Succinylcholine-induced Increases in Plasma Catecholamine Levels in Humans To the Editor
TL;DR: It is proposed that the elevation of plasma norepinephrine might contribute to the development of early adverse cardiovascular reactions to succinylcholine.
Abstract: Given the hypothesis that interaction of succinylcholine with nicotinic receptors releases endogenous catecholamines, plasma levels of epinephrine and norepinephrine were determined in anesthetized and manually ventilated patients immediately before and 2 mm after intravenous administration of succinylcholine. Anesthesia was induced with intravenous thiopental (3–4 mg/kg) followed by the administration of nitrous oxide and oxygen (1:1) and 0.5–1.0% halothane. Stimulation of the patients was avoided. Succinylcholine (1 mglkg) or metocurine (0.3 mg/kg) was injected intravenously and ventilation was controlled without intubation. Plasma norepinephrine levels increased from 301 pg/ml to 491 pg/ml (SEM = ±19 pg/ml, P < 0.01, N = 5) 2 min after the injection of succinylcholine; the increase in plasma epinephrine was not statistically significant. The time course of catecholamine elevation was studied in three additional patients. The increase of norepinephrine occurred immediately after the injection of succinylcholine, peaked (647 ± 67 pg/ml) around the third minute, and disappeared by the 10th min. The increase in epinephrine was less marked. Plasma levels of catecholamines did not change after the injection of metocurine (N = 2). The possibility that succinylcholine stimulates nicotinic receptors on the postganglionic sympathetic terminals is discussed. We propose that the elevation of plasma norepinephrine might contribute to the development of early adverse cardiovascular reactions to succinylcholine.
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TL;DR: Measurements of heart rate, arterial pressure and skin resistance have been used as indirect indices of the level of sympathetic activity to assess both the efficacy of premedication and depth of anaesthesia.
Abstract: Nociceptive surgical stimulation is accompanied by increased hypothalamopituitary activity which is generally referred to as the stress response to injury. This is manifest by a release of trophic hormones from the hypothalamus which in turn stimulate release of ACTH, TSH, GH, FSH, luteinizing hormone and prolactin in addition to ADH from the pituitary. Consequently, there is increased secretion of cortisol and thyroxine with suppression of insulin and increase in blood sugar concentrations. These responses may be partly attenuated by large doses of opioid analgesic drugs and some local anaesthetic techniques used during general anaesthesia. These endocrine changes have recently been reviewed elsewhere (Kaufman 1982, 1984; Weatherill and Spence, 1984). In addition, increased hypothalamic activity induced by nociceptive stimulation is accompanied by increased traffic in sympathetic efferent tracts. This is manifest by the well known signs which are conventionally used to diagnose unduly light levels of anaesthesia — notably dilatation of the pupils, sweating, tachycardia and hypertension. Thus measurements of heart rate, arterial pressure and skin resistance have been used as indirect indices of the level of sympathetic activity to assess both the efficacy of premedication and depth of anaesthesia. Increased sympathetic tone involves augmented release of noradrenaline by presynaptic sympathetic fibres and also increased secretion of catecholamines from the adrenal medulla. Thus attempts have been made for a number of years to assess sympathetic activity \"directly\" by measurement of plasma catecholamine concentrations. Until recently, assays were not available with sufficient sensitivity to measure resting concentrations of plasma catecholamines. However, with the advent of radioenzymatic assay (REA) and, over the past 5-6 years, high pressure liquid chromatography (HPLC) techniques for measurement of catecholamines in plasma, there has been a large
156 citations
TL;DR: It is concluded that lidocaine, 1.5 mg/kg IV, 2 min prior to laryngoscopy and intubation does not prevent hemodynamic reactions evoked by rapid sequence induction, and RPP reached a level considered potentially dangerous to patients with ischemic heart disease.
