Relative refractory period: A measure to detect early neuropathy in alcoholics

1987 ◽  
Vol 10 (4) ◽  
pp. 323-328 ◽  
Author(s):  
M. Kathryn Alderson ◽  
Jack H. Petajan
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.


2005 ◽  
Vol 14 (3) ◽  
pp. 249-250
Author(s):  
Mary G. Adams ◽  
Michele M. Pelter

1966 ◽  
Vol 45 (3) ◽  
pp. 475-488
Author(s):  
R. A. CHAPMAN

1. A method is described that enables the electrical responses of motor axons isolated from the leg nerve of the crab Carcinus to be studied close to or at the site of imposed electrical currents, while this area is continuously bathed by physiological solution. 2. The three classes of repetitive responses originally described by Hodgkin (1948) have occurred during the present work and additional features of these responses have been described. 3. The results support Hodgkin's original thesis that the development of the spike generating mechanisms determine the response frequency during a repetitive response, but a progressive lengthening of the relative refractory period occurs during this response and is considered to be the agency that causes the gradual slowing down of the response frequency, i.e. the adaption. 4. The processes of membrane restoration (repolarization and recovery) have been shown to be sensitive to applied currents; anodal current hastening and cathodal current slowing it. These phenomena provide a basis for interpreting the change in the duration of the relative refractory period observed during the repetitive response. 5. The differences between the form of the repetitive response in the crab axon and the predictions of the Hodgkin-Huxley equations is discussed and it seems likely that the rapid recovery of the membrane resistance during the repolarization phase of the crab axon action potential underlies this difference.


1994 ◽  
Vol 267 (1) ◽  
pp. H376-H382 ◽  
Author(s):  
D. G. Cable ◽  
T. E. Rath ◽  
E. R. Dreyer ◽  
J. B. Martins

Our purpose was to characterize Purkinje responses in vivo to alpha 1- and alpha 2-adrenergic stimulation in sinoaortically denervated and vagotomized dogs pretreated with metoprolol (1 mg/kg). We measured Purkinje relative refractory period (PRRP) responses to norepinephrine (NE) and phenylephrine (PE) with prazosin and/or yohimbine, WB-4101, and chloralethylclonidine (CEC) in varying doses. Results were as follows: PE infusion (25 micrograms.kg-1.min-1) prolonged PRRP (9.6 +/- 1.4 ms; a 4.1 +/- 0.4% change). Prazosin blocked PRRP prolongation with PE at 7 x 10(-8) M/kg (P < 0.05). Yohimbine did not attenuate PRRP prolongation with PE either alone or in combination with prazosin. NE infusion (0.8 micrograms.kg-1.min-1) also prolonged PRRP (9.2 +/- 2.3 ms; a 4.8 +/- 1.0% change). In contrast neither prazosin nor yohimbine at any dose (up to 10(-6) M/kg) totally blocked the prolongation with NE infusion. However, with prazosin (2 x 10(-7) M/kg) pretreatment, yohimbine blocked PRRP prolongation, significant at 7 x 10(-8) M/kg (P < 0.05). In separate experiments with yohimbine pretreatment at 7 x 10(-8) M/kg, PRRP prolongation with either PE or NE infusion was blocked equipotently with WB-4101 and CEC at 7 x 10(-8) M/kg. However, CEC did not block mean arterial pressure (MAP) responses to PE or NE infusion unlike WB-4101. We concluded that both subclasses of alpha 1-adrenergic antagonists equipotently block PRRP prolongation by alpha-agonists despite different effects on MAP. Purkinje refractoriness is also prolonged by alpha 2-adrenergic stimulation acting at the cell membrane.


2014 ◽  
Vol 112 (18) ◽  
Author(s):  
F. Selmi ◽  
R. Braive ◽  
G. Beaudoin ◽  
I. Sagnes ◽  
R. Kuszelewicz ◽  
...  

1958 ◽  
Vol 41 (4) ◽  
pp. 847-856 ◽  
Author(s):  
Werner R. Loewenstein

A period of supernormal excitability is left by a propagated impulse in a Pacinian corpuscle. The increase in excitability is found 6 to 10 msec. after an impulse occurs in the corpuscle. Supernormality is produced by either mechanically elicited dromic impulses, or by electrically excited antidromic impulses. Generator potentials do not cause supernormality. Local potentials discharged spontaneously by the corpuscle, and which fall on the supernormal trail left by an antidromic impulse, become enhanced in amplitude, an eventually are turned into propagated dromic potentials. The supernormal period is interpreted as caused by a negative after-potential left at the first intracorpuscular node of Ranvier which outlasts both the recovery time of the firing level and that of the generator potential during the corpuscle's relative refractory period.


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