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Phrenic nerve

Varagic, V. M. and Zugic, M., Interactions of xanthine derivatives, catecholamines, and glucose-6-phosphate on the isolated phrenic nerve diaphragm preparation of the rat, Pharmacology, 5, 275, 1971. [Pg.253]

Skeletal muscle Phrenic nerve/diaphragm Neuromuscular blockade... [Pg.636]

Brodin P, Rped A. (1984). Effects of eugenol on rat phrenic nerve and phrenic nerve-diaphragm preparations. Arch Oral Biol. 29(8) 611-15. [Pg.520]

Gallagher, J. and Shinnick, G.P., Effect of Gymnodium breve toxin in the rat phrenic nerve diaphragm preparation, Br. J. Pharmac., 69, 367, 1980. [Pg.188]

Phrenic-nerve hemidiaphragm preparations were preincubated in modified Krebs solution containing 1.0 x 10 6m [methyl-%]choline (specific activity 8 Ci/mmole) and 0.5 mM eserine salicylate for 30 min, followed by a brief rinse in eserine-containing modified Krebs solution but no label. Preparations were then incubated at 37°C in modified Krebs solution containing eserine for 120 min, taking duplicate 0.1 ml samples of the supernatant fluid at 10 min intervals. [Pg.361]

Holmes and Robins reported that 2-PAM I overcame neuromuscular blockade induced by DFP, TEPP, or sarin, but this could be demonstrated with the Isolated phrenic nerve-diaphragm preparation from the rat only after washing away excess OP compound. Intravenous injection of 2-PAM I overcame slowly neuromuscular blockade induced by OP compounds. The oxime, they found, also had a direct toxic action on muscle, reducing the ability of muscle to shorten and decreasing the ability of muscle fibers to conduct impulses. The same investigators reported that V (intraperltoneally at 150 mg/kg) had little, if any, effect on a sarin-induced blockade of neuromuscular transmission. [Pg.281]

Electrical Stimulation Devices. Bioelectrodes that transmit electrical signals into the body are generally known as electrical stimulation devices, examples of which include cardiac pacemakers, transcutaneous electronic nerve stimulators (TENs) for pain suppression, and neural prostheses such as auditory stimulation systems for the deaf and phrenic nerve stimulators for artificial respiratory control. In these, and other similar devices, electrodes transmit current to appropriate areas of the body for direct control of, or indirect influence over, target cells. [Pg.599]

Fig. (5). Effects of kuwanon G (1) and kuwanon H (2) on blood pressure. Electrocardiogram (ECG), phrenic nerve discharge (PN), and electroencephalogram (EEG) in a gallamine-immobilized rabbit... Fig. (5). Effects of kuwanon G (1) and kuwanon H (2) on blood pressure. Electrocardiogram (ECG), phrenic nerve discharge (PN), and electroencephalogram (EEG) in a gallamine-immobilized rabbit...
Table 5.7. EFFECT OF VITAMIN E ON RESPONSES OF RAT PHRENIC NERVE-DIAPHRAGM PREPARATION IN HYPOXIA... Table 5.7. EFFECT OF VITAMIN E ON RESPONSES OF RAT PHRENIC NERVE-DIAPHRAGM PREPARATION IN HYPOXIA...
Autoreceptor atria, urinary bladder Autoreceptor phrenic nerve Heteroreceptor inhibition of noradrenaline release in atria, vas deferens Agonist-induced bradycardia Inhibition of M current (Im) in sympathetic ganglia... [Pg.266]

Neuromuscular Phrenic nerve-diaphragm Ginsborg and Hirst 1972... [Pg.345]

Phrenic nerve-diaphragm preparation (frog xanthine-sensitive receptor) ... [Pg.345]

Giniatulhn RA, Sokolova EM (1998) ATP and adenosine inhibit transmitter release at the frog neuromuscular junction through distinct presynaptic receptors. Br J Pharmacol 124 839 44 Ginsborg BL, Hirst GD (1972) The effect of adenosine on the release of the transmitter from the phrenic nerve of the rat. J Physiol 224 629 15... [Pg.365]

Phrenic nerve stimulation for respiration is backed up by more than 10 years of experience [34]. It is used for patients where a high lesion of the spinal cord causes chronic respiratory insufficiency. The Vienna phrenic pacemaker stimulates the two branches of the phrenic nerves with four electrodes each. The cyclic combination of the electrodes, called roundabout stimulation, changes over time to prevent fatigue of the diaphragm during the 24 hours of stimulation per day. [Pg.138]

Figure 4.3. Representative set of spleen and hepatic sinus volumes, measured in vivo with MRI, during an 8 min simulated dive in a young elephant seal. The MRI images indicated that spleen emptying requires only two or so minutes. The contents are initially tranferred into the hepatic sinus and then RBCs are metered out into the blood more slowly, apparently through phrenic nerve control of the caval sphincter. Data from Thornton (2000). Figure 4.3. Representative set of spleen and hepatic sinus volumes, measured in vivo with MRI, during an 8 min simulated dive in a young elephant seal. The MRI images indicated that spleen emptying requires only two or so minutes. The contents are initially tranferred into the hepatic sinus and then RBCs are metered out into the blood more slowly, apparently through phrenic nerve control of the caval sphincter. Data from Thornton (2000).
A comparison between the chemiluminescence and the radioenzymatic assay methods that are used for the measurement of acetylcholine released from a rat phrenic nerve hemidiaphragm preparation was reported by Ehler et al. [57]. The comparison demonstrated quantitative equivalency and limits of detection for different analytes as 2 pmol. [Pg.74]

Pumiliotoxin B has both cardiotonic and myotonic activity in isolated atrial or rat phrenic nerve diaphragm preparations (97). The cardiotonic activity is markedly dependent on the structure of the pumiliotoxin (95). Subsequent studies on the activity of pumiliotoxin B in neuromuscular preparations were interpreted as due to an apparent facilitation of calcium translocation from internal storage sites (99 see review in Ref. 5). Inhibitory effects on the calcium-dependent ATPase of sarcoplasmic reticulum were shown to be due not to pumiliotoxin B, but to phenolic impurities, namely, fcis(2-hydroxy-3-terf-butyl-5-methylphenyl)methane, 3,5-di-/ert-butyl-4-hydroxytoluene (BHT), and nonylphenols (100). [Pg.222]

In rats, the phrenic nerve discharge was prolonged during respiratory depression. Since the toxin F7 has a potent anti-ChE activity, it is concluded that the respiratory failure induced by toxin F7 is peripheral in origin, chiefly, if not entirely, due to its anticholinesterase activity. [Pg.148]


See other pages where Phrenic nerve is mentioned: [Pg.270]    [Pg.327]    [Pg.17]    [Pg.64]    [Pg.243]    [Pg.243]    [Pg.271]    [Pg.38]    [Pg.218]    [Pg.360]    [Pg.361]    [Pg.386]    [Pg.63]    [Pg.19]    [Pg.20]    [Pg.54]    [Pg.28]    [Pg.270]    [Pg.295]    [Pg.191]    [Pg.184]    [Pg.280]    [Pg.435]    [Pg.164]    [Pg.340]    [Pg.347]    [Pg.354]    [Pg.362]    [Pg.174]    [Pg.251]    [Pg.140]   
See also in sourсe #XX -- [ Pg.243 ]

See also in sourсe #XX -- [ Pg.62 , Pg.63 , Pg.65 , Pg.74 , Pg.75 ]




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