Abstract: A double-blind, randomized trial was conducted in 16 women aged 20-48 yr, to assess the effect of intravenous lidocaine on the circulatory responses to rapid sequence induction of general anesthesia. None of the patients suffered from heart or lung diseases, all were scheduled for hysterectomy, and all were premedicated with 0.3 mg/kg diazepam orally 2 hr beforehand. Induction, preceded by preoxygenation, included simultaneous injection of thiopental and succinylcholine, without starting manual ventilation until the airway was secured with the endotracheal tube. Two minutes before laryngoscopy and intubation half of the patients received lidocaine, 1.5 mg/kg, intravenously (IV). The other half received an equal volume of saline. Cuff blood pressure was measured repeatedly by an automatic recording device, and heart rate and left ventricular ejection fraction (LVEF) were monitored by a portable nonimaging nuclear probe. After laryngoscopy and intubation, mean blood pressure increased 46%, heart rate 57%, and the rate pressure product (RPP) 84% from control values in patients given lidocaine, compared to 45, 66, and 113%, respectively, in the saline group (P greater than 0.05). Pronounced, but similar decreases in LVEF were observed in the two groups, to 0.40 from 0.65 in the lidocaine group and to 0.41 from 0.65 in the saline group. In all patients, RPP reached a level considered potentially dangerous to patients with ischemic heart disease. We conclude that lidocaine, 1.5 mg/kg IV, 2 min prior to laryngoscopy and intubation does not prevent hemodynamic reactions evoked by rapid sequence induction.
78 citations
TL;DR: Haemodynamic effects of atracurium in surgical patients under nitrous oxide, oxygen and isoflurane anaesthesia, and Histamine release by narcotics and muscle relaxants in humans.
Abstract: s of Scientific papers, International Anesthesia Research Society, 1984:102. Bormann BE, Smith RB, Bunegin L, Albin MS. Does succinylcholine raise intracranial pressure? (abstract). Anesthesiology 1980;53(suppl):S262. Paul WL, Bishko JR, Woodham B. Succinylcholine, d-tubocurarine, dimethyltubocurarine, and intracranial pressure in dogs. Anesth Analg 1981;60:269. Nigrovic V, McCullough LS, Wajskol A, Levin ]A, Martin JT. Succinylcholine-induced increases in plasma catecholamine levels in humans. Anesth Analg 1983;62:627-32. Hilgenberg JC, Stoelting RK, Harris WA. Haemodynamic effects of atracurium during enflurane-nitrous oxide anaesthesia. Br J Anaesth 1983;55(suppl):81S. MorrisRB, Cahalan MK, Miller RD, Wilkinson PL, Quasha AL, Robinson SL. The cardiovascular effects of vecurimium (ORG#NC45) and pancuronium in patients undergoing coronary artery bypass grafting. Anesthesiology 1983;58:438-30. Sokoll MD, Gergis SD, Mehta M, Kemmotsu 0, Rudd D. Haemodynamic effects of atracurium in surgical patients under nitrous oxide, oxygen and isoflurane anaesthesia. Br J Anaesth 1983;55(suppl):77-9S. Savarese JJ. Clinical use of muscle relaxants. In: 1984 Review course lectures. Cleveland: International Anesthesia Research Society, p. 148. Chapple DJ, Clark JS. Pharmacological action of breakdown products of atracurium and related substances. Br J Anaesth Moss J, Rosow CE. Histamine release by narcotics and muscle relaxants in humans. Anesthesiology 1983;59:330-9. Basta SJ, Savarese J J , Ali HH, Moss J, Gionfriddo M. Histamine-releasing potencies of atracunum, dimethyl tubocurarine and tubocurarine. Br J Anaesth 1983;55(suppl):105-6S. Marcus ML, Heistad DD, Ehrhardt JC, Abboud FM. Regulation of total and regional spinal cord blood flow. Circ Res 1977;41:128-34. Griffiths IR. Spinal cord blood flow in dogs: the effect of blood pressure. I Neurol Neurosurg Psychiatry 1973;36:914-20. Griffiths IR. Spinal cord blood flow in dogs. 2 . 