Biomedical subjects
Publications and source records attributed to H Meves.
This article deals with the clinical importance of the os styloideum carpi, and the differential diagnosis and therapy of painful styloid boss. Emphasis is laid on the importance of further studies, especially in pathomechanics.
The success of syndactyly operations depends to a considerable extent on the appropriate bandage-technique which according to the author's experience has proved to be highly effective.
1. Asymmetry currents were recorded from intracellularly perfused squid axons subjected to an equal number of exactly equal positive and negative voltage clamp pulses. The asymmetry currents consisted of an on-response at the beginning of the pulses and an off-response at the end of the pulses.2. The asymmetry currents were markedly reduced by 30 mM glutaraldehyde applied internally.3. Clamp pulses of varying height, superimposed on a holding potential of - 80 to - 100 mV, were used to study the voltage and time dependence of the asymmetry current. The magnitude of the on- and off-response increased with increasing pulse height along a sigmoid curve. The time constants of the on- and off-response depended on the potential during the depolarizing pulses; the time constant of the on-response had a maximum at an internal potential of - 12 mV, the time constant of the off-response was largest at positive internal potentials.4. Holding the membrane at a potential of - 80 to - 100 mV for several minutes led to a slow increase of the size of the asymmetry current.5. Changing the holding potential from - 80 or - 100 mV to a less negative potential caused a decrease of the asymmetry current. At holding potentials less negative than - 65 or - 60 mV the asymmetry current reversed its sign: the transient current at the beginning of the pulses turned into an inward current and the transient current at the end of the pulses became outward. No inactivation of the asymmetry current was seen in the range of holding potentials studied (V < - 3 mV).6. The results are generally consistent with the idea that the asymmetry currents are in some way related to the opening and closing of the Na gates; they suggest, however, that the asymmetrical charge movement does not simply reflect the voltage and time dependence of the m system.
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1. The Ca-sensitive photoprotein aequorin was injected into squid axons and the light response to stimulation or depolarizing voltage clamp pulses recorded.2. The effects of Mn(2+), Co(2+), Ni(2+), La(3+) and of the organic Ca antagonists D-600 and iproveratril on the early tetrodotoxin-sensitive and late tetrodotoxin-insensitive components of the light response were studied.3. The late tetrodotoxin-insensitive component can be blocked, reversibly, by concentrations of Mn, Co and Ni that reduce but do not block the tetrodotoxin-sensitive component. The late component can also be blocked by La(3+) and the organic Ca antagonists D-600 and iproveratril.4. Mn(2+), Co(2+), Ni(2+) and the drug D-600 all reduce the Na currents, but have little effect on either outward or inward K currents. Tetraethylammonium blocks the outward K current but has no appreciable effect on the tetrodotoxin-insensitive entry of Ca.5. Concentrations of Mn between 5 and 50 mM substantially reduce the light output during a train of action potentials; they also slightly reduce the rate of rise of the action potential.6. On pharmacological grounds it is concluded that the tetrodotoxin-insensitive component of Ca entry does not represent Ca ions passing through the K permeability channels. There must exist a potential-dependent late Ca channel that is distinct from the well known Na and K channels of the action potential. A possible function for this late Ca channel in the coupling of excitation to secretion is discussed.
1. Intracellular aequorin was used to monitor changes in Ca entry in response to maintained depolarization either produced electrically or by exposure to K-rich solutions.2. External K concentrations greater than 50 mM produce a phasic light response. The light rises to a peak in a few sec and then falls in 0.5-5 min to a new steady level that is always greater than the level in the absence of K.3. The phasic light response does not result from depletion of available aequorin at the periphery of the axon, but rather seems to reflect a phasic entry of Ca in response to depolarization.4. Similar phasic responses are produced by prolonged electrical depolarization. These results are consistent with depolarization serving both to activate and also to inactivate Ca entry.5. Following inactivation and after return to normal sea-water, there is an appreciable relative refractory period during which the response both to K-rich sea-water and electrical depolarization is reduced in size. Complete recovery takes 10-15 min.6. The response to 410 mM-KCl is dependent on the previous treatment of the preparation. Pre-treatment with 100 or 200 mM-KCl reduced the response to 410 mM-KCl. The potential for half inactivation was about -25 mV in 112 mM-Ca and -40 mV in 20 mM-Ca.7. The rate of onset of inactivation is potential dependent and is faster for depolarizations to zero potential than for smaller ones.8. The phasic Ca entry produced by K-rich solutions is insensitive to external tetrodotoxin and internal tetraethylammonium ions, but is blocked by external Mn(2+), Co(2+) and Ni(2+) ions and by the drugs D-600 and iproveratril. This suggests that the phasic Ca entry involves the late Ca channel.9. Recovery of the outward K current after a long depolarization is much faster than recovery of the late Ca entry system. This provides further support for the view that the late Ca channel and the K channel are distinct.
