Br.J. Anaesth. (1975), 47, 885
HEXAFLUORENIUM-SUXAMETHONIUM INTERACTION IN PATIENTS WITH NORMAL VERSUS ATYPICAL CHOLINESTERASE A. BARAKA SUMMARY
Hexafluorenium is a selective plasma cholinesterase inhibitor which has been used clinically to delay the hydrolysis of suxamethonium and hence to potentiate its neuromuscular blocking effect (Foldes et al., 1960). However, such potentiation has also been observed in the isolated frog sartorius muscle, and was attributed to a possible direct interaction between hexafluorenium and suxamethonium at the neuromuscular junction (Nastuk and Karis, 1964; Karis, Nastuk and Katz, 1966). In order to differentiate between the direct neuromuscular interaction and the plasma cholinesterase inhibitory effects of hexafluorenium in man, I compared the effect of hexafluorenium on suxamethonium block in a patient with atypical plasma cholinesterase activity with a control response obtained in another patient with normal enzymatic activity. METHOD
Two brothers undergoing eye surgery were investigated. One child was normal while the second child was an atypical cholinesterase homozygote (table I). Anaesthesia was maintained with nitrous oxide, oxygen (2:1) and halothane 0.5%. The ulnar nerve was stimulated by a Block-Aid monitor at 4-sec intervals. The resultant thumb adduction was monitored by a Grass force displacement transducer A. BARAKA, M.D., Department of Anesthesiology, American University Hospital, Beirut, Lebanon.
TABLE I. Dibucaine number (JDN) and the relative plasma cholinesterase activity in the two children. The cholinesterase activity was measured by the Michel method (1949), while the dibucaine number was estimated by the method described by Kalow and Genest (1957). Age (vr)
Body wt. (kg)
DN
Cholinesterase activity (%)
25
81
81
20
22
13
Genotype Normal homozygote Atypical homozygote
(FT 03) connected to a Grass polygraph (Baraka, 1975). After a steady twitch response was obtained, suxamethonium 0.1 mg/kg was injected i.v. and its neuromuscular block was recorded. After the recovery of normal neuromuscular transmission, hexafluorenium 0.3 mg/kg was injected, and this was followed 1 min later by suxamethonium 0.1 mg/kg. The resultant blocks were compared in the two children. RESULTS
In the normal homozygote child, suxamethonium 0.1 mg/kg produced muscle fasciculation, followed by transient and incomplete neuromuscular block. However, when suxamethonium was repeated after hexafluorenium 0.3 mg/kg, marked prolongation of the block and delay of recovery was observed. The potentiated block manifested tetanic fade and posttetanic facilitation (fig. 1).
Downloaded from http://bja.oxfordjournals.org/ at Deakin University Library on March 14, 2015
The effect of hexafluorenium 0.3 mg/kg on the neuromuscular block of suxamethonium 0.1 mg/kg in a child with homozygote atypical plasma cholinesterase activity and in one of his normal brothers has been compared. In the normal child, hexafluorenium produced a marked potentiation of suxamethonium block, while partially antagonizing the block in the atypical homozygote child. In both situations, the hexafluorenium-suxamethonium block appeared to be antidepolarizing in nature as indicated by tetanic fade and post-tetanic facilitation. It is concluded that, in man, hexafluorenium can modify the action of suxamethonium by two different mechanisms. In patients with normal plasma cholinesterase activity, the anti-esterase effect predominates and results in marked potentiation of suxamethonium block, while in atypical homozygotes a direct antidepolarizing action at the neuromuscular junction may result in a dimir-ished response.
BRITISH JOURNAL OF ANAESTHESIA
886
t SUXAMETHONIUM 0.1 mg/kg
PTF
t SUXAMETHONIUM 0.1 mg/kg
1 min
In the abnormal homozygote child, the injection of suxamethonium 0.1 mg/kg was not associated with any visible muscle fasciculation and was rapidly followed by a complete and prolonged neuromuscular block which was almost 10 times that produced by injecting the same dose in the normal child. After complete recovery, injection of suxamethonium after hexafiuorenium 0.3 mg/kg was not followed by a potentiated response, but rather by a slow and incomplete neuromuscular block which lasted for a period comparable to, or even less than, the control response. The block showed tetanic fade and post-tetanic facilitation (fig. 2).