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J Thorac Cardiovasc Surg 1969;57:203-13. Kouchoukos NT, Lell WA, Karp RB, Samuelson I”. Hemodynamic effects o f aortic clamping and decompression with a temporary shunt for resection of the descending thoracic aorta. Surgery 1979;85:25-30. Connolly JE. Kountz SL, Boyd RJ. Left heart bypass: experi1983;55(suppl): 11-5s. ticular reference to maintenance of maximal renal blood flow. J Thorac Cardiovasc Surg 1962;44577-88. 106. Cooley DA, Belmonte BA, De Bakey ME, Latson JR. Temporarv extracorporeal circulation in the surgical treatment of cardiac and aortic disease: report of 98 cases. Ann Surg 1957;145:898-914, 107. Gott VL. Heparinized shunts for thoracic vascular operations (editorial). Ann Thorac Surg 1972;14:219-20. 108. Kahn DR, Vathayanon S, Sloan H. Resection of descending thoracic aneurysms without left heart bypass. Arch Surg 109. Carlson DE, Karp RB, Kouchoukos NT. Surgical treatment of aneurysms of the descending thoracic aorta: an analysis of 85 patients. Ann Thorac Surg 1983;35:58-69. 110. De Bakey ME, McCollum CH, Graham JM. Surgical treatment of aneurysms of the descending thoracic aorta: long-term results in 500 patients. J Cardiovasc Surg 1978;19:571-6. 11 1. Najafi H, Javid H, Hunter J , Serry C, Monson D. Descending aortic aneurysmectomy without adjuncts to avoid ischemia. Ann Thorac Surg 1980;30:326-35. 112. Berendes JN, Bredee 11, Schipperheyn JJ, Mashhour YAS. Mechanisms of spinal cord injury after cross-clamping of the descending thoracic aorta. Circulation 1982;66(supplI):ll12-6. 113. Michenfelder JD, Gronert GA, Rehder K. Neuroanesthesia. Anesthesiology 1969;30:65-100. 113. Michenfelder ID, Theye RA. Canine systemic and cerebral effects of hypotension induced by hemorrhage, trimethaphan, halothane, or nitroprusside. Anesthesiology 1977;46:188-95. 115. Blaisdell FW, Cooley DA. The mechanism of paraplegia a h temporary thoracic aortic occlusion and its relationship to spinal fluid pressure. Surgery 1962;51:351-5. 116. Crundy BL, Nelson PB, Doyle E, Procopio PT. lntraoperative loss of somatosensoy-evoked potentials predicts loss of spinal cord function. Anesthesiology 1982;57:321-2. 117. Grundy BL, Nash CL JR, Brown RH. Arterial pressure manipulation alters spinal cord function during correction of scoliosis. Anesthesiology 1981;54:249-53. 118. Coles JG, Wilson GJ, Sima AF, Klement P, Tait GA. Intraoperative detection of spinal cord ischemia using somatosensory cortical evoked potentials during thoracic aortic occlusion. Ann Thorac Surg 1982;34:299-306. 119. Laschinger JC, Cunningham JN 111, Catinella FP, Nathan IM, Knopp EA, Spencer FC. Detection and prevention of intraoperative spinal cord ischemia after cross-clamping of the thoracic aorta: use of somatosensory evoked potentials. Surgery 1982;92: 11 09-17. 120. Crawford FA JR, Sade RM. Spinal chord injury associated with hvperthermia during aortic coarctation repair. J Thorac Cardiovasc Surg 1984;87:616-8. 121. Ekstedt J . CSF hydrodynamic studies in man. 2. Normal hydrodynamic variables related to CSF pressure and flow. J Neurol Neurosurg Psychiatry 1978;41:345-53. 122. McComb JG, Davson H, Hyman 5, Weiss MH. Cerebrospinal fluld drainage as influenced by ventricular pressure in the rabbit. J Neurosurg 1982;56:790-7. 123. Lindvall M, Edvinsson L, Owman CH. Neurogenic control of CSF production from the choroid plexus. In: Shulman K, Marmarou A, Miller JD, Becker DP, Houchwald GM, Brock M, eds. Intracranial pressure IV. New York: Springer-Verlag, 1980:43-50. 