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Biomedical subjects

J T Cheng

Publications and source records attributed to J T Cheng.

At least 235 records · Page 13Linked to original sources
PubMed1976

The uptake of delta9-tetrahydrocannabinol in choroid plexus and brain cortex in vitro and in vivo.

[3H]delta9 Tetrahydrocannabinol (delta9-THC) was actively transported by the choroid plexus and cerebral cortical slices of the rabbit when incubated as a BSA-microsuspension in artificial rabbit CSF. The transport system for delta9-THC in choroid plexus had a V max of 174 nmoles/mg tissue/h, approximately 9-fold greater than that observed for cortical slices. In vivo experiments demonstrated a preferential distribution of delta9-THC in choroid plexus at 1 h after intravenous injection. These results indicate that delta9-THC is actively accumulated by choroidal epithelium and may also be transported across the epithelial stroma into the capillary circulation. This suggests that the choroid plexus participates in the regulation of delta9-THC concentration in CSF and indirectly in brain by means of the "sink" function of the CSF.

Animals↗
PubMed1976

"Calcium-induced release of calcium" in rectal smooth muscle of mice.

Contractile responses to K, ACh, Ba and exogenous Ca of rectal strips from mice were recorded isotonically. These responses consisted of phasic contraction and subsequent tonic contraction. In Ca-depleted preparations exposed to Ca-free bath medium, the contractions by K and ACh disappeared but the contraction by Ba remained constant. This residual contraction by Ba is presumably due to a direct stimulation of Ba to contractile elements of muscle. Metabolic inhibitors (anoxia and DNP) abolished tonic contraction without affecting phasic contraction by exogenous Ca. In Ca-free bath medium, tonic contraction by exogenous Ca immediately disappeared whereas phasic contraction gradually decreased and about 3 hr later remained constant in parallel with the occurrence of residual contraction by Ba. After pretreatment with the removal of Na from bath medium, which produced Ca-release action, phasic contractions by exogenous Ca in Ca-free bath medium were depressed like those by K, ACh and Ba. These results suggest that the phasic contraction by exogenous Ca is produced mainly by release of Ca and partly by influx of Ca. Thus, it is suggested that the same mechanism of Ca-induced release of Ca from the storage sited as described in skeletal muscle is also operating in rectal smooth muscle of mice.

Acetylcholine↗
PubMed1976

Irreversible inhibitory effect of atropine on contractile responses to drugs in isolated rabbit ileum.

Effect of atropine sulfate (atropine) on the contractile responses to acetylcholine chloride (ACh), potassium chloride (K) and barium chloride (Ba) was investigated in isolated rabbit ileum. Tension of the strips suspended in the bath medium (Locke solution, 30 degrees C) was isotonically recorded. The K(ED50)- and Ba(ED50)-induced contractions were not affected by atropine at 3.0 X 10(-4) mM, which reversibly abolished the ACh(ED100)-contraction. After washout of 6.0 X 10(-4) mM atropine, the phasic, but not the tonic, component of ACh(ED50)-, K(ED50)- and Ba(ED50)- contractions was to some extent inhibited irreversibly. On the contrary, such irreversible inhibition of the phasic component was not produced by atropine methylbromide even in the high concentration of 3.0 X 10(-3) mM. The irreversible inhibitions by atropine of 6.0 X 10(-4) mM on the phasic component of ACh- and K-contractions were protected by pretreatment with a high concentration of ACh or K. Further, these irreversible inhibitions by atropine were potentiated by the absence of Ca and were abolished by the increase of Ca content in bath media. These results suggest that the irreversible inhibition of the contractile responses to drugs by atropine in high concentration may be due to the interference with the mobilization of Ca in the deep layer of the membrane, rather than by a blockade of muscarinic receptor sites.

Animals↗
PubMed1976

[Mechanism of the contracting actions of K, acetylcholine and Ba on the isolated rat rectum, with special reference to its relationship to Ca].

The contractile mechanism of K, ACh and Ba were investigated in relation to the mobilization of Ca in the rat's isolated rectum. Contractions by K, ACh and Ba consisted of the phasic contraction and the subsequent tonic contraction. From the effects of metabolic inhibition (anoxia, DNP) and Ca removal from bath solution on the contractions by these three agents, the following assumptions have been made: the phasic contractions by K and ACh are iduced by the release of Ca from the store sites and the passive influx of Ca, whereas that by Ba is induced by the release of Ca. Tht tonic contractions by K and ACh are maintained mainly by the active influx of Ca, whereas that by Ba is maintained by the active influx of Ca and the release of Ca. In addition, the direct stimulation to the contractile elements of muscle is partly concerned with the Ba-induced contraction. In the muscle cell membrane, three divisions of Ca store; the first is the store where Ca is most easily released, the second is the store where Ca is comparatively easily released and the third is the store where Ca is not easily released. K releases Ca from the first store, ACh does so from the first and second stores, and Ba does so from these three stores for producing contraction. These assumption were further supported by the analysis of the concentration action curves of the influence of Ca removal from bath solution on the phasic contractions and the tonic contractions induced by the three agents.

Acetylcholine↗