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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fatigue and recovery from fatigue were related to metabolism in single fibers of the frog semitendinosus muscle. The fibers were held at a sarcomere length of 2.3 microm in oxygenated Ringer solution at 15 degrees C and were stimulated for up to 150 s by a schedule of 10-s, 20-Hz tetanic trains that were interrupted by 1-s rest periods, after which they were rapidly frozen for biochemical analysis. Two kinds of fatigue were produced in relation to stimulus duration. A rapidly reversed fatigue occurred with stimulation for under 40 s and was evidenced by a decline in tetanic tension that could be overcome by 1 s of rest. A prolonged fatigue was caused by stimulation for 100-150 s. It was evidenced during stimulation by a fall in tetanic tension that could not be overcome by 1 s of rest, and after stimulation by a reduction, lasting for up to 82 min, in the peak tension of a 200-ms test tetanus. Fiber phosphocreatine (PCr) fell logarithmically in relation to stimulus duration, from a mean of 121 +/- 8 nmol/mg protein (SEM, n = 12) to 10% of this value after 150 s of stimulation. PCr returned to normal levels after 90-120 min of rest. Stimulation for 150 s did not significantly affect fiber glycogen and reduced fiber ATP by at most 15%. It is suggested that the prolonged fatigue caused by 100-150 s of tetanic stimulation was caused by long-lasting failure of excitation-contraction coupling, as it was not accompanied by depletion of energy stores in the form of ATP. One possibility is that H+ accumulated in fatigued fibers so as to interfere with the action of Ca2+ in the coupling process.
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PMID:Metabolic correlates of fatigue and of recovery from fatigue in single frog muscle fibers. 31 Aug 67

The characteristics of the neuromuscular block produced by streptomycin in vivo were studied on the sciatic-tibialis anterior nerve-muscle preparation of eight anaesthetized cats. The lungs of the animals were ventilated mechanically and normocarbia was maintained. During acute exposure to streptomycin (within 2 h), ED50 for blockade of the twitch was 56 (SEM +/- 5) mg kg-1 of the base. The characteristics of block were similar to those of neomycin-induced block in some aspects. There was absence of train-of-four fade and tetanic fade, partial sparing of the responses elicited at 10 Hz and 20 Hz, and total sparing of the 50 Hz tetanus, as well as the post-tetanic twitch. In contrast to neomycin-induced neuromuscular block, however, post-tetanic exhaustion was not observed and prolonged exposure to streptomycin (22-28 h) did not change the characteristics of the block. We conclude that, despite their chemical similarities, streptomycin and neomycin block neuromuscular transmission differently.
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PMID:Acute and subchronic neuromuscular blocking characteristics of streptomycin: a comparison with neomycin. 44 43

To determine whether the dose of atropine affects the rate of neostigmine-induced recovery from vecuronium-induced neuromuscular blockade, the authors monitored isometric adductor pollicis mechanical activity in 36 anesthetized (thiopental, fentanyl, nitrous oxide) adult patients (ASA physical status 1 or 2). Once surgery was completed and twitch height had spontaneously regained 25% of its initial value, the patients were randomly allocated into three groups (A10, A15, A20; n = 12 in each group) according to the dose of atropine (10, 15, or 20 micrograms/kg) that was mixed with 40 micrograms/kg neostigmine. Twitch height, train-of-four, and 50- and 100-Hz tetanic fade were recorded for 15 min after the administration of the reversal agents. No significant differences were found among the three groups in the final twitch height (95% +/- 2%), train-of-four (87% +/- 1%, 88% +/- 2%, 89% +/- 1%), and 50-Hz tetanic fade (90% +/- 1%, 94% +/- 1%, 93% +/- 1%) (mean +/- SEM). Fifteen minutes after reversal, fade in response to 100-Hz tetanus was statistically greater in the A10 group than in the two other groups (70% +/- 3% of control versus 84% +/- 4% and 81% +/- 2%) (mean +/- SEM, P less than 0.05). The present results demonstrate that larger doses of atropine facilitate neostigmine's reversal of vecuronium neuromuscular blockade. The clinical implications of the differences observed in this study remain to be determined.
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PMID:The influence of atropine dose on recovery from vecuronium-induced neuromuscular blockade. 809 86

