Differential effects of prazosin and yohimbine on fentanyl-induced muscular rigidity in rats.

Whereas muscular rigidity is a well-known phenomenon that is related to anesthesia induced by large doses of narcotic drugs, the precise underlying mechanism(s) remain to be fully elucidated. This study investigated the possible role of noradrenergic neurotransmission and the participation of alpha-adrenoceptors in this phenomenon. Male Sprague-Dawley rats, under ketamine-induced anesthesia (120 mg/kg, i.p.) and with proper control of respiration, body temperature and end-tidal CO2 were used. Intravenous administration of fentanyl (100 micrograms/kg) consistently caused a significant increase in the electromyographic (EMG) activity, recorded from both gastrocnemius and abdominal rectus muscles. This implied muscular rigidity was markedly antagonized by pretreatment with the specific alpha 1-adrenoceptor blocker, prazosin (50 or 250 micrograms/kg, i.v.). This antagonism occurred in spite of a high level of fentanyl in the plasma, as determined by radioimmunoassay. The specific alpha 2-adrenoceptor blocker, yohimbine (1.15 or 2.3 mg/kg, i.v.), on the other hand, not only failed to prevent fentanyl-induced activation of the EMG, but actually potentiated the response. It is concluded that noradrenergic neurotransmission, possibly originating from the locus coeruleus, may participate in the elicitation of muscular rigidity by fentanyl. Furthermore, this process may involve an excitatory action through alpha 1-, and an inhibitory action through alpha 2-adrenoceptors, in the spinal cord.

Striatal neurons but not nigral dopaminergic neurons in neonatal primary cell culture express endogenous functional N-methyl-D-aspartate receptors.

Developmental expression of N-methyl-D-aspartate (NMDA) receptor subunits were determined and compared in striatal and nigral neurons in neonatal primary cell cultures. In striatal neurons, NR1, NR2A and NR2B mRNAs and immunoreactivity, and NR2D mRNA were found and the maximal levels of NR1 mRNA and immunoreactivity expression were found at 6 day-in-vitro (DIV). NMDA receptors found at this stage in striatal neurons are likely to contain NR1 plus NR2A, NR2B and NR2D subunits. In nigral neurons, NR1 and NR2B mRNAs and immunoreactivity, and NR2D mRNA were found and the maximal level of NR1 immunoreactivity expression was found at 10 DIV. Unlike striatal neurons, NMDA receptors found in nigral neurons are likely to contain NR1 plus NR2B and NR2D subunits only. NMDA-induced toxicity assays showed that striatal neurons were most susceptible to cell death at around 10 DIV but nigral neurons were not susceptible to NMDA-induced cell death at all stages. In addition, patch clamp analysis revealed that functional NMDA receptors could only be found in striatal neurons but not in nigral dopaminergic neurons in vitro. The present results indicate that striatal and nigral neurons are programmed to express distinct NMDA receptor subunits during their endogenous development in cell cultures. Despite dopaminergic neurons in culture display NMDA receptor subunits, functional NMDA receptors are not assembled. The present findings have demonstrated that dopaminergic neurons in vitro may behave very differently to their counterparts in vivo in terms of NMDA receptor-mediated responses. Our results also have implications in transplantations using dopaminergic neurons in vitro in treatments of Parkinson's disease.

Differential expression of N-methyl-D-aspartate receptor subunit messenger ribonucleic acids and immunoreactivity in the rat neostriatum during postnatal development.

