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Three cases of severe anaphylaxis to gallamine triethiodide are described. All reported cases of anaphylaxis to gallamine have occurred in women, and all the confirmed cases in Australasia. There is evidnece that women may be exposed to some substance which leaves them sensitive to gallamine triethiodide.
The fate of gallamine triethiodide has been investigated in patients undergoing cholecystectomy with choledochostomy (group I), pelvic operations (group II) and orthopaedic operations (group III). Following a single i.v. injection of gallamine 2.5 mg kg(-1) the disappearance of the drug from the serum occurred in three phases with half-lives of less than 5, 30, 138 min, less than 5, 39, 141 and less than 5, 48, 144 min in the respective groups. Twenty-four hours after injection the renal excretion of the unchanged drug was 53% (15-100%) of the administered dose in group I, 67% (40-90%) in group II and 95% (89-100%) in group III. The biliary excretion of gallamine appeared to be negligible in man. The relationship between renal excretion and duration of action of gallamine, and the influence of some intraoperative factors on drug disposition, are discussed.
The cardiovascular effects of gallamine triethiodide and succinylcholine chloride were studied in Beagle dogs during controlled halothane anesthesia. Small but significant increases in heart rate and mean arterial presssure were observed 1 minute after intravenous injection of succinylcholine chloride. Intravenous injection of gallamine triethiodide did not produce significant cardiovascular changes.
.1 mol/L CaCl2 0.5 microliters, 0.06 mol/L ACh 0.5 microliters, 5.4 x 10(-3) mol/L gallamine triethiodide (cholinergic nicotinic receptor blocker) 0.5 microliter and 14.4 x 10(-3) mol/L atropine (cholinergic muscarinic receptor blocker) 0.5 microliter were injected through bilateral intracranial cannulae in rat habenula. Pain threshold was measured by the latency of tail-flick reflex elicited by radiant heat exposure before and after intracerebral injection. CaCl2 significantly reduced the basic pain threshold and weakened the effect of the acupuncture analgesia. ACh apparently antagonized the effect of acupuncture analgesia. Gallamine triethiodide could recover the pain threshold almost to the raised level by acupuncture, but atropine only strengthened the effect on pain threshold weakly and briefly. The results suggest that the antagonistic effect of Ca2+ may be mediated via ACh in habenula.
The onset, depth and recovery from paralysis produced by gallamine triethiodide were studied using the tibialis anterior muscle/sciatic nerve preparation in mongrel dogs, during changes in blood flow to this muscle. A roller pump was used to effect the blood flow changes via an aorto-femoral shunt. The onset and depth of paralysis were related directly to muscle blood flow. There was no correlation between the rate of recovery from paralysis and the blood flow to the muscle.
Gallamine triethiodide, a drug commonly used in neurophysiological experiments, causes statistically significant and inconsistent changes in the information-carrying capacity of trains of action potentials generated by members of a population of gamma motor neurons recorded from the same cat under the same conditions during the same time period.
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Two cases are described in which patients developed acute anaphylactic reactions to precurarising doses of gallamine. Life threatening complications can arise from the use of small doses of drugs as adjuncts to anaesthesia and raises the question whether the benefits of precurarisation outweigh the risks of anaphylaxis.
A patient suffered profound anaphylactoid reaction during anaesthesia. Intradermal skin testing confirmed the clinical impression that gallamine caused the reaction. The method of testing is discussed. Previous reports of hypersensitivity to the drug are reviewed, and the use of adrenaline, antihistamines and corticosteroids in patient management are considered.
A reversed-phase, ion-pair high-performance liquid chromatographic (HPLC) method for the determination of gallamine and its impurities is described. The separation is achieved on a Nucleosil C18 column with acetonitrile-aqueous phosphate buffer (pH 3.0) (31:69, v/v) containing 0.1 M sodium perchlorate as eluent and on-line UV detection at 200 nm. The method is sensitive (the detection limit is 0.7 ng injected) and reproducible, with a peak area coefficient of variation of 0.19% (n = 15; 3 micrograms injected) and 1.65% (n = 15; 10 ng injected) for a gallamine assay; the detector response is linear over the concentration range 0.5-250 micrograms/ml of gallamine triethiodide with a correlation coefficient of 0.9997. The method has been used to isolate the two main impurities contained in gallamine triethiodide batches; their structures have been determined by NMR and fast atom bombardment mass spectrometry. Various gallamine triethiodide batches have been analysed and the HPLC results compared with those obtained by thin-layer chromatography.