1. Voltage clamp experiments were carried out on squid axons perfused with an isotonic solution of 25 mM-CsF + sucrose and placed in a Na-free solution of 100 mM-CaCl(2) + sucrose.2. Depolarizing voltage steps produced inward currents of 4-6 muA/cm(2) peak amplitude which decayed slightly during a 60 msec pulse; the inward current disappeared when the internal potential reached +50 to +60 mV and became outward for larger depolarizations.3. Tetrodotoxin completely blocked the inward current and part of the outward current. No inward currents were seen with 100 mM-MgCl(2) + sucrose as the external solution. Substituting acetate for external Cl(-) did not abolish the tetrodotoxin-sensitive outward currents.4. It is concluded that the inward current is carried by Ca and the tetrodotoxin-sensitive outward current by Cs ions, both moving through the Na channel.5. The reversal potential of the tetrodotoxin-sensitive current was in the average +54 mV. Raising the external Ca concentration or adding NaCl to the external solution increased the reversal potential; lowering the external Ca concentration or replacing the internal CsF by a Na salt decreased the reversal potential.6. From the reversal potentials of the tetrodotoxin-sensitive current measured with varying external and internal solutions the relative permeabilities of the Na channel were calculated as P(Ca)/P(Cs) = 1/0.6, P(Ca)/P(Na) = 1/10 to 1/7 and P(Cs)/P(Na) = 1/22 to 1/9 by means of the constant field equation. The permeability ratios suggest that under these experimental conditions the Na channel is still primarily permeable to Na ions, although its selectivity is relatively small.7. The time course of the tetrodotoxin-sensitive Ca inward current was different from the time course of the Na inward current. The Na current consisted of an initial peak followed by a more slowly decaying component, the Ca current showed only the slow component.8. The slowly inactivating tetrodotoxin-sensitive Ca inward currents give rise to the long lasting action potentials which have first been observed by Tasaki and coworkers under similar conditions.
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1. Axons perfused with a K-free solution containing 300 mM-NaF + sucrose to maintain isotonicity (referred to as 300 mM-NaF) and placed in K-free artificial sea-water usually depolarized spontaneously to around 0 mV. The membrane could be hyperpolarized to -70 to -100 mV with a small inwardly directed current; in one experiment the holding current was measured and was found to be less than 20 muA/cm(2).2. Membrane currents associated with a step depolarization from a potential which varied from -70 to -100 mV showed three phases: (a) an initial capacitative transient, (b) an early current which was inward for small depolarizations and outward for large ones, (c) a smaller maintained current. The currents in (b) and (c) are considered to be carried by Na ions since they both reversed direction at the same potential which was on the average within 0.3 mV of the equilibrium potential for Na ions, 10.4 mV at 0 degrees C and 11 mV at 16.5 degrees C, as estimated from measurements made with a cation-sensitive glass electrode.3. The instantaneous current-voltage relation was determined at the time of peak current and at the end of a long prepulse when the current had reached a steady level. In both cases the curve was approximately linear with a slight deviation at negative potentials.4. Prepulses, lasting 11-48 msec, to a potential of 33-64 mV (0-3.5 degrees C) produced a shift in the equilibrium potential of 0.6-3.3 mV. This small change can be accounted for by assuming that Na ions accumulate in the Frankenhaeuser-Hodgkin space.5. Both peak and steady-state components of Na current were blocked by tetrodotoxin (10(-7) g/ml.) in the external solution.6. The values of peak and steady-state Na conductance were strongly voltage-dependent for V less than -20 mV; for V more negative than -40 mV the peak and steady-state values increased e-fold for a change in potential of 4 and 6-8 mV respectively. At positive potentials the peak conductance was relatively independent of potential, whereas the steady-state curve showed an increase; at 50 mV the steady-state conductance was on the