The present study was performed to investigate the patterns of gene expression of N-methyl-D-aspartate (NMDA) receptors (NRs) in the rat neostriatum during postnatal development. Reverse transcriptase-polymerase chain reactions (RT-PCR) indicated that levels of NR1, NR2A and NR2D mRNAs reached peak levels between postnatal days 7 (PND 7) and PND 14. The levels of NR2B and NR2C mRNAs were low at PND 1 and their levels increased at PND 7 and remained high in adults. Immunofluorescence combined with image analysis revealed that the levels of NR1 immunoreactivity rose to its maximum at PND 14. In contrast, NR1 immunoreactivity rose progressively in perikarya of striatal neurons. Levels of NR2A immunoreactivity in the neostriatum were highest in adults. However, levels of NR2A immunoreactivity were higher in striatal neurons at PND 1 and PND 7. Levels of NR2B immunoreactivity were highest at PND 7. In the perikarya of striatal neurons however, the highest levels of NR2B immunoreactivity were detected at PND 14 and adult striatal neurons. In addition, double immunofluorescence revealed that the levels of NR1 immunoreactivity increased but the levels of NR2A immunoreactivity were the same in parvalbumin (PV)-positive striatal interneurons of PND 14 and adult rats. NR2B immunoreactivity was not detected in PV-positive neurons of PND 14 rats, but intense NR2B labeling was seen in PV-positive neurons of adult rats. Last but not least, in choline acetyltransferase (ChAT)-positive striatal interneurons of PND 14 and adult rats, levels of NR1 and NR2A immunoreactivity was seen to increase. Level of NR2B immunoreactivity remained the same in ChAT-positive neurons of PND 14 and adult rats. The present results indicate that there are differential patterns of expression of NR mRNAs and immunoreactivity in the neostriatum during different stages of postnatal development. Different combinations of NR have been found in different subpopulations of striatal neurons at different developmental stages. NR1, NR2A and NR2B are the major NMDA receptor subunits expressed during development. The change in patterns of expression of NR may be related to the functional maturation of neurons in the neostriatum.

Subtypes of Guanine-Nucleotide-Binding Regulatory Proteins at the Locus coeruleus Involved in Fentanyl-Induced Muscular Rigidity in the Rat.

Previous results from our laboratory have established that the G(o) subtype of guanine nucleotide (GTP)-binding regulatory protein at the locus coeruleus (LC) may participate in the elicitation of muscular rigidity by fentanyl. The present study further examined the involvement of other subtypes of GTP-binding regulatory proteins at the LC in this process, using Sprague-Dawley rats anesthetized with ketamine (120 mg/kg, i.p., with 30 mg/kg/h i.v. infusion supplements) and under mechanical ventilation. Intravenous administration of fentanyl (100 &mgr;g/kg) induced a significant increase in electromyographic signals recorded from the sacrococcygeus dorsi lateralis muscle. Power spectral analysis revealed that this was accomplished by a decrease in the mean power frequency and an increase in the root mean square values of the signals. The above responses were appreciably antagonized by pretreating animals with bilateral microinjection into the LC of pertussis toxin (80 or 160 fmol), N-ethylmaleimide (16 pmol) or 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (100 or 200 fmol); but not by cholera toxin (120 or 240 fmol), forskolin (240 or 480 pmol) or N-ethylmaleimide at a higher dose (32 pmol). These results suggest that, in addition to G(o) protein, fentanyl-induced muscular rigidity may also involve other pertussis toxin-sensitive GTP-binding regulatory proteins, possibly G(i) and G(p) subtypes, in the signal transduction processes following activation of &mgr;-opioid receptors at the LC. Copyright 1995 S. Karger AG, Basel

Antagonization of fentanyl-induced muscular rigidity by neurotensin at the locus coeruleus of the rat.

We evaluated the interaction between neurotensin (NT) and mu-opioid receptors at the locus coeruleus (LC), using fentanyl-induced muscular rigidity as our experimental index. Adult, male Sprague-Dawley rats anesthetized with ketamine (120 mg/kg, i.p., with 24 mg/kg/h i.v. infusion supplements) were used. Intravenous injection of fentanyl (100 micrograms/kg) consistently promoted a significant increase in the electromyographic activity recorded from the sacrococcygeus dorsalis lateralis muscle. This implied muscular rigidity was appreciably and dose-dependently antagonized by prior intracerebroventricular (i.c.v.) application of NT (15, 30 or 60 nmol/5 microliter). Microinjection of the tridecapeptide (300 or 600 pmol/100 nl) into the bilateral LC produced similar results. This suppressive effect of NT on fentanyl-induced muscular rigidity was antagonized by simultaneously administered NT antiserum (1:80), or partially blocked by its antagonist, (D-Trp11)-NT (300 pmol), but not by normal rabbit serum (1:80). These results suggest that NT may interact with the mu-opioid receptors at the LC, resulting in the suppression of fentanyl-induced muscular rigidity in the rat.