The effects of increasing the extracellular K+ concentration on the capacity to generate action potentials and to contract were tested on unfatigued muscle fibers isolated from frog sartorius muscle. The goal of this study was to investigate further the role of K+ in muscle fatigue by testing whether an increased extracellular K+ concentration in unfatigued muscle fibers causes a decrease in force similar to the decrease observed during fatigue. Resting and action potentials were measured with conventional microelectrodes. Twitch and tetanic force was elicited by field stimulation. At pHo (extracellular pH) 7.8 and 3 mmol K+.L-1 (control), the mean resting potential was -86.6 +/- 1.7 mV (mean +/- SEM) and the mean overshoot of the action potential was 5.6 +/- 2.5 mV. An increased K+ concentration from 3 to 8.0 mmol.L-1 depolarized the sarcolemma to -72.2 +/- 1.4 mV, abolished the overshoot as the peak potential during an action potential was -12.0 +/- 3.9 mV, potentiated the twitch force by 48.0 +/- 5.7%, but did not affect the tetanic force (maximum force) and the ability to maintain a constant force during the plateau phase of a tetanus. An increase to 10 mmol K+.L-1 depolarized the sarcolemma to -70.1 +/- 1.7 mV and caused large decreases in twitch (31.6 +/- 26.1%) and tetanic (74.6 +/- 12.1%) force. Between 3 and 9 mmol K+.L-1, the effects of K+ at pHo 7.2 (a pHo mimicking the change in interstitial pH during fatigue) and 6.4 (a pHo known to inhibit force recovery following fatigue) on resting and action potentials as well as on the twitch and tetanic force were similar to those at pHo 7.8. Above 9 mmol K+.L-1 significant differences were found in the effect of K+ between pHo 7.8 and 7.2 or 6.4. In general, the decrease in peak action potential and twitch and tetanic force occurred at higher K+ concentrations as the pHo was more acidic. The results obtained in this study do not support the hypothesis that an accumulation of K+ at the surface of the sarcolemma is sufficiently large to suppress force development during fatigue. The possibility that the K+ concentration in the T tubules reaches the critical K+ concentration necessary to cause a failure of the excitation-contraction coupling mechanism is discussed.
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PMID:Effects of K+ on the twitch and tetanic contraction in the sartorius muscle of the frog, Rana pipiens. Implication for fatigue in vivo. 149 91

A small dose of tetanus toxin (2-5 ng; 10 mouse LD50) injected into the rat hippocampus produces a chronic epileptic syndrome in which epileptic discharges recur intermittently for 6-8 weeks. Hippocampal slices prepared during this period and maintained in vitro generate both evoked and spontaneous epileptic discharges. The present study used slices prepared 8-18 days after injection of tetanus toxin or vehicle solution into both hippocampi to test whether or not synaptic inhibition was selectively impaired in this experimental epilepsy. Intracellular recordings were made from CA3 pyramidal layer neurones within the tetanus toxin focus, which was identified by field potential recordings of synchronous bursts evoked by afferent stimulation. The intrinsic properties of these neurones did not differ from comparable cells in control-injected rats. All cells generated excitatory postsynaptic potentials (EPSPs) following stimulation of stratum radiatum in CA3. In control slices EPSPs were followed by a 'fast' inhibitory postsynaptic potential (IPSP), peaking at 25-30 ms, with a mean amplitude (+/- SEM) of -6.7 mV (+/- 0.66). In the epileptic slices these were absent, and the EPSP prolonged so that the potential at 30 ms was a depolarisation of +6.6 mV (+/- 2.75). The slow IPSP at 120 ms dropped to -0.27 mV (+/- 0.18) from -3.97 mV (+/- 1.43) (11 cells in each group). The loss of IPSPs cannot be attributed to a shift in reversal potentials in the toxin-injected group because no IPSPs were unmasked by current injection (n = 11). IPSPs also occurred spontaneously in the neurones in control slices, with a mean amplitude of -1.30 mV. Their frequency decreased by a factor of 13 in cells from the chronic focus induced by tetanus toxin (P less than 0.0001, analysis of variance), but their amplitude did not change significantly (mean of -1.22 mV). Spontaneous EPSPs were significantly more frequent and slightly smaller in the toxin-injected group (mean amplitudes 1.35 and 1.13 mV respectively). Together these studies support the hypothesis that the chronically recurring seizures induced by low doses of tetanus toxin can be attributed to a substantial, persistent and selective reduction of inhibitory neurotransmission in the hippocampus.
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PMID:Sustained and selective block of IPSPs in brain slices from rats made epileptic by intrahippocampal tetanus toxin. 161 77

