Quantitative studies of enkephalin's coexistence with gamma-aminobutyric acid, glycine and neurotensin in amacrine cells of the chicken retina.

Previous double-label studies demonstrate that enkephalin coexists with gamma-aminobutyric acid, glycine or neurotensin in amacrine cells of the chicken retina. The present study utilizes double- and triple-label paradigms to quantitatively analyze these coexisting relationships. Twenty-eight percent of enkephalin-like immunoreactive amacrine cells were found to exhibit high-affinity uptake of [3H]GABA, while 53% of enkephalin-amacrine cells specifically accumulate [3H]glycine. Moreover, the present study predicts that at least 26% of enkephalin-amacrine cells which accumulate [3H]glycine should also be immunoreactive for neurotensin.

Animals↗
PubMed1987

Interactions between enkephalin and gamma-aminobutyric acid in the larval tiger salamander retina.

Both double-label and intracellular electrophysiological recording techniques were utilized to investigate the interactions between enkephalin and gamma-aminobutyric acid in the larval tiger salamander retina. Double-label studies revealed that the vast majority (greater than 96%) of enkephalin-immunostained amacrine cells also exhibit high affinity uptake of [3H]gamma-aminobutyric acid. Electrophysiological evidence demonstrated that morphine and gamma-aminobutyric acid exert opposite effects on a population of On-Off ganglion cells. gamma-Aminobutyric acid decreased the activity of these cells, while enkephalin increased their activity. These findings support the idea that opiate-mediated pathways inhibit GABAergic pathways in the vertebrate retina.

Animals↗
PubMed1987

Intrarenal converting enzyme inhibition in rabbit.

The role of the intrarenal renin-angiotensin system on the control of renal blood flow in the rabbit was pursued in this investigation. Blood pressure (BP) and renal blood flow (RBF) were monitored in New Zealand white rabbits anesthetized with pentobarbital. Control RBF and changes in RBF elicited by infusions of angiotensin I (AI) were determined by electromagnetic flowmetry. In Group 1 (n = 7), BP and RBF responses to AI infused i.a. and i.v. were evoked in the control period and the effects of a low i.a. dose of captopril to inhibit selectively renal angiotensin converting enzyme (ACE) and then a high i.a. dose to inhibit maximally renal ACE were determined. Low dose captopril depressed the RBF response to i.a. AI by 67% without an effect on the response to i.v. AI. RBF was increased by 15.0% and renal vascular resistance (RVR) was decreased by 14.4% by low dose captopril. High dose captopril had no further effect on the response to i.a. AI, but decreased the RBF response to i.v. AI by 72%. RBF and RVR were further changed by high dose captopril. In Groups 2 and 3, high dose captopril was administered after either indomethacin or saline vehicle. Captopril increased RBF, decreased RVR, and blocked responses to AI similarly whether prostaglandin synthesis was inhibited or not. The results indicate that renal vasodilation in the rabbit can be produced by selective renal ACE inhibition with a low dose of captopril, but that systemic ACE inhibition also contributes to this effect when a high dose is given.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1986

Effects of the rate and composition of fluid replacement on the pharmacokinetics and pharmacodynamics of intravenous furosemide.

Effects of differences in the rate and composition of intravenous fluid replacement for urine loss on the pharmacokinetics and pharmacodynamics of furosemide were evaluated using the dog as a model animal. Each of six dogs received 8-hr constant intravenous infusion of 20 mg (15 mg used in one dog) of furosemide with 0% replacement (treatment I), 50% replacement (treatment II), and 100% replacement (treatment III) with lactated Ringer's solution, as well as with 100% replacement with 5% dextrose in water (treatment IV). Most pharmacokinetic parameters, such as plasma clearance, steady-state volume of distribution, mean residence time, and terminal half-life, were essentially the same in all four treatments. Renal clearances and urinary excretion rates of the drug in treatments II-IV were essentially the same, but about 20% higher than those in treatment I. In spite of the similarities in kinetic properties, diuretic and/or natriuretic effects from furosemide were markedly different among the four treatments. For example, mean 10-hr urine outputs were 646, 1046, 3156, and 1976 ml and mean 10-hr sodium excretions were 87.0, 142, 383, and 97.2 mmole for treatments I-IV, respectively. Except for treatment III, diuresis and/or natriuresis were found to be time-dependent, generally decreasing with time until reaching a low plateau during later hours of infusion. The present findings also showed that no fluid replacement and 100% replacement with 5% dextrose solution both produced the same degree of severe acute tolerance in natriuresis, indicating the insignificance of water compensation in tolerance development; in treatment II, where neutral sodium balance was achieved, the development of acute tolerance in diuresis and natriuresis can mainly be attributed to negative water balance under this special condition; at steady state the hourly diuresis and natriuresis could differ up to about ten times between treatments. Some implications for the kinetic/dynamic relationship or modeling, in the clinical use, and in the bioequivalence evaluation of dosage forms are discussed.

Animals↗
PubMed1986

Analysis of influence of extra- and intrarenally formed angiotensin II on renal blood flow.

