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P Lipfert

Publications and source records attributed to P Lipfert.

27 records · Page 2Linked to original sources
PubMed1993

[The circulatory effect of conduction anesthesia near the spinal cord. Pathogenesis, prophylaxis and therapy of heart circulation complications].

Major conduction anaesthesia is not harmless. Based on new findings about sympathetic blockade, it was analysed whether circulatory side effects after spinal or epidural anaesthesia, in particular cardiocirculatory arrest, correlate with the level of segmental spread and whether prophylactic or therapeutic measures are effective. With spinal or epidural anaesthesia in healthy, unpremedicated patients, blood pressure, heart rate, and cardiac output remain within +/- 20% of normal independent of the height of segmental spread. However, in patients with circulatory diseases and/or premedication blood pressure often drops more than 20%, especially when cranial spread exceeds T4. Cardiocirculatory arrest during major conduction anaesthesia: (1) is preceded by an interval of 10-20 min recognisable by narrowing of the pulse pressure and continuous decreases in blood pressure and heart rate; (2) does not correlate with the level of segmental spread; and (3) is possibly caused by reduced filling of the heart and/or vagal activity. Infusion of crystalloid or colloid solutions may diminish the drop in blood pressure, whereas vasopressors reduce the frequency and extent of cardiocirculatory side effects. As yet, however, there is no safe prophylaxis to prevent cardiocirculatory arrest. Cardiopulmonary resuscitation after circulatory arrest must be combined with early administration of catecholamines.

Anesthesia, Epidural↗
PubMed1989

Toxic effects of triethyldodecylammoniumbromide (TEA-C12) on myelinated nerve fibers and blood-nerve barrier in the mouse.

The blocking effect of triethyldodecylammoniumbromide (TEA-C12), applied locally to the sciatic nerve, was studied in 28 adult BDF1 mice. Clinical parameters, electrophysiological recordings of muscle action potentials evoked by stimulation at the sciatic notch, and morphological aspects are presented. Our results show that both the minimal blocking concentration and half the minimal blocking concentration induce flaccid paresis of the treated hind-limb. There was a complete, long-lasting nerve conduction block due to Wallerian degeneration of the myelinated nerve fibers. In contrast, pain sensation was abolished only on day 4 after application of the minimal blocking concentration, but was preserved during the rest of the time that nerve conduction block was observed. This correspond to the electron microscopic finding of preservation of unmyelinated nerve fibers. Recovery of nerve conduction was characterized electrophysiologically by occurrence of minute polyphasic regeneration potentials between day 18 and 21, clinically by advanced restitution of muscle force on day 64, and morphologically by nerve regeneration. TEA-C12 also induced a disturbance of the blood-nerve barrier, demonstrated using an intraperitoneally administered biotinylated IgG tracer in the endoneurial space. The morphological features of the acute axonal changes of the myelinated nerve fibers including the degeneration of the axonal mitochondria suggest that the neurotoxic effect of TEA-C12 is possibly mediated by interference with the axonal energy supply. The selective affection of myelinated nerve fibers separates TEA-C12 from other neurotoxins that induce changes of the axonal microorganelles or complete Wallerian degeneration of myelinated and unmyelinated nerve fibers. The selectivity for myelinated nerve fibers and the supposed pathogenetic mechanism exhibit some similarities with the human polyneuropathy caused by acute arsenic acid intoxication.

Action Potentials↗
PubMed1989

Tachyphylaxis to local anesthetics does not result from reduced drug effectiveness at the nerve itself.