Gallamine triethiodide pancuronium bromide or d-tubocurarine was infused intravenously at different rates in urethane anaesthetized rats. When given in neuromuscular blocking doses gallamine triethiodide produced significant hypotension if the rate of infusion exceeded 2 mg/min whereas neither pancuronium bromide nor d-tubocurarine produced a marked change in blood pressure in neuromuscular blocking doses.
After intravenous infusion maintaining a neuromuscular blocking concentration very little gallamine enters the cerebrospinal fluid (CSF) of the intact anesthetized cat even after several days. After a similar intravenous infusion in the decerebrate cat gallamine enters the CSF slowly over 4 days eventually reaching a concentration similar to that in the plasma. This procedure is accompanied by very strong twitching in many muscles and the occurrence of slow waves in the inferior olive in synchrony with the twitches. A large dose (4 mg) of gallamine triethiodide injected directly into the cisterna magna of an intact anesthetized cat produced twitching within 1 min and slow waves in the inferior olive in good synchrony with the twitches; the effects lasted at least 43 h. Injection of a quantity of gallamine triethiodide (about 130 micrograms) sufficient to mimic the concentration in the CSF obtained after 3-4 days of neuromuscular block in the decerebrate cat (50-120 micrograms/ml gallamine) had extremely weak effects lasting for at most 1 h. However, this weak effect is probably due to the anesthetic because injection of a similar quantity into an (unanesthetized) decerebrate cat at any time after decerebration had strong effects. After intracisternal injection of gallamine the concentration in the CSF reaches very low levels within 12 h but twitching and activity in the inferior olive persists for 1-2 days. The reasons for this prolonged action are now being investigated. The effects of gallamine are compared with the condition of reticular reflex myoclonus.
Sixty coldwater and warmwater fish ranging in weight from 2 to 35 kg were injected intramuscularly with the hypnotics alphaxalone-alphadolone and metomidate hydrochloride and the non-depolarising muscle relaxant gallamine triethiodide using a laser-aimed underwater dart gun. Alphaxalone-alphadolone produced sufficient sedation for easy netting within five to 20 minutes at doses between 0.3 and 0.5 ml/kg, with induction being somewhat faster in warmwater species. The pattern of induction was similar with metomidate but required doses of 40 to 60 mg/kg. The muscle relaxant gallamine triethiodide showed promise as a practical agent for the capture and handling of large fish by virtue of its smooth induction of paralysis at doses between 1 and 3 mg/kg and its reversible supplementation with orally administered metomidate hydrochloride.
In an attempt to assess the universal validity of the conditioned taste aversion (CTA) paradigm, various types of poisoning (UC) were associated with the gustatory CS. Water deprived rats were habituated for two days to the drinking box, where water was available for 15 min. On Day 3, access to the CS (0.1% saccharin 15 min) was followed after 30 min by a sublethal dose of the poison (0.15 M LiCl, 4% body weight; 0.1 M sodium malonate, 1% body weight; pyrrolopyrimidine drug BW 58-271, 15 mg/kg; sodium cyanide 4 mg/kg; sodium iodoacetate 40 mg/kg; sodium fluoride 30 mg/kg; gallamine triethiodide 40 mg/kg). Rats injected with the last drug were maintained under artificial respiration until muscular paralysis disappeared. After 4 days of recovery, water deprivation schedule was resumed on Days 8 and 9. During the retention test on Day 10 saccharin consumption dropped by 60% in the LiCl poisoned rats, but not CTA developed in animals poisoned by pyrrolopyrimidine, gallamine, malonate and cyanide. CTA of intermediate intensity was evoked by iodoacetate and fluoride. The absence of CTA was not due to the amnesic effect of poisoning, since LiCl administration to NaCN poisoned rats produced CTA of usual intensity. It is concluded that CTA is not related to the overall severity of poisoning but rather to the effect of the poison on specific interoceptors.