Different trends in modulation of NMDAR1 and NMDAR2B gene expression in cultured cortical and hippocampal neurons after lead exposure.

Exposure to heavy metal lead (Pb(2+)) has been reported to cause problems in cognitive functions of the brain, e.g. memory loss and difficulties in mental development. N-Methyl-D-aspartate receptors (NRs) are important molecules that are known to be involved in mediation of learning and memory. In order to investigate the effects of Pb(2+) on the gene expression of NR1 and NR2B subunits in neurons, primary cell cultures of rat cortical and hippocampal neurons were employed. After treatments with different concentrations of Pb(2+) ions in culture medium (0, 5, 10, 25 and 50 microM), the cellular localization of Pb(2+) in neurons was evaluated by laser scan confocal microscopy by using a Pb(2+) ion specific fluorescence probe. In addition, the gene expression of NR1 and NR2B subunits was determined by reverse transcriptase-polymerase chain reaction, immunofluorescence and Western blotting. The results of the present study showed that both cortical and hippocampal neurons accumulated intracellular Pb(2+) in accordance with the concentrations of Pb(2+) ions present in the culture medium. After Pb(2+) treatments, levels of NR1 mRNA, immunoreactivity and protein were found to be unchanged but levels of NR2B mRNA, immunoreactivity and protein were found to be significantly increased in cortical neurons. In contrast, both NR1 and NR2B mRNAs, immunoreactivity and proteins were found to be significantly decreased in hippocampal neurons. The changes in gene expression were found to be dose dependent in accordance with the Pb(2+) concentrations. The present results indicate that Pb(2+) has a differential effect on the expression of NR1 and NR2B subunits in cortical and hippocampal neurons, respectively. It is likely that the toxic effects of Pb(2+) may cause differential damage to different types of memory that are mediated by cortical and hippocampal neurons, respectively.

Involvement of spinal adenosine A1 and A2 receptors in fentanyl-induced muscular rigidity in the rat.

In the present study, using hydrophilic adenosine antagonists either selective to A1 or A2 receptors, we investigated the central and spinal adenosinergic participation in fentanyl-induced muscular rigidity. Adult Sprague-Dawley rats were anesthetized with ketamine and were under mechanical ventilation. Fentanyl (100 micrograms/kg, i.v.) consistently elicited electromyographic (EMG) activation in the sacrococcygeal dorsalis lateralis muscle. This implied muscular rigidity was not blocked by i.c.v. administration of the adenosine A1 antagonist, 1-allyl-3,7-dimethyl-8-p-sulfophenyl-xanthine (ADSPX; 20 or 40 nmol/2.5 microliters), except at higher dose (80 nmol). Equimolar doses of the adenosine A2 antagonist, 3,7-dimethyl-1-propargylxanthane (DMPX), did not exert any inhibitory effect on fentanyl-induced rigidity. Intrathecal (i.t.) administration of the same doses of ADSPX (20, 40 or 80 nmol/10 microliters) appreciably suppressed the EMG activation. However, the rigidity was only inhibited by 40 or 80 nmol (i.t.) of DMPX, but not by the lowest dose. High-dose (80 nmol, i.t.) adenosine A1 or A2 antagonist per se did not induce motor impairment or hindlimb paralysis in conscious animals. These results suggest that adenosine A1 and A2 receptors in the spinal cord may play a more crucial role than those in the central nervous system (CNS) in fentanyl-induced muscular rigidity in rats.

Involvement of locus coeruleus and noradrenergic neurotransmission in fentanyl-induced muscular rigidity in the rat.