DISCUSSION
This investigation has shown that hexafiuorenium potentiates markedly the neuromuscular block of suxamethonium in patients with normal plasma cholinesterase activity. On the other hand, in patients with atypical esterase activity, the interaction of hexafiuorenium with suxamethonium is not followed by a potentiated response, but rather by an incomplete neuromuscular block which lasts for a period comparable to, or even less than, the control response. Such findings suggest that the potentiation of suxamethonium block by hexafiuorenium in normal patients is mainly the result of a selective
t SUXAMETHONIUM 0.1 mg/kg
f HEXAFLUORENIUM (0.3 mg/kg) t
1 min
SUXAMETHONIUM (0.1 mg/kg)
FIG. 2. Tracings of the twitch response to ulnar nerve stimulation in the atypical homozygote child. Upper tracing shows that suxamethonium 0.1 mg/kg produces a complete and prolonged neuromuscular block. Tetanus is maintained and there is no significant post-tetanic facilitation. Lower tracing shows the effect of the same dose of suxamethonium after hexafiuorenium 0.3 mg/kg. The resulting block is slower in onset, less in degree, shows early recovery and is characterized by tetanic fade and post-tetanic facilitation.
Downloaded from http://bja.oxfordjournals.org/ at Deakin University Library on March 14, 2015
FIG. 1. Tracings of the twitch response to ulnar nerve stimulation in the normal homozygote child. Upper tracing shows the transient neuromuscular block produced by suxamethonium 0.1 mg/kg. Lower tracing shows the effect of the same dose of suxamethonium after hexafiuorenium 0.3 mg/kg. A marked prolongation of the block associated with delayed recovery is observed. The block is characterized by tetanic fade and post-tetanic facilitation.
HEXAFLUORENIUM-SUXAMETHONIUM INTERACTION
REFERENCES
Baraka, A. (1974). Neuromuscular effects of galanthamine versus neostigmine and hexafluorenium. 4th Euro. Coner. Anesthesiol., Madrid. (1975). Potentiation of suxamethonium blockade by neostigmine in a patient with atypical cholinesterase. Br. J. Anaesth., 47, 416. Foldes, F., Hillmer, K , Molloy, R., and Monte, A. (1960). Potentiation of the neuromuscular effect of succinylcholine by hexafluorenium. Anesthesiology, 21, 50. Kalow, W. (1959). The distribution, destruction and elimination of muscle relaxants. Anesthesiology, 20, 505. Genest, K. (1957). A method for the detection of atypical forms of human serum cholinesterase: determination of dibucaine numbers. Can. J. Biochem., 35, 339. Karis, J., Nastuk, W., and Katz, R. (1966). The action of tacrine on neuromuscular transmission: a comparison with hexafluorenium. Br. J. Anaesth., 38, 762.
Michel, M. (1949). An electrometric method for the determination of red blood cell and plasma cholinesterase activity. J. Lab. Clin. Med., 34, 1564. Nastuk, W., and Karis, J. (1964). The blocking action of hexafluorenium on neuromuscular transmission and its interaction with succinylcholine. J. Pharmacol. Exp. Ther., 144, 236. INTERACTION DE L'HEXAFLUORENIUM ET DU SUXAMETHONIUM SUR DES MALADES AYANT UNE CHOLINESTERASE NORMALE PAR RAPPORT A UNE CHOLINESTERASE ATYPIQUE RESUME
On a compare l'effet de l'hexafluorenium a raison de 0,3 mg/kg sur le blocage neuromusculaire par le suxamethonium a 0,1 mg/kg d'un enfant homozygote ayant une activite de cholinesterase du plasma atypique, a celui d'un de ses freres normaux. Sur l'enfant normal, 1'hexafluorenium produit une potentialisation marquee du blocage par le suxamethonium, alors qu'il oppose partiellement le blocage sur l'enfant homozygote atypique. Dans les deux cas, le blocage par l'hexafluorenium-suxamethonium semblait, par nature, etre antidepolarisant comme l'indique l'affaiblissement tetanique et la facilitation post tetanique. On en conclut que, chez l'homme, 1'hexafluorenium peut modifier l'action du suxamethonium par deux mecanismes differents. Chez les malades ayant une activite de cholinesterase avec plasma normal, l'effet anti-esterase predomine et resulte en une potentialisation du blocage par le suxamethonium, alors que chez un homozygote atypique, toute action directe antidepolarisante a la jointure neuromusculaire peut aboutir a une reponse diminuee. HEXAFLUORENIUM-SUXAMETHONIUMGEGENWIRKUNGEN IN PATIENTEN MIT NORMALER, BEZW. ATYPISCHER CHOLINESTERASE ZUSAMMENFASSUNG