123. Mann ID, Cookson SL, Mann ES. Differential effects of pentobarbital, ketamine hydrochloride, and enflurane anesthesia on CSF formation rate and outflow resistance in the rat. In: Shulman K, Marmarou A, Miller ID, Becker DP, Hochwald 1968;97:336-40. PRINCIPLES OF NEUROANESTHESIA ANESTH ANALG 173 1985;64: 143-74 GM, Brook M, eds. Intracranial pressure IV. New York: Springer-Verlag, 1980;466-70. 125. Artru AA. Anesthetics produce prolonged alterations of CSF dynamics (abstract). Anesthesiology 1982;57:356. 126. Artru AA, Nugent M, Michenfelder JD. Enflurane causes a prolonged and reversible increase in the rate of CSF production in the dog. Anesthesiology 1982;57:255-60. 127. Myers RR, Shapiro HM. Paradoxical effect of enflurane on choroid plexus metabolism: clinical implications. Abstracts of Scientific Papers, American Society of Anesthesiologists Annual Meeting, 1978;489-90. 128. Artru A. Relationship between cerebral blood volume and CSF pressure during anesthesia with halothane or enflurane in dogs. Anesthesiology 1983;58:533-9. 129. Maffeo CJ, Bedford RF, Van Landingham K, Butler AB. CSF outflow resistance and ICP during pentobarbital and halothane anesthesia in the cat (abstract). Anesthesiology 1982;57367. 130. Artru AA. Isoflurane does not increase the rate of CSF production in the dog. Anesthesiology 1984;60:193-7. 131. Miller JD, Sullivan HG. Severe intracranial hypertension. 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Hamill J, Bedford RF, Pobereskin LH, Weaver D, Colohan A. Lidocaine before endotracheal intubation: LTA or IV? (abstract). Anesthesiology 1980;53(supp1):26. 146. Javid M. Cited by Shapiro HM (132) 147. Marshall LF,
61 citations
TL;DR: Compared with use of the ETT, the PLMA™ reduced cisatracurium requirement, oxygen desaturation, and time to discharge from both the postanesthesia care unit and the hospital.
Abstract: BACKGROUND The stress responses from tracheal intubation are potentially dangerous in patients with higher cardiovascular risk, such as obese patients. The primary outcome objective of this study was to test whether, in comparison with the endotracheal tube (ETT), the Proseal™ Laryngeal Mask Airway (PLMA™) (Laryngeal Mask Airway Company, Jersey, United Kingdom) reduces blood pressure and norepinephrine responses and the amounts of muscle relaxants needed in obese patients. METHODS We assessed hemodynamic and hormonal stress responses, ventilation, and postoperative recovery in 75 morbidly obese patients randomized to receive standardized anesthesia with either an ETT or the PLMA™ for laparoscopic gastric banding. RESULTS In repeated-measures ANOVA, mean arterial blood pressure and plasma norepinephrine were significantly higher in the ETT group than in the PLMA™ group. In individual pairwise comparisons, blood pressure rose higher in ETT than PLMA™ patients after insertion and removal of airway devices, and after recovery. In ETT compared with PLMA™ patients, plasma norepinephrine was higher after induction of carboperitoneum (mean ± SD, 534 ± 198 and 368 ± 147 and pg/ml, P = 0.001), after airway device removal (578 ± 285 and 329 ± 128 pg/ml, P < 0.0001), and after recovery in postanesthesia care unit (380 ± 167 and 262 ± 95 and pg/ml, P = 0.003). Compared with use of the ETT, the PLMA™ reduced cisatracurium requirement, oxygen desaturation, and time to discharge from both the postanesthesia care unit and the hospital. CONCLUSIONS PLMA™ reduces stress responses and postoperative complaints after laparoscopic gastric banding.