Whereas muscular rigidity is a well-known side effect that is associated with high-dose fentanyl anesthesia, a paucity of information exists with regard to its underlying mechanism(s). We investigated in this study the possible engagement of locus coeruleus of the pons in this phenomenon, using male Sprague-Dawley rats anesthetized with ketamine. Under proper control of respiration, body temperature and end-tidal CO2, intravenous administration of fentanyl (50 or 100 micrograms/kg) consistently promoted an increase in electromyographic activity recorded from the gastrocnemius and abdominal rectus muscles. Such an induced muscular rigidity by the narcotic agent was significantly antagonized or even reduced by prior electrolytic lesions of the locus coeruleus or pretreatment with the alpha-adrenoceptor blocker, prazosin. Microinjection of fentanyl (2.5 micrograms/50 nl) directly into this pontine nucleus, on the other hand, elicited discernible electromyographic excitation. It is speculated that the induction of muscular rigidity by fentanyl may involve the coerulospinal noradrenergic fibers to the spinal motoneurons.

Involvement of coerulospinal noradrenergic pathway in fentanyl-induced muscular rigidity in rats.

Unilateral, site-specific microinjection of fentanyl (2.5 micrograms/50 nl) into the locus coeruleus (LC) in Sprague-Dawley rats anesthetized with ketamine evoked a significant increase in the electromyographic activity recorded from both caudal lateral extensor and gastrocnemius muscles. This correlate of opiate-induced muscular rigidity was appreciably antagonized by a pretreatment with the specific alpha 1-adrenoceptor blocker, prazosin (250 micrograms/kg, i.v.). On the other hand, an equimolar dose (0.65 mumol/kg) of the specific alpha 2-adrenoceptor blocker, yohimbine (0.23 mg/kg, i.v.) failed to prevent the occurrence of fentanyl-induced EMG activation. We suggest that the coerulospinal noradrenergic pathway may be directly involved in the elicitation of muscular rigidity by fentanyl, possibly via alpha 1-adrenoceptors in the spinal cord.

Spinal cord localization of the motoneurons innervating the sacrococcygeus dorsi lateralis muscle and their noradrenergic nerve terminals in rats.

We examined in the present study the spinal cord localization of motoneurons innervating the caudal portion of the sacrococcygeus dorsi lateralis (SCDL) muscle and their noradrenergic nerve terminals in Sprague-Dawley rats, using horseradish peroxidase (HRP) and dopamine-beta-hydroxylase (DBH) double-labeling techniques. Retrogradely HRP-labeled motoneurons innervating the caudal part of the SCDL muscle were located ipsilaterally in the ventromedial aspect of the ventral horn (lamina IX) in spinal segments of S2-S4. These cells were polygonal in shape, with an average soma diameter of 37.0 +/- 1.1 microns (mean +/- S.E.M., n = 95) and amounted to 33.6 +/- 5.7 (n = 7) in the horizontal plane. Of note was the presence of abundant DBH-positive nerve terminals arborizing on the soma and dendrites of HRP-labeled motoneurons. These results provided anatomical evidence to further support our previous findings that the coerulospinal noradrenergic neurotransmission is involved in the mediation of fentanyl-induced muscular rigidity.

Antagonization of fentanyl-induced muscular rigidity by denervation of the coerulospinal noradrenergic pathway in the rat.

The present study examined the effect of denervating the coerulospinal noradrenergic pathway on the muscular rigidity elicited by fentanyl in Sprague-Dawley rats anesthetized with ketamine. We demonstrated that the dopamine-beta-hydroxylase-positive nerve terminals arborizing on spinal motoneurons that innervate the sacrococcygeus dorsi lateralis (SCDL) muscle were significantly eliminated by DSP4 treatment. Unilateral microinjection of fentanyl (2.5 micrograms/50 nl) into the locus coeruleus of these animals also failed to evoke discernible increase in the electromyographic activity recorded from the SCDL muscle. These results lend further support for our previous finding that the coerulospinal noradrenergic neurotransmission is critically involved in fentanyl-induced muscular rigidity.

Involvement of G(o) alpha subtype of guanine nucleotide-binding regulatory protein at the locus coeruleus in fentanyl-induced muscular rigidity in the rat.