Verglichen wurde die Wirkung von Hexafluorenium (0,3 mg/kg) auf den neuromuskularen Block durch Suxamethonium (0,1 mg/kg) bei einem Kind mit gleichanlaeiger, atypischer Plasma-Cholinesteraseaktivitat, mit der Wirkung auf einen seiner normalen Briider. Beim normalen Kind rief Hexafluorenium eine deutliche Verstarkung des Suxamethonium-Blocks, wahrend es beim atypischen gleichanlagigen Kind dem Block teilweise entgegenwirkte. In beiden Fallen schien der Hexafluorenium-Suxamethonium-Block anti-depolarisierend zu sein, angezeigt durch tetanisches Nachlassen und posttetanische Bahnung. Zusammenfassend wird festgestellt, daB Hexafluorenium beim Menschen die Wirkung von Suxamethonium durch zwei verschiedene Mechanismen modifizieren kann. Bei Patienten mit normaler PlasmaCholinesteraseaktivitat uberwiegt die Antiesterase-Wirkung und fuhrt zu einer deutlichen Verstarkung des Suxamethonium-BIocks, wahrend bei atypischen Homozygoten eine direkte anti-depolarisierende Wirkung an der neuromuskularen Verbindung zu einer verringerten Reaktion fiihren kann. INTERACCION HEXAFLUORONIUM— SUXAMETONIUM EN PACIENTES CON COLINESTERASA NORMAL COMPARADOS CON LOS DE COLINESTERASA IRREGULAR SUMARIO
Se comparo el efecto de 0,3 mg/kg de hexafluoronium sobre el bloqueo neuromuscular de 0,1 mg/kg de suxa-
Downloaded from http://bja.oxfordjournals.org/ at Deakin University Library on March 14, 2015
inhibition of the plasma cholinesterase activity (Foldes et al., 1960), and that it is not secondary to a direct interaction at the post-junctional membrane. In atypical esterase homozygotes, the plasma cholinesterase plays no part in elimination of suxamethonium, since there is virtually no hydrolysis of the drug at the normal pH of the blood and in the clinical concentrations used (Kalow, 1959). Under such conditions, hexafluorenium will not change the hydrolysis of suxamethonium and hence will not potentiate its neuromuscular block. The mechanism of suxamethonium block following hexafluorenium in both the normal and atypical patients appears to be antidepolarizing in nature, as indicated by tetanic fade and post-tetanic facilitation (Baraka, 1974). This might be explained by the findings of Nastuk and Karis (1964) and Karis, Nastuk and Katz (1966) that hexafluorenium prevents the depolarization of the post-junctional membrane by suxamethonium and other depolarizing agents, including the chemical transmitter acetylcholine. Therefore, it may be concluded that, in man, hexafluorenium can modify the action of suxamethonium both indirectly by delaying its hydrolysis by the plasma cholinesterase and directly by inhibiting its depolarizing activity at the postjunctional membrane. In normal patients, the inhibitory effect of hexafluorenium on the enzymatic hydrolysis predominates and a marked potentiation of suxamethonium block occurs, while in atypical esterase homozygotes, the antidepolarizing neuromuscular interaction may result in a diminished response.
887
888 metonium en un nino con actividad homozigotica irregular de la colinesterasa del plasma y la de uno de sus hermanos normales. En el niiio normal, el hexafluoronium produce una importante potenciacion del bloqueo por suxametonium, a la vez que antagoniza parcialmente el bloqueo en el niiio con homozigotos irregulares. En ambas situaciones, el bloqueo hexafluoronium-suxametonium parece ser antidespolarizante por naturaleza como indica el desvanecimiento tetanico y la facilitation post-tetanica. Se
BRITISH JOURNAL OF ANAESTHESIA concluyo que, en el hombre, el hexafluoronium puede modificar la action de suxametonium por medio de dos mecanismos diferentes. En pacientes con actividad normal de la colinesterasa del plasma, predomina el efecto del antiesterasa y da como resultado una potenciacidn importante del bloqueo por suxametonium a la vez que homozigotos irregulares. Una action directa de antidespolarizaci6n en la union neuromuscular puede dar como resultado una respuesta disminuida.