50 citations
Cites background from "Succinylcholine-induced Increases i..."
...devoid of effect and succinylcholine has a very short effect on circulating catecholamines.(28) Second, although we did not...
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...releasing effect that may contribute, at most, to catecholamine increase at the time of intubation but not at later time-points.(27,28) Hence, smaller stress responses in PLMATM patients do not appear to be accounted for by chronic therapies or anesthesia drugs....
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TL;DR: It is proposed that patients might be better served by using NE rather than PE as the primary vasopressor to combat hypotension during general anesthesia.
Abstract: May 2016 • Volume 122 • Number 5 www.anesthesia-analgesia.org 1707 Copyright © 2016 International Anesthesia Research Society DOI: 10.1213/ANE.0000000000001239 The induction of general anesthesia is associated with sympatholysis1 and a decrease in circulating norepinephrine (NE) and epinephrine (E) concentrations.2,3 Yet, the associated hypotension is commonly treated with phenylephrine (PE), a synthetic vasoconstrictor.4,5 Theoretically, NE might better combat this general anesthesia–induced hypotension by restoring decreased circulating concentrations of this catecholamine and maintaining cardiac output (CO). However, NE is rarely used in these circumstances. In this article, I will propose that patients might be better served by using NE rather than PE as the primary vasopressor to combat hypotension during general anesthesia.
46 citations
References
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TL;DR: Some statistical techniques for analyzing the kinds of studies typically reported in Circulation Research are described and particular emphasis is given to the comparison of means from more than two populations.
Abstract: Some statistical techniques for analyzing the kinds of studies typically reported in Circulation Research are described. Particular emphasis is given to the comparison of means from more than two populations, the joint effect of several experimentally controlled variables, and the analysis of studies with repeated measurements on the same experimental units.
4,060 citations
"Succinylcholine-induced Increases i..." refers methods in this paper
...Only this comparison was of interest (m = 1, using the Bonferroni method) and because only an increase in circulating catecholamines was postulated by the hypothesis, P values for the single tail t-test were taken directly from the tables (18)....
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TL;DR: Modification of the original single isotope radioenzymatic assay of Passon and Peuler permits the direct and simultaneous analysis of norepinephrine, epinephrine and dopamine in plasma samples of 50 μl or less.
2,028 citations
"Succinylcholine-induced Increases i..." refers methods in this paper
...Plasma from the second sample was separated by centrifugation, removed by aspiration, and frozen ( - 20°C) until analyzed for epinephrine and norepinephrine by a radioenzymatic method (17)....
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TL;DR: Since significant smoking-associated increments, in pulse rate, blood pressure and blood lactate/pyruvate ratio, preceded measurable increments in plasma catecholamine concentrations, but were adrenergically mediated, these changes should be attributed to norepinephrine released locally from adrenergic axon terminals within the tissues rather than to increments in circulating catechlamines.
Abstract: We studied the effects of cigarette smoking, sham smoking and smoking during adrenergic blockade in 10 subjects to determine whether smoking released the sympathetic neurotransmitter norepinephrine, as well as the adrenomedullary hormone epinephrine, and whether smoking-associated hemodynamic and metabolic changes were mediated through adrenergic mechanisms. Smoking-associated increments in mean (±S.E.M.) plasma norepinephrine (227±23 to 324±39 pg per milliliter, P<0.01) and epinephrine (44±4 to 113±27 pg per milliliter, P<0.05) were demonstrated. Smoking-associated increments in pulse rate, blood pressure, blood glycerol and blood lactate/pyruvate ratio were prevented by adrenergic blockade; increments in plasma growth hormone and cortisol were not. Since significant smoking-associated increments, in pulse rate, blood pressure and blood lactate/pyruvate ratio, preceded measurable increments in plasma catecholamine concentrations, but were adrenergically mediated, these changes should be attribut...