Possible development of tachyphylaxis to local anesthetics in the nerve itself (time-dependent change in axonal conduction properties) was studied in the aortic nerve of eight rabbits anesthetized with urethane. The nerve was immersed in Tyrode solution with or without bupivacaine at pH 7.4 and 38 degrees C in a trough molded from the surrounding tissues. After control measurements the nerve was exposed to increasing bupivacaine concentrations until complete nerve block at minimal blocking concentration. Subsequently, bupivacaine concentrations were reduced and kept constant for 4 h (partial block). Finally, intact nerve function was confirmed after bupivacaine washout with Tyrode solution. For quantification total nerve activity was recorded continuously and related to drug concentrations. Two findings argue against the occurrence of tachyphylaxis at the nerve itself: 1) nerve activity decreased rather than increased over time in the presence of constant bupivacaine concentrations during partial block; and 2) for the same bupivacaine concentration, nerve activity during partial block was always lower than during the initial blocking experiments. Thus, drug effectiveness increased rather than decreased over time, which cannot be reconciled with the theory that tachyphylaxis might be mediated by changes in axonal conduction properties.

Anesthetics, Local↗
PubMed1989

[Tachyphylaxis to local anesthetics].

Tachyphylaxis to local anesthetics is defined as decrease in duration, segmental spread, or intensity of a regional block after repeated doses of equal size, i.e. to maintain a given level of effect the dose has to be increased. In contrast, time-dependent variations in pain or circadian changes in the duration of local anesthetic action only simulate the occurrence of tachyphylaxis (pseudotachyphylaxis). Tachyphylaxis appears neither to be linked to structural (ester vs amide) or pharmacological properties of the local anesthetics (short- vs long-acting) nor to technique (surface anesthesia, conduction block, spinal, caudal, or epidural anesthesia, brachial plexus block) or mode of administration (intermittent vs continuous). There is even disagreement about the clinical significance of tachyphylaxis because some authors found it in almost every patient, others less often whereas a third group did not find tachyphylaxis at all. The mechanisms underlying tachyphylaxis are open to debate. Changes in pharmacokinetics (local alterations of disposition and absorption; decrease of perineural pH) and pharmacodynamics (antagonistic effects of nucleotides or increased sodium concentration; increase in afferent input) have been implicated. None of the theoretical considerations presented are strong enough to explain tachyphylaxis. However, results from isolated nerve preparations suggest that pharmacokinetics rather than pharmacodynamics might play a role in the development of tachyphylaxis.

Anesthetics, Local↗
PubMed1989

[The local anesthetic effect of tetrodotoxin on the natural spike activity of the depressor nerve in rabbits].

Tetrodotoxin (TTX) has been presented as an ultra-long-acting local anesthetic. Because its duration of action on myelinated nerve fibers of warm-blooded animals is unknown the effect of TTX on natural spike activity (A-delta fibers) of rabbit aortic nerve in vivo was studied. In 13 animals, a segment of the aortic nerve was placed in a perfusion chamber and exposed to increasing concentrations of TTX (n = 8) and, for comparison, of procaine (n = 8), which like TTX has a high pka. Total nerve activity and its change as related to drug concentrations was recorded continuously (concentration effect curves). The half-lives (t1/2) of onset time after drug administration and recovery following drug washout were also determined. TTX blocked nerve activity in a concentration-related manner, as did procaine; however, the potency of TTX (EC50 = 3.3 +/- 0.8.10(-9), cm = 1.3 +/- 0.4.10(-8) mol/l) was about 50,000 times higher than that of procaine (EC50 = 1.6 +/- 0.2.10(-4), cm = 2.5 4/- 0.3.10(-4) mol/l). Onset time did not differ statistically (p = 0.08) between TTX (t1/2 = 3.5 +/- 0.4 min) and procaine (t1/2 = 2.2 +/- 0.5 min). Most importantly, TTX block could not be reversed within 1-5 h of drug washout (n = 5) or was reversed incompletely (13%, 66%, and 90% of control activity) with t1/2 16 to 21 min. In contrast, all the procaine-blocked nerves recovered completely (t1/2 = 3.0 +/- 0.4 min). TTX blocks myelinated A-delta fibers of warm-blooded animals with lower concentrations and for a longer time than nonmyelinated fibers.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1987

Studies of local anesthetic action on natural spike activity in the aortic nerve of cats.