Downloaded from http://bja.oxfordjournals.org/ at Deakin University Library on March 14, 2015
HEXAFLUORENIUM-SUXAMETHONIUM INTERACTION IN PATIENTS WITH NORMAL VERSUS ATYPICAL CHOLINESTERASE A. BARAKA SUMMARY
Hexafluorenium is a selective plasma cholinesterase inhibitor which has been used clinically to delay the hydrolysis of suxamethonium and hence to potentiate its neuromuscular blocking effect (Foldes et al., 1960). However, such potentiation has also been observed in the isolated frog sartorius muscle, and was attributed to a possible direct interaction between hexafluorenium and suxamethonium at the neuromuscular junction (Nastuk and Karis, 1964; Karis, Nastuk and Katz, 1966). In order to differentiate between the direct neuromuscular interaction and the plasma cholinesterase inhibitory effects of hexafluorenium in man, I compared the effect of hexafluorenium on suxamethonium block in a patient with atypical plasma cholinesterase activity with a control response obtained in another patient with normal enzymatic activity. METHOD
Two brothers undergoing eye surgery were investigated. One child was normal while the second child was an atypical cholinesterase homozygote (table I). Anaesthesia was maintained with nitrous oxide, oxygen (2:1) and halothane 0.5%. The ulnar nerve was stimulated by a Block-Aid monitor at 4-sec intervals. The resultant thumb adduction was monitored by a Grass force displacement transducer A. BARAKA, M.D., Department of Anesthesiology, American University Hospital, Beirut, Lebanon.
TABLE I. Dibucaine number (JDN) and the relative plasma cholinesterase activity in the two children. The cholinesterase activity was measured by the Michel method (1949), while the dibucaine number was estimated by the method described by Kalow and Genest (1957). Age (vr)
Body wt. (kg)
DN
Cholinesterase activity (%)
25
81
81
20
22
13
Genotype Normal homozygote Atypical homozygote
(FT 03) connected to a Grass polygraph (Baraka, 1975). After a steady twitch response was obtained, suxamethonium 0.1 mg/kg was injected i.v. and its neuromuscular block was recorded. After the recovery of normal neuromuscular transmission, hexafluorenium 0.3 mg/kg was injected, and this was followed 1 min later by suxamethonium 0.1 mg/kg. The resultant blocks were compared in the two children. RESULTS
In the normal homozygote child, suxamethonium 0.1 mg/kg produced muscle fasciculation, followed by transient and incomplete neuromuscular block. However, when suxamethonium was repeated after hexafluorenium 0.3 mg/kg, marked prolongation of the block and delay of recovery was observed. The potentiated block manifested tetanic fade and posttetanic facilitation (fig. 1).
Downloaded from http://bja.oxfordjournals.org/ at Deakin University Library on March 14, 2015
The effect of hexafluorenium 0.3 mg/kg on the neuromuscular block of suxamethonium 0.1 mg/kg in a child with homozygote atypical plasma cholinesterase activity and in one of his normal brothers has been compared. In the normal child, hexafluorenium produced a marked potentiation of suxamethonium block, while partially antagonizing the block in the atypical homozygote child. In both situations, the hexafluorenium-suxamethonium block appeared to be antidepolarizing in nature as indicated by tetanic fade and post-tetanic facilitation. It is concluded that, in man, hexafluorenium can modify the action of suxamethonium by two different mechanisms. In patients with normal plasma cholinesterase activity, the anti-esterase effect predominates and results in marked potentiation of suxamethonium block, while in atypical homozygotes a direct antidepolarizing action at the neuromuscular junction may result in a dimir-ished response.
BRITISH JOURNAL OF ANAESTHESIA
886
t SUXAMETHONIUM 0.1 mg/kg
PTF
t SUXAMETHONIUM 0.1 mg/kg
1 min
In the abnormal homozygote child, the injection of suxamethonium 0.1 mg/kg was not associated with any visible muscle fasciculation and was rapidly followed by a complete and prolonged neuromuscular block which was almost 10 times that produced by injecting the same dose in the normal child. After complete recovery, injection of suxamethonium after hexafiuorenium 0.3 mg/kg was not followed by a potentiated response, but rather by a slow and incomplete neuromuscular block which lasted for a period comparable to, or even less than, the control response. The block showed tetanic fade and post-tetanic facilitation (fig. 2).