Previous work from our laboratory suggested that locus coeruleus (LC) and the coerulospinal noradrenergic pathway are intimately related to the elicitation of muscular rigidity by fentanyl. The present study attempted to identify the subtype of guanine nucleotide-binding regulatory protein that may participate in this process, using Sprague-Dawley rats anesthetized with ketamine and under mechanical ventilation. Immunofluorescent staining with a polyclonal antiserum directed against a 39-kDa protein that corresponds to the alpha subunit of G(o) revealed the presence of G(o) alpha immunoreactivity in neurons of the LC. Bilateral microinjection of the same G(o) alpha antiserum into the LC also significantly blunted the enhanced electromyographic activity recorded from the sacrococcygeus dorsalis lateralis muscle induced by intravenous administration of fentanyl (100 micrograms/kg). These results suggest that G(o) alpha protein at the LC may participate in the signal transduction process that underlies muscular rigidity induced by high-dose fentanyl.

Involvement of potassium and calcium channels at the locus coeruleus in fentanyl-induced muscular rigidity in the rat.

Previous work from our laboratory suggested that Go alpha protein at the locus coeruleus (LC) may be involved in the signal transduction process that underlies muscular rigidity induced by fentanyl. The present study further evaluated the roles of K+ and L-type Ca2+ channels, gating of which is known to be associated with activation of Go alpha protein, in this process, using Sprague-Dawley rats anesthetized with ketamine. Bilateral microinjection into the LC of tetraethylammonium chloride (100 or 200 pmol), a K+ channel blocker, and S(-)-Bay K 8644 (0.5 nmol), a Ca2+ channel activator, produced significant antagonization of the EMG activation elicited by fentanyl (100 micrograms/kg, i.v.), as recorded from the sacrococcygeus dorsalis lateralis muscle. On the other hand, local application to the bilateral LC of diazoxide (10 or 20 nmol), an ATP-dependent K+ channel activator, and nifedipine (0.25 or 0.5 pmol), a L-type Ca2+ channel blocker, was ineffective in blunting fentanyl-induced muscular rigidity. These results suggest that activation of K+ channels and/or inhibition of L-type Ca2+ channels secondary to triggering of the Go alpha protein at the LC may underlie the signal transduction process in the mediation of fentanyl-induced muscular rigidity.

Inhibition by intrathecal prazosin but not yohimbine of fentanyl-induced muscular rigidity in the rat.

We evaluated the effect of intrathecally administered prazosin, alpha 1-adrenoceptor antagonist, or yohimbine, alpha 2-adrenoceptor antagonist, on fentanyl-induced muscular rigidity. Adult, male Sprague-Dawley rats were anesthetized with ketamine and were under mechanical ventilation. Fentanyl given intravenously (100 micrograms/kg) or microinjected into the bilateral locus coeruleus (LC) (2.5 microgram/50 nl) consistently evoked a significant increase in the electromyographic activity recorded from the sacrococcygeus dorsalis lateralis muscle. This implied muscular rigidity was appreciably antagonized by prior intrathecal (10 microliters) administration of prazosin (5 or 10 nmol), but not equimolar dose of yohimbine. These results suggest that the spinal alpha 1-adrenoceptors in the coerulospinal noradrenergic pathway play a key role in fentanyl-induced muscular rigidity.

Chemical sympathectomy for neuropathic pain: does it work? Case report and systematic literature review.

OBJECTIVE: To determine if chemical sympathectomy successfully reduces limb neuropathic pain. DESIGN: Systematic literature review of the effectiveness of phenol or alcohol sympathectomy for extremity neuropathic pain. PATIENT: A 29-year-old female with complex regional pain syndrome of both lower extremities after back surgery who was submitted to bilateral lumbar chemical sympathectomy. SEARCH STRATEGY: The Cochrane Database of Systematic Reviews, the Cochrane Controlled Trials Register, Medline, and EMBASE were systematically searched. OUTCOME MEASURES: (1) For the patient in question: spontaneous pain, allodynia, pinprick hyperalgesia, pressure evoked pain; (2) For the literature review: meaningful versus nonmeaningful pain relief based on degree and duration (>2 weeks) of pain relief. RESULTS: (1) The case reported experienced partial temporary relief of pain primarily related to selective modulation of allodynia, but not deep pain or pinprick hyperalgesia; (2) 44% of 66 patients in 13 studies that met the authors' inclusion criteria experienced meaningful pain relief. Whereas 19% experienced no meaningful relief, for the remaining 37% of the patients no conclusions regarding duration and degree of relief could be drawn due to poor reporting of outcomes. CONCLUSIONS: Based on the case reported and systematic literature review, chemical sympathectomy seems to have at best a temporary effect, limited to cutaneous allodynia. Despite the popularity of chemical sympatholysis, only few patients and poorly defined outcomes are reported in the literature, substantiating the need for well-designed studies on the effectiveness of the procedure.