1. The activity of primary afferent axons was recorded in rats that had received a chronic constriction injury (CCI) to the common sciatic nerve. The CCI gives rise to a painful peripheral neuropathy that is characterized by allodynia, hyperalgesia, and, probably, spontaneous pain (or dysesthesia). In the majority of animals, these neuropathic pain symptoms begin 2 days postinjury; sciatic nerve afferents were examined just before and just after the time of symptom onset, at 1 and 3 days postinjury. 2. We used two stimulating electrodes, one proximal to the injury and the other distal, to activate the injured sciatic nerve while we recorded from individual primary afferent axons in microfilaments teased from the L4-L6 dorsal roots. Measurements of conduction velocities (calculated from the proximal electrode) and evaluation of conduction through the site of injury were made from 181 A beta, 135 A delta, and 60 C-fibers. 3. The percentage of axons that did not conduct through the injury site at 1 day postinjury was 85% for the A beta fibers and 55% for the A delta fibers, but only 9% for the C-fibers. By day 3, these percentages had increased to 89% for the A beta fibers, 87% for the A delta fibers, and 32% for the C-fibers. Some axons were activated from the distal stimulating electrode at currents greater than 5-10 times those required from the proximal electrodes, but their distally evoked responses did not have the longer latencies expected from a more distant site of activation. Control experiments confirmed that such high-threshold responses were due to current spread from the distal electrode to a site proximal to the nerve injury. 4. Spontaneous discharges were observed in 35% of A beta fibers, 15% of A delta fibers, and 3% of C-fibers (data from 1 and 3 days postinjury combined). Of the 55 A beta fibers exhibiting spontaneous discharge, 89% did not conduct through the injury site; the same was true of 65% of the A delta fibers (n = 20). Both of the two spontaneously discharging C-fibers conducted through the injury. The frequency of the spontaneous discharge of the myelinated fibers ranged from 10 to 50 Hz and was usually regular or bursting. 5. Intravenous administration of gallamine triethiodide (Flaxedil), a K+ channel blocker, either induced activity in previously silent fibers or increased the frequency of spontaneous activity in 50% (21/42) of A beta fibers and 19% (3/16) of A delta fibers.(ABSTRACT TRUNCATED AT 400 WORDS)
'Lissive anaesthesia', the administration of a small dose of a non-depolarising muscle relaxant to a patient breathing nitrous oxide, oxygen and an anaesthetic vapour, is a technique popularly employed for minor procedures. In this study, the effects of intravenous gallamine triethiodide (40 mg) on the blood-gas status of 20 patients under general anaesthesia with oxygen, nitrous oxide and halothane after pethidine and atropine premedication, were assessed. The results are compared with those obtained from a control group of 10 patients anaesthetised in an identical manner, but omitting the muscle relaxant drug. All patients in both the relaxant and control groups in this study developed respiratory acidaemia. The rise in mean arterial carbon dioxide tension was, however, greater after injection of gallamine. Significant hypoxia or metabolic acidaemia was not encountered, except in one grossly obese patient in the gallamine group. The implications of these findings are discussed.
The activity of myelinated primary afferents was recorded from the dorsal roots 1-3 days after creation of a painful peripheral neuropathy in rats. The effects on spontaneous discharge of acute transections at various points along the injured sciatic nerve and the dorsal root were determined, as were the effects of K+ channel blockers applied topically to two putative sites of impulse origin: the injured region of the nerve and the dorsal root ganglion (DRG). Transections just proximal to the nerve injury and just distal to the DRG failed to halt the discharge, but spontaneous discharge disappeared when the transection was made just proximal to the DRG (i.e. between the DRG and recording electrode). K+ channel blockers (4-aminopyridine and gallamine triethiodide) applied to the DRG increased the frequency of spontaneous discharge or initiated activity from silent fibers. Applications of K+ channel blockers to the injured region of the nerve were without effect. Thus, the spontaneous discharge and the sensitivity to K+ channel blockade seen in A beta and A delta primary afferents at the time of the onset of the neuropathic pain syndrome appear to originate in the DRG.
The active and passive length-tension curves of small strips of cat external anal sphincter (EAS) were examined in vitro. The striated muscle fibers were arranged perpendicular to the long axis of the longitudinal smooth muscle cells of the longitudinal layer of the anal canal. Histological examination indicated that the strips were comprised of striated muscle fibers oriented in the long axis of the strip. Electrical field stimulation elicited twitch and tetanus responses that were not altered by the administration of gallamine triethiodide (10(-6) to 10(-4) M), a neuromuscular blocking agent. At 37 degrees C the time from the onset of the twitch contraction to the development of peak force ranged from 30 to 37 ms, the time from peak force to one-half relaxation ranged from 20 to 25 ms. The maximum active twitch and tetanus tension (Po) averaged 0.23 and 0.90 kg/cm2, respectively. Active tension could be developed over a range of 0.6-1.4 optimum length (Lo). The passive length-tension curve showed that the muscle had significant passive tension at lengths below the Lo for tension development and a high passive tension at Lo (average of 44% of active isometric twitch tension, 12.2% of active isometric tetanus tension) and above Lo. We conclude that the passive length-tension curve for the EAS is stiffer than that of typical mammalian skeletal muscles. We suggest that this difference is related to the adaptation of the EAS to its sphincteric function as a component of a hollow organ.