Previous studies have indicated that intrarenal converting enzyme (CE) inhibition had no influence on renal blood flow (RBF). The present study examined the effect of intrarenal CE inhibition with captopril on the distribution of left (L) RBF in the anesthetized rabbit. Systemic arterial blood pressure and LRBF were measured in pentobarbital anesthetized rabbits, the latter by electromagnetic flowmetry. Radiolabeled 15-mu microspheres (85Sr and 141Ce) were used to determine RBF distribution. A dose of captopril that blocked the LRBF response to angiotensin I (ANG I), 0.3 microgram/kg/min i.a., but had no effect on the response to ANG I i.v. was established. Captopril administered i.a. at 0.2 microgram/kg/min for 20 min into the left renal artery decreased the response to ANG I i.a. by 71% without any effect on the response to ANG I i.v. The deep to superficial cortical blood flow ratio was unaffected by infusion of captopril i.a. in normal rabbits. In animals treated with furosemide, the ratio was increased by captopril infusion. However, the ratio change occurred in the infused and noninfused kidneys, negating a selective intrarenal effect. In the second part of this investigation the influence of a maximally effective i.a. dose of captopril was determined on intrarenal CE and RBF. The dose of 6.4 micrograms/kg/min of captopril increased LRBF slightly, but decreased the RBF response to ANG I i.a. only by 30%. Induction of a secondary pathway of intrarenal conversion of ANG I to ANG II is suggested by the latter results.

Angiotensin I↗
PubMed1986

Strophanthidin inotropy in cardiac Purkinje fibers under conditions that vary cellular sodium or calcium.

The role of sodium and calcium on strophanthidin inotropy was studied in canine cardiac Purkinje fibers perfused in vitro under conditions that vary cellular sodium and calcium. With high concentrations of strophanthidin (greater than or equal to 10(-7) M), force increases more in the presence of low [Ca]0 or high [Na]0 and less in the presence of a low sodium-calcium concentration solution than in Tyrode solution. In a solution with a low concentration of sodium-calcium containing strophanthidin, restoring [Na]0 to normal decreases and then re-increases force: when [Na]0 is decreased again, the force transiently overshoots. These effects of strophanthidin are exaggerated by metabolic inhibitors. In a low [Ca] solution, low concentrations of strophanthidin (3 X 10(-8) or 5 X 10(-8) M) re-increase force a little or not at all. On recovery, the transient force increase is not exaggerated by low strophanthidin and is absent after manganese exposure. The inotropy of low concentrations of strophanthidin is potentiated by norepinephrine, high [Ca]0 (4 mM), or by lowering [Na]0. Thus, the present results suggest that the inotropic action of high strophanthidin concentrations depends primarily on sodium and secondarily on calcium, and that the inotropic action of low concentrations of strophanthidin involves a modification of the cell response to calcium.

Animals↗
PubMed1985

[Regulation of adenosine triphosphatase activity in mitochondria, chloroplasts and erythrocytes by anions, adenosine diphosphate and alcohols].

The effects of sulfite, bicarbonate, thiocyanate, methanol, ethanol, glycerol, dimethy sulfoxide and ADP on the ATPase activity of the coupling factor from liver mitochondria (F1) and pea chloroplasts (CF1) and of the anion-sensitive ATPase from rat erythrocytes were investigated. Under steady-state conditions of ATP hydrolysis catalyzed by F1, CF1, and erythrocyte ATPase, three Km values for each of the enzymes, three activation constants for sulfite and three inhibition constants for thiocyanate were determined. The efficiency and direction of the effects of anions, alcohols and ADP strongly depend on temperature and substrate (Mg-ATP) concentration. The mechanisms of modification by anions and alcohols of the ATPase activities are discussed.

Adenosine Diphosphate↗
PubMed1985

Effects of diacetyl monoxime on cardiac excitation-contraction coupling.

Diacetyl monoxime (DAM) is a negative inotropic agent. To identify the mechanism of its actions, electrical and mechanical studies with various cardiac tissues were carried out. DAM (0.2-20 mM) inhibited the contractile force in both normal and 22 mM KCl-depolarized (in presence of 10(-6) M isoproterenol) guinea-pig papillary muscles in a concentration-dependent manner. In general, there was a lack of major effects of DAM on sarcolemmal electrical properties. The fast action potentials were somewhat depressed and the slow action potentials were slightly enhanced. In chemically skinned pig ventricular muscles, the myofibrillar contraction induced in 6.25 pCa was inhibited by DAM in a similar concentration range. DAM also produced an apparent decrease in sensitivity toward Ca++ in this preparation. Myofibrillar adenosine triphosphatase assay showed similar results as in the skinned muscles. All DAM effects were reversible upon washout and could be partially antagonized by raising [Ca++]. Taken together, the negative inotropic effect of DAM cannot be ascribed to an inhibitory effect on the slow inward current, as suggested previously. An inhibitory effect at the myofibril level is a distinct possibility. Additional effects of DAM on the sarcoplasmic reticulum cannot be ruled out.

Action Potentials↗