1,094 citations
"Succinylcholine-induced Increases i..." refers background in this paper
...This release is observed both in animals in vivo (11,12) and in isolated organs in vitro, including the heart (13,14) and spleen (15)....
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TL;DR: Measurements of heart rate, arterial pressure and skin resistance have been used as indirect indices of the level of sympathetic activity to assess both the efficacy of premedication and depth of anaesthesia.
Abstract: Nociceptive surgical stimulation is accompanied by increased hypothalamopituitary activity which is generally referred to as the stress response to injury. This is manifest by a release of trophic hormones from the hypothalamus which in turn stimulate release of ACTH, TSH, GH, FSH, luteinizing hormone and prolactin in addition to ADH from the pituitary. Consequently, there is increased secretion of cortisol and thyroxine with suppression of insulin and increase in blood sugar concentrations. These responses may be partly attenuated by large doses of opioid analgesic drugs and some local anaesthetic techniques used during general anaesthesia. These endocrine changes have recently been reviewed elsewhere (Kaufman 1982, 1984; Weatherill and Spence, 1984). In addition, increased hypothalamic activity induced by nociceptive stimulation is accompanied by increased traffic in sympathetic efferent tracts. This is manifest by the well known signs which are conventionally used to diagnose unduly light levels of anaesthesia — notably dilatation of the pupils, sweating, tachycardia and hypertension. Thus measurements of heart rate, arterial pressure and skin resistance have been used as indirect indices of the level of sympathetic activity to assess both the efficacy of premedication and depth of anaesthesia. Increased sympathetic tone involves augmented release of noradrenaline by presynaptic sympathetic fibres and also increased secretion of catecholamines from the adrenal medulla. Thus attempts have been made for a number of years to assess sympathetic activity \"directly\" by measurement of plasma catecholamine concentrations. Until recently, assays were not available with sufficient sensitivity to measure resting concentrations of plasma catecholamines. However, with the advent of radioenzymatic assay (REA) and, over the past 5-6 years, high pressure liquid chromatography (HPLC) techniques for measurement of catecholamines in plasma, there has been a large
156 citations
TL;DR: Though SCh induces a small release of K+ in normal muscle, it produces a potentially lethal efflux in the presence of increased sensitivity, and this K+-releasing action of SCh persists for 2 to 3 months in patients who have sustained burns or trauma, and perhaps 3 to 6 months in Patients with upper motor neuron lesions.
Abstract: SCh is unequivocally contraindicated in the management of patients who have sustainded thermal trauma or direct muscle trauma and those who have neurologic disorders involving motor deficits, including tetanus. The mechanism is clear in some, but not all, of these conditions, and is related to increased chemosensitivity of the muscle membrane due to the development of receptor sites in extrajunctional areas. Though SCh induces a small release of K+ in normal muscle, it produces a potentially lethal efflux in the presence of increased sensitivity. This K+-releasing action of SCh begins about 5 to 15 days after injury and persists for 2 to 3 months in patients who have sustained burns or trauma, and perhaps 3 to 6 months in patients with upper motor neuron lesions.
112 citations
"Succinylcholine-induced Increases i..." refers background in this paper
...At the present time succinylcholine-induced hyperkalemia has been considered as the primary or even the only pathophysiologic event leading to hemodynamic crises associated with succinylcholine (3,6)....
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...attributed to the extensive depolarization of the affected muscles due to the interaction of succinylcholine with the greatly increased number of receptors for acetylcholine in denervated muscle fibers (3,6)....
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...Occasionally, fatal hemodynamic crises have been observed in, but not limited to, patients with burns (l), tetanus (2), spinal cord or lower motor neuron injuries (3), polyneuropathy (4), or previous irradiation (5)....
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