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Biomedical subjects

J T Cheng

Publications and source records attributed to J T Cheng.

At least 217 records · Page 12Linked to original sources
PubMed1985

Effects of adenosine on contractile response of circular muscle in electrically stimulated guinea-pig ileum.

The action of adenosine on the electrically induced mechanical response of circular muscle in isolated guinea-pig ileum has been investigated. Electrical stimulation (0.1 Hz) elicited the twitch response, which was completely abolished by tetrodotoxin (0.2 microM), morphine (1 microM) and atropine (0.1 microM). Adenosine (0.1-100 microM) markedly depressed the twitch response in a concentration-dependent manner, and the concentration-depression curve for adenosine was significantly shifted to the right in the presence of theophylline (30 microM). On the other hand, the contractile responses induced by acetylcholine (1-300 microM) were not effected by adenosine at all. The present investigation suggests that the twitch response is mediated through acetylcholine released from the intramural cholinergic nerves supplying the circular muscle of guinea-pig ileum, and adenosine has an inhibitory effect on the cholinergic transmission, probably via P1-purinoceptors.

Acetylcholine↗
PubMed1984

Reversal of akinesia and release of festination by morphine or GABA applied focally to the nucleus reticularis tegmenti pontis.

Focal application of 5 micrograms of morphine sulfate to the nucleus reticularis tegmenti pontis (NRTP) in rats reversed the akinesia induced by 5 mg/kg systemic haloperidol or 40 mg/kg systemic morphine and released festinating forward locomotion. gamma-Aminobutyric acid (200 micrograms) applied to this nucleus also reversed such akinesia. Intraventricular naloxone (10 micrograms) or picrotoxin (0.1 microgram), respectively, blocked the effects of such focally applied drugs. Thus, morphine and gamma-aminobutyric acid appear to act physiologically on the cells of the NRTP. The results suggest that systemic morphine, in addition to producing immobility, simultaneously facilitates a readiness for locomotion by inactivating a final common inhibitory system in the region of the NRTP.

Animals↗
PubMed1984

Mechanism of alteration of sodium potassium pump of erythrocytes from patients with chronic renal failure.

We examined intracellular electrolytes, K influx, and [3H]ouabain-binding capacity of erythrocytes from 32 normal subjects and 45 patients with end-stage renal failure on dialysis, including 16 with high intracellular Na (mean 17.3 +/- 3.9 mmol/liter cell water). The [3H]ouabain-binding capacity of erythrocytes with high cell Na was markedly reduced as compared with that of erythrocytes from normal subjects (274 +/- 52 vs. 455 +/- 59 sites/cell, P less than 0.001). The mean serum creatinine was higher in the uremic group with high cell Na. There was a significant linear correlation between intracellular Na and [3H]ouabain-binding in both normal and uremic subjects. Cross-incubation of normal cells with uremic plasma for 24 h failed to reduce [3H]ouabain-binding capacity of normal cells. In spite of a substantial increase in cell Na, K pump influx was not higher in uremic erythrocytes with high cell Na. When intracellular Na was altered with nystatin (cell Na equal to 120 mmol/liter cell water in both groups), K pump influx was proportional to the number of Na-K pump sites so that the ion turnover rate per pump site was similar in the two groups. Uremic plasma failed to depress K pump influx of normal erythrocytes. The passive net influx of Na in uremic cells with high intracellular Na was not different from that observed in erythrocytes from normal subjects. When erythrocytes were separated by age on Percoll density gradients, the number of Na-K pump sites of the youngest uremic cells was significantly lower than that of the youngest normal cells, suggesting that decreased synthesis of Na-K pump sites, rather than accelerated loss of Na-K pump sites during aging, was responsible for the decrease in [3H]ouabain-binding capacity of erythrocytes from uremic subjects. Taken together, these findings suggest that a decrease in the number of Na-K pump sites plays a major role in the abnormality of Na-K pump of erythrocytes from patients with chronic renal failure.

Adult↗
PubMed1983

The inhibition of movement by morphine or haloperidol depends on an intact nucleus reticularis tegmenti pontis.

Electrolytic damage of the nucleus reticularis tegmenti pontis (NRTP) in rats produces a form of accelerating forward locomotion, indicating that this region is part of a system that inhibits locomotion and movement. In animals with such damage, 5 mg/kg haloperidol does not block forward locomotion although it produces complete akinesia in normal rats [2]. Our present results demonstrate that doses of morphine sulfate that render normal rats completely akinetic (40, 50, or 60 mg/kg) also fail to block forward locomotion. Furthermore, 200 micrograms gamma-aminobutyric acid applied intracranially in the region of the NRTP can reverse the akinesia produced by systemically administered haloperidol or morphine. We suggest that there are two types of akinesia--direct and indirect--and that morphine and haloperidol may produce akinesia indirectly via an inhibitory system which includes the NRTP.

Animals↗
PubMed1983

Hypoglycemic effect of guava juice in mice and human subjects.

Guava is a plentiful fruit in Taiwan and it was taken from the plants of Psidium guajava Linn. (Myrtaceae). According to the folklore in Chinese Medicine, gauva was useful in the treatment of diabetes mellitus. In the present study, acute i.p. treatment with 1 g/kg guava juice produced a marked hypoglycemic action in normal and alloxan-treated diabetic mice. Although effective duration of guava is more transient and it is less potent than chlorpropamide and metformin, blood glucose lowering effect of guava also can be obtained by oral administration in maturity-onset diabetic and healthy volunteers. Thus, it is suggested that guava may be employed to improve and/or prevent the disease of diabetes mellitus.