average 0.44 times the peak value for temperatures -0.3 to 4 degrees C and 0.24 times the peak value for a temperature of 16.5 degrees C.7. Following an 18-164 min perfusion period with 300 mM-NaF, the delayed K currents with 300 mM-KF were reduced in amplitude to less than one-tenth the initial level. This apparent removal of the delayed rectifier was not accompanied by any significant change in either the relation between peak early current and voltage or the associated equilibrium potential.8. In an experiment in which tetrodotoxin was used to block the early channel, K currents were determined before and after NaF perfusion. In both cases the kinetics on depolarization followed the Hodgkin-Huxley n(4) relationship and the rate constants were similar, although after NaF perfusion the amplitude was reduced to 0.07 times the control level.9. In axons perfused with 300 mM-KF, following removal of the delayed rectifier by 300 mM-NaF, the ratio of steady-state Na current: peak Na current was estimated to be about half the value obtained with NaF. A similar decrease was obtained in an axon which was perfused with 300 mM-CsF; on subsequent perfusion with 300 mM-KF, following 35 min with CsF, about half the original delayed current was present.10. The general conclusion is that in axons perfused with 300 mM-NaF the Na conductance is not fully inactivated by depolarizations which last for tens of milliseconds. The maintained component may underlie the plateau phase of long lasting action potentials which have been recorded under similar conditions.
1. Voltage clamp experiments were carried out on squid giant axons internally perfused with 300 mM-NaF + sucrose. K-free artificial sea-water, -0.3 to 3.5 degrees C, was used externally.2. Membrane currents were corrected for capacitative and leakage components, and the resulting Na current was converted to Na conductance, g(Na). An attempt was made to fit changes in g(Na) according to the Hodgkin-Huxley model, namely [Formula: see text]. According to the model g(Na) is a constant, m(infinity) and h(infinity) are steady-state values which depend only on voltage, tau(m) (-1) and tau(h) (-1) are rate constants which also are functions only of voltage.3. Stepwise depolarizations from the holding potential (-67 to -83 mV) to a potential which varied from -10 to +63 mV resulted in an exponential decline of h from its initial level to a final, non-zero level. If the test depolarization was preceded by a positive prepulse (duration, 19-105 msec; voltage, -6 to 94 mV) the rate constant for h, tau(h) (-1), was increased roughly threefold with practically no change in the final level.4. The steady-state level of h was studied by using prepulses of varying amplitude followed by a test depolarization. In one such experiment a value of 0.34 was obtained for a 105 msec prepulse to -49 mV. The same value for the steady level of h was obtained from analysing a record taken at +52 mV. If the potential was switched from -49 to +52 mV there was a transient increase in g(Na) although h(infinity) had the same value at these two potentials.5. Recovery from depolarization was studied by repolarizing the fibre for varying lengths of time, then applying a test depolarization. If the first depolarization was strongly positive (for example, 70 mV), so that the steady level of h was large (0.39), the currents associated with the test pulse could not be fitted on the basis of an exponential increase in h during the recovery period. Rather, the results suggested that on repolarization h rapidly decreased initially, then slowly increased.6. These results can be explained by assuming that h is given by the sum of two components, h(1) and h(2). Changes are represented kinetically by h(1) right harpoon over left harpoon x right harpoon over left harpoon h(2), where x signifies the inactive state. The distribution is shifted to the left at negative potentials and to the right for positive ones. The resulting Na conductance is comprised of two types: the first type, g(Na)m(3)h(1), is similar to the Hodgkin-Huxley system and underlines the usual transient increase in g(Na) associated with depolarization; the second type, g(Na)m(3)h(2), is maintained with depolarization and gives rise to a steady level of g(Na).