DISCUSSION
This investigation has shown that hexafiuorenium potentiates markedly the neuromuscular block of suxamethonium in patients with normal plasma cholinesterase activity. On the other hand, in patients with atypical esterase activity, the interaction of hexafiuorenium with suxamethonium is not followed by a potentiated response, but rather by an incomplete neuromuscular block which lasts for a period comparable to, or even less than, the control response. Such findings suggest that the potentiation of suxamethonium block by hexafiuorenium in normal patients is mainly the result of a selective
t SUXAMETHONIUM 0.1 mg/kg
f HEXAFLUORENIUM (0.3 mg/kg) t
1 min
SUXAMETHONIUM (0.1 mg/kg)
FIG. 2. Tracings of the twitch response to ulnar nerve stimulation in the atypical homozygote child. Upper tracing shows that suxamethonium 0.1 mg/kg produces a complete and prolonged neuromuscular block. Tetanus is maintained and there is no significant post-tetanic facilitation. Lower tracing shows the effect of the same dose of suxamethonium after hexafiuorenium 0.3 mg/kg. The resulting block is slower in onset, less in degree, shows early recovery and is characterized by tetanic fade and post-tetanic facilitation.
Downloaded from http://bja.oxfordjournals.org/ at Deakin University Library on March 14, 2015
FIG. 1. Tracings of the twitch response to ulnar nerve stimulation in the normal homozygote child. Upper tracing shows the transient neuromuscular block produced by suxamethonium 0.1 mg/kg. Lower tracing shows the effect of the same dose of suxamethonium after hexafiuorenium 0.3 mg/kg. A marked prolongation of the block associated with delayed recovery is observed. The block is characterized by tetanic fade and post-tetanic facilitation.
HEXAFLUORENIUM-SUXAMETHONIUM INTERACTION
REFERENCES
Baraka, A. (1974). Neuromuscular effects of galanthamine versus neostigmine and hexafluorenium. 4th Euro. Coner. Anesthesiol., Madrid. (1975). Potentiation of suxamethonium blockade by neostigmine in a patient with atypical cholinesterase. Br. J. Anaesth., 47, 416. Foldes, F., Hillmer, K , Molloy, R., and Monte, A. (1960). Potentiation of the neuromuscular effect of succinylcholine by hexafluorenium. Anesthesiology, 21, 50. Kalow, W. (1959). The distribution, destruction and elimination of muscle relaxants. Anesthesiology, 20, 505. Genest, K. (1957). A method for the detection of atypical forms of human serum cholinesterase: determination of dibucaine numbers. Can. J. Biochem., 35, 339. Karis, J., Nastuk, W., and Katz, R. (1966). The action of tacrine on neuromuscular transmission: a comparison with hexafluorenium. Br. J. Anaesth., 38, 762.
Michel, M. (1949). An electrometric method for the determination of red blood cell and plasma cholinesterase activity. J. Lab. Clin. Med., 34, 1564. Nastuk, W., and Karis, J. (1964). The blocking action of hexafluorenium on neuromuscular transmission and its interaction with succinylcholine. J. Pharmacol. Exp. Ther., 144, 236. INTERACTION DE L'HEXAFLUORENIUM ET DU SUXAMETHONIUM SUR DES MALADES AYANT UNE CHOLINESTERASE NORMALE PAR RAPPORT A UNE CHOLINESTERASE ATYPIQUE RESUME
On a compare l'effet de l'hexafluorenium a raison de 0,3 mg/kg sur le blocage neuromusculaire par le suxamethonium a 0,1 mg/kg d'un enfant homozygote ayant une activite de cholinesterase du plasma atypique, a celui d'un de ses freres normaux. Sur l'enfant normal, 1'hexafluorenium produit une potentialisation marquee du blocage par le suxamethonium, alors qu'il oppose partiellement le blocage sur l'enfant homozygote atypique. Dans les deux cas, le blocage par l'hexafluorenium-suxamethonium semblait, par nature, etre antidepolarisant comme l'indique l'affaiblissement tetanique et la facilitation post tetanique. On en conclut que, chez l'homme, 1'hexafluorenium peut modifier l'action du suxamethonium par deux mecanismes differents. Chez les malades ayant une activite de cholinesterase avec plasma normal, l'effet anti-esterase predomine et resulte en une potentialisation du blocage par le suxamethonium, alors que chez un homozygote atypique, toute action directe antidepolarisante a la jointure neuromusculaire peut aboutir a une reponse diminuee. HEXAFLUORENIUM-SUXAMETHONIUMGEGENWIRKUNGEN IN PATIENTEN MIT NORMALER, BEZW. ATYPISCHER CHOLINESTERASE ZUSAMMENFASSUNG