Adolescent↗
PubMed1982

Amphotericin B nephrotoxicity: increased renal resistance and tubule permeability.

Two groups of rats received amphotericin-B (Amp). One group (AA) received a single acute dose of 1 mg/kg i.v. The second (CA) received 10 mg/kg i.p. daily for 4 days. In AA rats, measurements 1 to 5 hr after Amp were compared with their own preinfusion values. Inulin clearance, (CIn, 4.5 ml X min-1 X kg-1 per kidney pre vs. 1.3 post), renal plasma flow (RPF, 12.0 ml X min-1 X kg-1 vs. 7.4), and the estimated pressure in the glomerular capillaries (Pgc, 52 mm Hg vs. 40), were all significantly decreased while renal vascular resistance (5.2 mm Hg/ml vs. 12.0) was increased. Only 45% of the 3H-inulin injected into surface tubules was recovered in the urine as contrasted with 100% recovery before injection. This suggests that tubule permeability was increased, but there was no histologic evidence of renal tubule necrosis. Twenty-four hours after intravenous Amp, CIn and RPF returned to normal. Data from CA rats were compared with values from sham-treated pairfed (PF) control rats. Again, CIn (4.22 ml X min-1 X kg-1 in PF vs. 2.69 in CA), RPF (16.1 ml X min-1 X kg-1 vs. 8.3), and Pgc (48 mm Hg vs. 38) were decreased, and renal vascular resistance (4.9 mm Hg/ml vs. 8.0) was increased. The recovery of 3H-inulin in the urine was slightly, but significantly, decreased (96% vs. 83%). These findings demonstrate that Amp decreases renal function by at least two mechanisms. An increase in renal vascular resistance is most important, although increased tubule permeability with a "backleak" of tubule fluid also contributes to renal dysfunction, particularly after intravenous Amp.

Amphotericin B↗
PubMed1981

Galloping induced by pontine tegmentum damage in rats: a form of "Parkinsonian festination" not blocked by haloperidol.

Localized lesions or local applications of gamma-aminobutyric acid (GABA) in the nucleus reticularis tegmenti pontis (NRTP) of rats cause rapidly accelerating forward locomotion. Such "festination" can coexist with blockade of the dopamine system. We suggest that (i) the akinesia produced by dopamine deficiency results at least in part from release of excessive inhibition of locomotion by a neural system whose final common inhibitory path includes the region of the NRTP and (ii) when it occurs in addition to nigrostriatal damage, destruction in the region of the NRTP might be the cause of a form of festination seen in some patients suffering from Parkinsonism.

Animals↗
PubMed1981

Effect of pH value on the drug-initiated contractility of small intestine "in vitro".

The influence of different pH values in nutrient media on the drug-initiated contractility of rectal smooth muscle was isometrically investigated. The following results were obtained: (1) The response to drugs is potentiated in alkali media and is reduced in acidic media. (2) Facilitated responses in alkali media were lost with the removal of CaCl2 and the reduction of responses was markedly enhanced with the increase in H+ or in the absence of CaCl2. (3) Analysis with an atomic absorption spectrophotometer, shows that H+ may compete with Ca2+ in transmembrane transport. (4) Removal of NaCl can elicit the release of Ca2+ and this action was diminished in acidic conditions. (5) The contractile system of muscle cells was also inhibited by lowering pH values in nutrient media. Thus, interference with mobilization of Ca2+ by H+ is considered to be responsible for modifying the contractions of rectal smooth muscle in mice.

Animals↗
PubMed1977

Mechanisms of amitriptyline induced hypothermia in the rat.

Effects of amitriptyline on rectal temperature of male rats were studied at the ambient temperature of 25 degrees C. Drugs were administered intraperitoneally. Amitryptyline elicited a dose related hypothermia. The hypothermia was attenuated by phenoxybenzamine 10 mg/kg, haloperidol 2 mg/kg, diphenhydramine 5 mg/kg, atropine 20 mg/kg, and cyproheptadine 5 mg/kg. Propranolol, at a dose of 5 mg/kg, had no effect on the hypothermia. Theophylline 50 mg/kg and dibutyryl cyclic AMP 20 mg/kg inhibited the hypothermia produced by anitriptyline. Pretreatment with parachloroamphetamine (PCA), 2 or 5 mg/kg daily for 3 days, strongly antagonized the hypothermia. In addition, pretreatment with parachlorophenylalanine (PCPA), 100 mg/kg daily for three days, reduced the brain 5-hydroxytryptamine (5-HT) concentration to 20% of the control level and completely blocked the hypothermia response. When brain 5-HT concentration recovered to 50% of the control level in PCPA treated rats following the administration of 10 mg/kg 5-hydroxytryptophan (5-HTP) the hypothermia induced by amitriptyline was restored. However, the administration of 5-HT, 5 mg/kg, to PCPA treated rats did not increase brain 5-HT concentration or restore the amitriptyline induced hypothermia (AIH). Results suggest that amitriptyline interacts with several transmitter substances to produce hypothermia. Since the ability of amitriptyline to produce hypothermia was correlated with brain 5-HT content, 5-HT might play an important role in the mediation of AIH.

Amitriptyline↗