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Sökning: (WFRF:(Gustafsson P.)) > (1980-1989)

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1.
  • Gustafsson, D, et al. (författare)
  • Effects of calcium antagonists on myogenic and neurogenic control of resistance and capacitance vessels in cat skeletal muscle
  • 1988
  • Ingår i: Journal of Cardiovascular Pharmacology. - 0160-2446. ; 12:4, s. 22-413
  • Tidskriftsartikel (refereegranskat)abstract
    • The effects of five different calcium antagonists (diltiazem, felodipine, nifedipine, nimodipine, and verapamil) on cat skeletal muscle resistance and capacitance vessels were studied in a whole organ preparation. These calcium antagonists seemed to have the similar qualitative effects on these vascular functions. Calcium antagonists were found to be potent inhibitors of myogenic vascular reactivity (here defined as the maximal increase in flow resistance evoked by a sudden rise of transmural pressure). Basal vascular tone and vascular tone induced by low frequency stimulation of sympathetic nerves were both less sensitive to these drugs than vascular tone induced by myogenic vascular reactivity. Sympathetically mediated vascular tone at high stimulation frequencies seemed to be least sensitive. Further, resistance vessels were much more sensitive to these drugs than capacitance vessels. Finally, basal tone in the large bore arterioles were more sensitive than in the small bore arterioles, a surprising finding which was interpreted with the aid of computer simulations using a mathematical model of local vascular control in cat skeletal muscle. The model suggested that this difference could be due to a delicate interaction between myogenic vascular reactivity and metabolic vascular control. It is suggested that the inhibition of myogenic vascular reactivity is a factor contributing to the edema formation of calcium antagonists.
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2.
  • Gogan, P., et al. (författare)
  • On re‐excitation of feline motoneurones: its mechanism and consequences.
  • 1984
  • Ingår i: The Journal of Physiology. - : Wiley. - 0022-3751 .- 1469-7793. ; 350, s. 81-91
  • Tidskriftsartikel (refereegranskat)abstract
    • Conditions required for re‐excitation of lumbosacral motoneurones, i.e. for double impulses in the motor axons associated with a single soma‐dendritic action potential, were examined in cats anaesthetized with pentobarbitone and paralysed with gallamine triethiodide. Simultaneous recording from a motoneurone (intracellular, and in some experiments also extracellular), and from its axon in a ventral root, was used to assess the relations between the soma and the double axonal action potentials. Action potentials (greater than 70 mV) evoked by brief depolarizing current pulses applied intracellularly were never observed to cause re‐excitation. Re‐excitation could, however, be regularly induced by procedures which increased the delay between the initial segment and soma‐dendritic components of these potentials. Re‐excitation could be evoked (i) when brief hyperpolarizing pulses were applied before the onset of the soma‐dendritic spikes, (ii) when the depolarizing pulses were applied on a background of long hyperpolarizing pulses or (iii) when two action potentials were evoked in a quick succession (by two brief depolarizing pulses). No relationship was found between the presence of re‐excitation of motor axons and the presence of the delayed depolarization which follows the soma‐dendritic spikes. Neither re‐excitation nor delayed depolarization were found to be dependent upon re‐excitation of the initial segment. These observations are thus at variance with previous suggestions that the initial segment spikes induce the re‐excitation of motor axons and that the initial segment spikes cause the delayed depolarization following soma‐dendritic spikes. Since re‐excitation of a motor axon occurred without any signs of a second initial segment spike, it is concluded that it is initiated at the level of the axon, most likely at the first node of Ranvier. Re‐excitation of motor axons was also observed during repetitive firing induced by intracellular current injection. However, it occurred then only occasionally, and only under strong depolarizing drive. It is thus not expected to be a common phenomenon under natural conditions of repetitive firing. © 1984 The Physiological Society
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