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  • 1
    Electronic Resource
    Electronic Resource
    Evidence for bilateral vagal innervation of postganglionic parasympathetic neurons in chicken heart (1983)
    Springer
    Journal of neural transmission 56 (1983), S. 239-247 
    Details
    ISSN: 1435-1463
    Keywords: Parasympathetic nervous system ; acetylcholine ; heart
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Stimulation of the cervical vagus nerves caused an output of acetylcholine (ACh) from the isolated chicken heart, which almost exclusively was released from the postganglionic neurons: (+)-tubocurarine (3×10−4 M) reduced the output to 12±6% (n=7) of the control. Stimulation of the two nerve trunks was equally effective in releasing ACh.-Evidence that a large number of postganglionic neurons receives bilateral innervation was based on two experimental series. (1.) The sum of the ACh outputs evoked by unilateral (separate) nerve stimulation of the right and the left vagus was higher than the bilaterally evoked output (100%) and increased with increasing frequencies (10, 20 and 40 Hz) from 115±13% to 131±9% (n=13). In the presence of 10−4 M 4-aminopyridine, unilaterally evoked output (40 Hz) was further increased from 131 to 176±5% (n=21).-(2.) In the presence of 4-aminopyridine plus hemicholinium-3 (2×10−5 M), unilateral nerve stimulation at 40 Hz evoked an output of ACh that decreased from 477 to 79 pmol g−1min−1 during a 20 min-period of stimulation due to transmitter depletion. Thereafter output of ACh evoked by stimulation of the contralateral nerve was reduced by 73% as compared to the control value (475 pmol g−1min−1; output without the preceding 20 min-stimulation).-It is concluded that a large number of parasympathetic postganglionic neurons of the chicken heart receives a dual excitatory input from both right and left vagus nerve.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01243281
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  • 2
    Electronic Resource
    Electronic Resource
    Interstitial washout and hydrolysis of acetylcholine in the perfused heart (1982)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 318 (1982), S. 295-300 
    Details
    ISSN: 1432-1912
    Keywords: Acetylcholine ; Choline ; Perfused heart ; Cholinesterase ; Interstitial washout
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The efflux of acetylcholine, of radioactively labelled acetylcholine and choline, into the venous effluent of the perfused chicken heart was studied to determine the kinetics of both interstitial washout and hydrolysis of acetylcholine. Stimulation of both cervical vagus nerves (e.g., for 5 s at 40 Hz) caused a release of acetylcholine, which appeared partially unhydrolyzed in the venous effluent, and reduced force of contraction and heart rate. For comparison labelled acetylcholine or choline was infused for 5 s into the heart and again the venous efflux of either substance was determined. It was found that the kinetics of efflux of acetylcholine or choline from the interstitial space were of first order. The mean half times were 16.2 s (after infusion of acetylcholine) and 17.9 s (after nerve stimulation) for acetylcholine and 17.9 s (after infusion of choline) for choline. In the interstitial space, radioactivity (sum of [3H]-acetylcholine and [3H]-choline formed from [3H]-acetylcholine) released by nerve stimulation declined mono-exponentially with a rate constant of 0.069 s−1 and a half time of 10 s (due to washout), whereas the concentration of unhydrolyzed [3H]-acetylcholine decreased in a multi-exponential fashion due to both washout and hydrolysis. The interstitial concentration of [3H]-acetylcholine reached the 50% level after 2.5 s. In conclusion, the long persistence of unhydrolyzed acetylcholine in the interstitial space of the heart appears to be due to an apparently low rate of hydrolysis. This, in turn, is responsible for the importance of diffusion and washout of acetylcholine from the interstitial space as significant factors of synaptic removal of acetylcholine. Moreover, the results support the notion that the sustained interstitial concentration of acetylcholine determines the long duration of cardiac responses to vagal stimulation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00501168
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  • 3
    Electronic Resource
    Electronic Resource
    4-Aminopyridine antagonizes the inhibitory effect of pentobarbital on acetylcholine release in the heart (1980)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 312 (1980), S. 7-13 
    Details
    ISSN: 1432-1912
    Keywords: ACh release ; 4-Aminopyridine ; Heart ; Pentobarbital ; Tetracaine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Effects of pentobarbital on acetylcholine (ACh) release, force of contraction and nervous conduction were studied in isolated heart preparations and in cervical vagus nerves, respectively. 4-Aminopyridine and tetracaine were used as pharmacological tools to eludicate the mode of action of pentobarbital. 1. 4-Aminopyridine (10−4 M) markedly increased the overflow of ACh from the isolated chicken heart evoked by electrical stimulation (1–50 Hz, 1 ms, 40 V) of the cervical vagus nerves. This effect of 4-aminopyridine was highest at low frequencies of stimulation (+ 226% at 1 Hz) and declined with increasing frequencies to reach a minimum augmentation of 22% at 30 Hz. 2. Pentobarbital and tetracaine dose-dependently decreased the evoked overflow of ACh from the isolated chicken heart. Half-maximal inhibition was observed at concentrations (IC50) of 1.4×10−4 M and 4×10−6 M, respectively. Much higher concentrations of pentobarbital were required to inhibit the conduction in vagal B-fibres (IC50=3×10−3 M) whereas the IC50 values of tetracaine for both inhibitory effects were nearly identical. 3. 4-Aminopyridine (10−4 M) antagonized the inhibitory effect of PB on the evoked overflow of ACh and shifted the concentration-response curve to the right. The 4-aminopyridine/pentobarbital antagonism was equally pronounced whether the release of ACh was evoked by vagal stimulation (preganglionic) or by field stimulation (pre- and postganglionic). 4. The negative inotropic effect of vagal stimulation in isolated atria of cats and chickens was weakened by pentobarbital (1–5×10−4 M) and enhanced by 4-aminopyridine (10−4 M). Again, 4-aminopyridine (10−4 M) antagonized the effect of pentobarbital. 5. In contrast to the effects of pentobarbital, the inhibition of ACh overflow produced by tetracaine was not antagonized by 4-aminopyridine. 6. The results strongly support the previous suggestion (Lindmar et al., 1979) that the inhibition by pentobarbital of the evoked overflow of ACh from the postganglionic parasympathetic neurones of the heart is due to a reduction of the Ca2+ inward current into the nerve terminals.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00502566
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    Paper (German National Licenses)
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