Verglichen wurde die Wirkung von Hexafluorenium (0,3 mg/kg) auf den neuromuskularen Block durch Suxamethonium (0,1 mg/kg) bei einem Kind mit gleichanlaeiger, atypischer Plasma-Cholinesteraseaktivitat, mit der Wirkung auf einen seiner normalen Briider. Beim normalen Kind rief Hexafluorenium eine deutliche Verstarkung des Suxamethonium-Blocks, wahrend es beim atypischen gleichanlagigen Kind dem Block teilweise entgegenwirkte. In beiden Fallen schien der Hexafluorenium-Suxamethonium-Block anti-depolarisierend zu sein, angezeigt durch tetanisches Nachlassen und posttetanische Bahnung. Zusammenfassend wird festgestellt, daB Hexafluorenium beim Menschen die Wirkung von Suxamethonium durch zwei verschiedene Mechanismen modifizieren kann. Bei Patienten mit normaler PlasmaCholinesteraseaktivitat uberwiegt die Antiesterase-Wirkung und fuhrt zu einer deutlichen Verstarkung des Suxamethonium-BIocks, wahrend bei atypischen Homozygoten eine direkte anti-depolarisierende Wirkung an der neuromuskularen Verbindung zu einer verringerten Reaktion fiihren kann. INTERACCION HEXAFLUORONIUM— SUXAMETONIUM EN PACIENTES CON COLINESTERASA NORMAL COMPARADOS CON LOS DE COLINESTERASA IRREGULAR SUMARIO
Se comparo el efecto de 0,3 mg/kg de hexafluoronium sobre el bloqueo neuromuscular de 0,1 mg/kg de suxa-
Downloaded from http://bja.oxfordjournals.org/ at Deakin University Library on March 14, 2015
inhibition of the plasma cholinesterase activity (Foldes et al., 1960), and that it is not secondary to a direct interaction at the post-junctional membrane. In atypical esterase homozygotes, the plasma cholinesterase plays no part in elimination of suxamethonium, since there is virtually no hydrolysis of the drug at the normal pH of the blood and in the clinical concentrations used (Kalow, 1959). Under such conditions, hexafluorenium will not change the hydrolysis of suxamethonium and hence will not potentiate its neuromuscular block. The mechanism of suxamethonium block following hexafluorenium in both the normal and atypical patients appears to be antidepolarizing in nature, as indicated by tetanic fade and post-tetanic facilitation (Baraka, 1974). This might be explained by the findings of Nastuk and Karis (1964) and Karis, Nastuk and Katz (1966) that hexafluorenium prevents the depolarization of the post-junctional membrane by suxamethonium and other depolarizing agents, including the chemical transmitter acetylcholine. Therefore, it may be concluded that, in man, hexafluorenium can modify the action of suxamethonium both indirectly by delaying its hydrolysis by the plasma cholinesterase and directly by inhibiting its depolarizing activity at the postjunctional membrane. In normal patients, the inhibitory effect of hexafluorenium on the enzymatic hydrolysis predominates and a marked potentiation of suxamethonium block occurs, while in atypical esterase homozygotes, the antidepolarizing neuromuscular interaction may result in a diminished response.
887
888 metonium en un nino con actividad homozigotica irregular de la colinesterasa del plasma y la de uno de sus hermanos normales. En el niiio normal, el hexafluoronium produce una importante potenciacion del bloqueo por suxametonium, a la vez que antagoniza parcialmente el bloqueo en el niiio con homozigotos irregulares. En ambas situaciones, el bloqueo hexafluoronium-suxametonium parece ser antidespolarizante por naturaleza como indica el desvanecimiento tetanico y la facilitation post-tetanica. Se
BRITISH JOURNAL OF ANAESTHESIA concluyo que, en el hombre, el hexafluoronium puede modificar la action de suxametonium por medio de dos mecanismos diferentes. En pacientes con actividad normal de la colinesterasa del plasma, predomina el efecto del antiesterasa y da como resultado una potenciacidn importante del bloqueo por suxametonium a la vez que homozigotos irregulares. Una action directa de antidespolarizaci6n en la union neuromuscular puede dar como resultado una respuesta disminuida.
Downloaded from http://bja.oxfordjournals.org/ at Deakin University Library on March 14, 2015