1. Membrane currents during step depolarizations were measured in axons which were perfused with 300 mM-NaF and placed in K-free artificial sea-water, -0.3-4 degrees C. The Na conductance was fitted by the modified Hodgkin-Huxley model, g(Na) = g(Na)m(3)(h(1) + h(2)). Changes in h(1) and h(2) were assumed to follow [Formula: see text] where x represents the inactive state.2. The rate constants and steady-state values for m were in agreement with the Hodgkin-Huxley equations except that the experimental relationship of m(infinity) (3) against V was shifted 10-15 mV in the negative direction. This discrepancy, which was not found in an experiment with choline sea-water, can be explained on the basis of a resistance in series with the membrane between the voltage measuring electrodes.3. At 0 degrees C the rate constants (in msec(-1)) associated with changes in h(1) and h(2) were fitted using the following equations: beta(h1) = 0.5/{exp [- (V + 32)/10] + D(1)exp (- V/V(1))}, alpha(h2) = pexp (V/V(2)), beta(h2) = pexp (V/V(2) - V/23.5) + pD(2), with the condition that at 0 mV, (alpha(h2) + beta(h2)) = p(D(2) + 2) = 0.55 msec(-1). The experiments gave average values D(1) = 3.6, V(1) = 240 mV, p = 0.08 msec(-1) and V(2) = 70 mV. The average value of g(Na) was 66 mmho/cm(2).4. At negative voltages where m(infinity) (3) against V is steep, the points for beta(h1) and alpha(h2)/beta(h2) from axons in Na sea-water were not fitted well by the above equations whereas data from an axon in choline sea-water were. These discrepancies can be explained on the basis of a series resistance.5. Measurements made at 16-17 degrees C indicated that g(Na) has a Q(10) of 1.6, tau(m) (-1) a Q(10) of 2.8 and beta(h1) a Q(10) of 3.5. The ratio alpha(h2)/beta(h2) was decreased relative to the value at 0 degrees C and could be fitted by using Q(10) = 0.6.6. Measurements made with 250 mM-NaF + 50 mM-KF inside gave rate constants which were very similar to those obtained with 300 mM-NaF. Perfusion with 300 mM-KF appeared to double the value of beta(h1), relative to that obtained with 300 mM-NaF, and to reduce alpha(h2)/beta(h2) by about half.7. The voltage dependence of alpha(h2) makes it likely that following depolarization recovery from the inactive state x occurs via x --> h(1) rather than x --> h(2) --> h(1).
1. Voltage clamp experiments were carried out on squid giant axons which were perfused internally with 300 mM-NaF + sucrose and placed in K-free artificial sea-water at 16-17 degrees C. On stepwise depolarization (V = -38.5 to 68 mV) the Na conductance g(Na) rapidly reached a peak value and then declined to a new level; this ;maintained' level was slowly inactivated in an exponential manner with a rate constant which varied from 0.3 to 1.1 sec(-1). This process was not influenced appreciably by replacing 50 mM-NaF with KF.2. On repolarization to a potential which varied between -73 and -101 mV the slow inactivation was removed with a rate constant of 0.11-0.73 sec(-1).3. Prolonged depolarization also produced a slow inactivation of the ability of the membrane to give a transient increase in g(Na). This effect developed at a rate about (1/3)-(1/2) that associated with the inactivation of the ;maintained' component; on repolarization, recovery of the peak g(Na) was 1-2 times as fast as recovery of the ;maintained' g(Na).4. In experiments on fibres perfused with 300 mM-KF after internal NaF had removed the usual delayed K conductance, depolarization resulted in an outward current which developed in an exponential manner with a time constant of a fraction of a second. The equilibrium potential for this component was more negative than -50 mV.5. Long-lasting action potentials were computed on the basis of the above slow changes and, except for the period of final repolarization, were found to be in satisfactory agreement with experimental records. The discrepancies suggest that there may be additional slow changes in permeability which could not be resolved in the present experiments.
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