1. The effects of atropine and glycopyrrolate on neuromuscular transmission and on muscle contraction, were studied, in the rat diaphragm preparation, by analyzing their effects on the indirectly (and directly)-elicited twitch (0.2 Hz), tetanic (50 Hz for 20 sec duration), post-tetanic twitch responses (at 5 sec after the tetanus), and on the phenomenon of post-tetanic twitch potentiation (PTP), which is thought to be of a presynaptic origin, i.e. due to increased transmitter release. 2. Atropine (0.001-10 microM) increased the indirectly-elicited twitch tension by 22 +/- 2.1% (control 0.9 +/- 0.1 g, P less than 0.02), the tetanus by 15 +/- 1.1% (control 3.9 +/- 0.7 g, P less than 0.05), the post-tetanic twitch response by 33 +/- 3.1% (control 1.2 +/- 0.1 g, P less than 0.01) and the PTP value by 36 +/- 1.9% (control 33 +/- 2.3%, P less than 0.01, means +/- SEM = 6). 3. Atropine (0.001-10 microM) had little effect on the directly-elicited twitch tension, but in high concentrations (e.g. 20 microM), it blocked the twitch tension. 4. In contrast, glycopyrrolate (0.1-100 microM) had little effect on the twitch tension (direct or indirect), but it significantly reduced the tetanus (by 38 +/- 3.5%, P less than 0.01), the post-tetanic twitch response (by 17 +/- 1.2%, P less than 0.05) and the PTP values (by 24 +/- 3.1% P less than 0.02). 5. In the presence of hemicholinium (1.3 microM) the responses to atropine and glycopyrrolate were altered (decreased), indicating a possible action on presynaptic mechanism of transmission. 6. It is concluded that atropine and glycopyrrolate produce different (opposite) effects at the rat neuromuscular junction, atropine enhances whereas glycopyrrolate depresses neuromuscular transmission. The effects of these two antimuscarinic drugs may be exerted at the presynaptic nerve terminals, i.e. on presynaptic muscarinic receptors, which are involved in the feedback mechanism of transmitter release.
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PMID:Effects of atropine and glycopyrrolate on neuromuscular transmission in the rat phrenic nerve-diaphragm preparation. 283 47

Immune regulatory changes after tetanus booster immunization were studied by measuring T-cell proliferation and surface Ia expression after cocultivation of T cells with autologous tetanus toxoid pulsed macrophages. Both soluble and aluminium-absorbed tetanus toxoid was used as antigen. T cells proliferated readily prior to immunization, if TTAl was used as an antigen (when proliferation was measured by the uptake of [3H]thymidine: mean +/- SEM 64.5 +/- 11.5 X 10(3) dpm). The proliferative response of the peripheral blood T cells studied decreased significantly to 29.3 +/- 9.3 X 10(3) dpm (P less than 0.01) 1 week postimmunization, returned to preimmunization values after 2 to 4 weeks, and increased further thereafter. Surface Ia expression paralleled the proliferative response at every point pre- and postimmunization. Serum antibody levels increased steadily during the first weeks. These results demonstrate a functional parallel to the previously described changes in T-cell phenotypes (M. M. Eibl, J. W. Mannhalter, and G. Zlabinger, N. Engl. J. Med 310, 198, 1984) after tetanus booster immunization.
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PMID:Reduced antigen-induced proliferation and surface Ia expression of peripheral blood T cells following tetanus booster immunization. 387 79

