Hypokalemia shortens relative refractory period of peripheral sensory nerves in man

1977 ◽  
Vol 216 (1) ◽  
pp. 67-71 ◽  
Author(s):  
K. Maurer ◽  
H. C. Hopf ◽  
K. Lowitzsch
Author(s):  
V.J. Montpetit ◽  
S. Dancea ◽  
L. Tryphonas ◽  
D.F. Clapin

Very large doses of pyridoxine (vitamin B6) are neurotoxic in humans, selectively affecting the peripheral sensory nerves. We have undertaken a study of the morphological and biochemical aspects of pyridoxine neurotoxicity in an animal model system. Early morphological changes in dorsal root ganglia (DRG) associated with pyridoxine megadoses include proliferation of neurofilaments, ribosomes, rough endoplasmic reticulum, and Golgi complexes. We present in this report evidence of the formation of unique aggregates of microtubules and membranes in the proximal processes of DRG which are induced by high levels of pyridoxine.


1957 ◽  
Vol 190 (2) ◽  
pp. 383-390 ◽  
Author(s):  
Paul F. Cranefield ◽  
Brian F. Hoffman ◽  
Arthur A. Siebens

The strength-interval curve of dog ventricular myocardium has been measured with anodal and cathodal stimulation. During diastole the anodal threshold is higher than the cathodal. As anodal stimuli are applied progressively earlier the anodal threshold first rises above and then falls to levels below the anodal diastolic threshold. During most of the relative refractory period the anodal threshold is lower than the cathodal threshold. At all times during the late relative refractory period and throughout diastole excitation of double origin (anodal and cathodal) is evoked by sufficiently strong stimuli; this simultaneous origin of excitation at two points does not evoke fibrillation. During the early relative refractory period, however, only the anode is able to excite. Differences between anodal and cathodal thresholds are not attributable to asynchronous repolarization at the two electrode sites. The ‘no-response’ phenomenon occurs only when the anodal threshold is markedly lower than the cathodal.


2013 ◽  
Vol 108 (10) ◽  
pp. 1634-1643 ◽  
Author(s):  
Eduardo E Valdez-Morales ◽  
Jeff Overington ◽  
Raquel Guerrero-Alba ◽  
Fernando Ochoa-Cortes ◽  
Charles O Ibeakanma ◽  
...  

1992 ◽  
Vol 263 (1) ◽  
pp. G29-G37
Author(s):  
O. D. Hottenstein ◽  
G. Remak ◽  
E. D. Jacobson

Cessation of perivascular nerve stimulation (NS) elicits a transient increase in intestinal blood flow above the prestimulatory value. This enhancement of blood flow constitutes the phenomenon of post-nerve stimulation hyperemia (PSH). We investigated the involvement of peptidergic sensory nerves in intestinal PSH. In anesthetized rats the velocity of blood flowing through the anterior mesenteric artery (VBF) was measured with a pulsed Doppler velocimeter. PSH was induced by 4 min of postganglionic electrical NS (5 Hz). PSH was abolished by distal periarterial application of tetrodotoxin and intra-arterial lidocaine, which suggests a peripheral sensory nervous mechanism for PSH. The increase in conductance at peak PSH was blocked by pretreatment with the selective, primary afferent neurotoxin capsaicin administered as 1) subcutaneous injection in neonatal life, 2) topical application to periarterial nerves, or 3) injection into the jejunal lumen. In rats pretreated with reserpine, NS evoked a hyperemic response, which was blocked by capsaicin. Treatment with adenosine deaminase inhibited PSH considerably less than capsaicin, suggesting a lesser role for adenosine in PSH. Our findings support the hypothesis that postganglionic NS activates both adrenergic and peptidergic nerves and that the latter release vasodilator peptides in the gut during PSH.


2009 ◽  
Vol 65 ◽  
pp. S212 ◽  
Author(s):  
Seiji Komagata ◽  
Shanlin Chen ◽  
Ryuichi Hishida ◽  
Minoru Shibata ◽  
Katsuei Shibuki

Nature ◽  
1975 ◽  
Vol 254 (5496) ◽  
pp. 146-148 ◽  
Author(s):  
RAINER F. FOELIX

2019 ◽  
Vol 61 (1) ◽  
Author(s):  
R. Van Rensburg ◽  
H. Reuter

Pain is a complex and unique experience. It encompasses several pathways, involving nociceptive signal generation (transduction) and propagation (transmission), as well as perception and modulation of the nociceptive stimuli. Nonsteroidal anti-inflammatory drugs (NSAIDs) primarily exert their analgesic effects through inhibition of cyclooxygenase (COX) enzymes, thereby attenuating prostaglandin synthesis. The COX-2 selective NSAIDs (coxibs) and aspirin have also been shown to reduce colorectal cancers, presumably by prostaglandin-inhibition mechanisms. Paracetamol appears to have both peripheral and central effects. The postulated mechanism for its peripheral effects is indirect COX inhibition, while the central effects are thought to be mediated by modulation of descending pain inhibition pathways. Topical analgesics are available in various formulations. The topical NSAIDs have the same mechanism of action as the systemic formulations, but with less systemic absorption and effects. The local anaesthetics provide a dense sensory block via inhibition of nerve impulse transmission, and are available in percutaneous and transdermal preparations. Capsicum is effective for neuropathic pain, and acts by stimulating and then desensitising peripheral sensory nerves.


Sign in / Sign up

Export Citation Format

Share Document