The aortic nerve was used to study the blocking action of procaine and bupivacaine on natural spike activity. In anesthetized cats, a segment of the aortic nerve was placed in a perfusion chamber and exposed to increasing drug concentrations, varying pH, while temperature remained constant. Total nerve activity was recorded continuously, and its change was related to drug concentration. The half-time of recovery following drug wash-out was also determined. At pH 7.4, the minimal blocking concentration was 0.5 X 10(-3) mol/l for procaine and 0.05 X 10(-3) mol/l for bupivacaine, the half-times of recovery 1.4 and 3.0 min, respectively. Procaine and bupivacaine reversibly blocked natural spike activity at the same concentrations as they blocked electrically evoked activity. The aortic nerve, whose physiologic spike traffic can be followed continuously for hours, may be used to advantage for studying the long-term effects of local anesthetics in vivo.

Action Potentials↗
PubMed1987

Ultralong-lasting nerve block: triethyldodecyl ammonium bromide is probably a neurotoxin rather than a local anesthetic.

The profile and duration of action of triethyldodecyl ammonium bromide (TEA-C12) on natural spike activity of rabbit aortic nerve was examined. To study the profile of action, a segment of the aortic nerve of anesthetized rabbits was placed in a perfusion chamber and exposed to increasing concentrations of TEA-C12 and, for comparison, of procaine. Total nerve activity was recorded continuously and its change related to drug concentrations (concentration/effect curves). The half-lives of onset time after drug administration and recovery following drug-washout were also determined. To study the duration of conduction block induced by TEA-C12, the aortic nerve of anesthetized rabbits was exposed to a concentration slightly higher than the minimal blocking concentration for an average time of 130 min after complete conduction block occurred. Three to 40 days later, the nerves were examined both neurophysiologically and neuropathologically. TEA-C12 blocked nerve activity in a concentration-related manner, as did procaine; however, the onset time (t1/2) was much slower for TEA-C12 (9.2 min) than for procaine (2.2 min). Most importantly, TEA-C12 block could not be reversed within 9 h of drug-washout, whereas all the procaine-blocked nerves completely recovered (t1/2 = 3.0 min). Nerve activity was completely blocked by TEA-C12 and nerve block was accompanied by severe morphological damage with complete loss of myelinated nerve fibers and severe axonal edema of the remaining axons for about 4 weeks. Nerve function completely recovered, but with only partial morphological restoration between day 30 and 40 after the initial block.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMedDate not supplied

Minimal blocking concentrations of bupivacaine and procaine in an exclusively nociceptive system in humans.

BACKGROUND AND OBJECTIVES: Prior to this investigation, there was no approach to compare both the potency of local anesthetics and their time course of action in a reproducible nociceptive system in humans. We tested whether the vascularly isolated vein segment is appropriate for such an approach. METHODS: In six healthy men, a hand vein segment was vascularly isolated and intraluminally stimulated with electropulses of constant current intensity. The subjects rated pain between threshold and maximally tolerable pain on a visual analogue scale. For determining minimal blocking concentrations (a measure of potency), the vein segment was continuously perfused with Tyrode's solution with increasing concentrations of bupivacaine or procaine for at least 10 minutes each until pain was completely blocked. Subsequently, the respective local anesthetic was rinsed off with Tyrode's solution to determine the time course of recovery. RESULTS: Both bupivacaine and procaine blocked pain in a concentration-related fashion, the minimal blocking concentrations being 1.6 (0.6-1.9; median and range) mmol/L for bupivacaine and 15.0 (7.5-22.5) mmol/L for procaine. Whereas the onset of block (time of 50% block) did not differ significantly between bupivacaine and procaine [43 s (range, 3-80) vs 53 s (range, 30-115)], local anesthesia lasted significantly longer after application of bupivacaine [278 s (range, 215-325)] than after procaine [183 s (range, 125-225)]. CONCLUSIONS: The vascularly isolated vein segment is well suited to compare in vivo the properties of local anesthetics with a minimally invasive approach at a reproducible nociceptive system in humans.

Adult↗