Post-tetanic potentiation (PTP) was elicited at the frog sartorius and cutaneous pectoris neuromuscular junctions. A 30-sec, 30-Hz tetanus produced a 2- to 3-fold post-tetanic increase in endplate potential (EPP). In surface-recorded responses this PTP decayed in a double exponential way with time constants of 12.7 sec +/- 2.4 (SEM) and 146.8 sec +/- 36.6. In acute experiments 0.2 to 0.8 mM phenytoin (5,5-diphenylhydantoin, DPH) dramatically and reversibly reduced the early component. The late component was also reduced, although to a lesser extent and often not reversibly. DPH reduced PTP even when there was no failure of the EPP during the tetanus. Thus, the DPH effect did not require a complete block of the presynaptic action potential. At longer exposures and higher DPH concentrations EPP failures did develop, and this was associated with a more profound suppression of PTP. PTP was also elicited in tetrodotoxin (TTX)-containing solutions using electronic stimulation of nerve terminals to elicit transmitter release. This PTP had a much shorter duration (about 30 sec) than that seen in normal Ringer's solution and was followed by depression of EPP amplitudes. Thus, sodium entry into nerve terminals enables a mechanism which greatly prolongs PTP. DPH had no effect on PTP in TTX. These results, together with others in the literature, suggest that the reduction of PTP by DPH involves a graded reduction of sodium influx into nerve terminals during high rates of axon stimulation. The development of all-or-none failures of the presynaptic action potential results in even greater suppression of PTP.
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PMID:On the mechanism by which phenytoin blocks post-tetanic potentiation at the frog neuromuscular junction. 405 60

The time course of force and stiffness during a twitch was determined at 6 and 26 degrees C in frog semitendinosus muscle bundles using the transmission time technique of Schoenberg, M., J.B. Wells, and R.J. Podolsky, 1974, J. Gen. Physiol. 64:623-642. Sarcomere shortening due to series compliance was also measured using a laser light diffraction technique. Following stimulation, stiffness developed more rapidly than force, but had a slower time course than published Ca2+ transients determined from light signals using Ca2+ sensitive dyes (Baylor, S.M., W.K. Chandler, and M.W. Marshall, 1982, J. Physiol. (Lond.). 331:139-177). Stiffness (S) did not reach its tetanic value during a twitch at 6 or 26 degrees C, although at 6 degrees C, it approached close to this value with S-twitch/S-tetanus = 0.82 +/- 0.07 (+/- SEM). During relaxation, force fell more rapidly than stiffness both for a twitch and also a tetanus. Also in this paper, several of the assumptions inherent in using the transmission time technique for the measurement of stiffness are considered in detail.
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PMID:Stiffness, force, and sarcomere shortening during a twitch in frog semitendinosus muscle bundles. 660 49

This prospective study evaluated host resistance in a surgical population who walked into the hospital for elective surgery. Patients were stratified into Hospital Reactive (HR, n = 19) if they reacted to two or more of five recall skin test antigens and Walk-in Anergic (WA, n = 26) if they did not react to the antigens. The WA patients were slightly older (74.4 +/- 1.8 years, +/- SEM versus 66.7 +/- 2.7 p less than 0.05). Diagnosis in the HR and WA group were: tumors 13/19 versus 21/26, diverticulitis 3/19 versus 0/19, and miscellaneous 3/19 versus 5/26. Twenty-five laboratory normal controls (LN) were also studied. There were no significant differences in the following parameters between the HR and WA groups: stage of disease; hemoglobin; circulating leukocyte count; polymorphonuclear cell counts; total lymphocyte counts (both groups lower than LN, p less than 0.05), monocyte counts (both higher than LN, p less than 0.05); per cent E-rosettes and lymphocyte blastogenesis to mitogens (phytohemagglutinin, concanavalin-A) and antigens (purified protein derivative and tetanus); phagocytosis of preopsonised Staphylococcus aureus 502A, at 5, 10, and 20 minutes; alpha, beta, and gamma globulins; C3, and total hemolytic complement (CH50) levels; C-reactive protein; and ANA and DNA levels. The HR group demonstrated an increase in the rate of killing of Staphylococcus 502A at 10, 20, 40, and 80 minutes compared to the LN group but the WA group did not show this augmentation (p less than 0.001). The serum albumins were: LN = 4.46, HR = 3.98, WA = 3.43 g/dl (p less than 0.05). Degree and duration of surgery was the same in the HR and WA groups. There were no major sepsis episodes (bacteremia or proven intracavitary abscess) in the HR patients versus 25% in the WA patients (p less than 0.05). There was one death (6%, pulmonary embolus) in the HR group and 8 (40%) in the WA group (p less than 0.05). Antibiotic prophylaxis was equal but the WA patients received therapeutic antibiotics more frequently (65% versus 11% p less than 0.05). Of all the host immunocompetence tests measured in this study, the delayed type hypersensitivity skin test response and the serum albumin were variables abnormal between the survivors and those who died.
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PMID:The walk-in anergic patient. How best to assess the risk of sepsis following elective surgery. 671 20


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