Fast detection of venous air embolism in Doppler heart sound using the wavelet transform.

The introduction of air bubbles into the systemic circulation can result in significant morbidity. Real-time monitoring of continuous heart sound in patients detected by precordial Doppler ultrasound is, thus, vital for early detection of venous air embolism (VAE) during surgery. In this study, the multiscale feature of wavelet transforms (WT's) is exploited to examine the embolic Doppler heart sound (DHS) during intravenous air injections in dogs. As both humans and dogs share similar physiological conditions, our methods and results for dogs are expected to be applicable to humans. The WT of DHS at scale 2j (j = 1, 2) selectively magnified the power of embolic, but not the normal, heart sound. Statistically, the enhanced embolic power was found to be sensitive (P < 0.01 at 0.01 ml of injected air) and correlated significantly (P < 0.0005, r = 0.83) with the volume of injected air from 0.01 to 0.10 ml. A fast detection algorithm of O(N) complexity with unit complexity constant for VAE was developed (processing speed = 8 ms per heartbeat), which confirmed the feasibility of real-time processing for both humans and dogs.

Bilateral hydrothorax caused by left external jugular venous catheter perforation.

We report a case of bilateral hydrothorax secondary to perforation of the superior vena caval wall, which was caused by a double-lumen central venous catheter used for catheterization of the left jugular vein. A patient undergoing craniectomy developed a right pleural effusion followed by a left hydrothorax 12 hours after the operation. There are several possible explanations for this phenomenon. The horizontal course of the left brachiocephalic vein, heart contraction, mechanical ventilation, changes in patient position, and solutions of high osmolality can promote vascular erosion by the catheter tip. High hydrostatic pressure in the thorax associated with a congenital or an acquired interpleural communication may cause bilateral hydrothorax. We suggest that it is always preferable to cannulate a central vein through the right side. When the left external jugular vein has to be cannulated, an intravascular ECG may be helpful to determine the position of the catheter tip. Chest roentgenogram should be obtained early to confirm catheter position. Furthermore, the distal port of the double-lumen central venous catheter should be used perioperatively for continuous surveillance of the central venous pressure waveform to ensure early warning of venous perforation.

Modification of tonic-clonic convulsions by atracurium in multiple-monitored electroconvulsive therapy.

STUDY OBJECTIVE: To determine the effect of two different doses of atracurium on the modification of tonic-clonic convulsions in multiple-monitored electroconvulsive therapy (MMECT). To compare recovery time and adverse reactions of these doses. DESIGN: Clinical study. Anesthesiologist was blinded in the evaluation of post-electroconvulsive therapy (ECT) myalgia and other side effects. SETTING: University-affiliated veterans general hospital. PATIENTS: Two groups of twelve psychiatric inpatients who suffered from major depression or catatonic-type schizophrenia that failed to respond to tricyclic antidepressant therapy. INTERVENTIONS: Under single-channel, prefrontal electroencephalographic (EEG) monitoring, patients were given either 0.3 mg/kg or 0.5 mg/kg of atracurium intravenously (IV) after anesthetic induction with methohexital 1 mg/kg i.v. MEASUREMENTS AND MAIN RESULTS: Evoked electromyographic responses of the adductor pollicis muscle was obtained by train-of-four stimulation of the ulnar nerve at the wrist every 20 seconds. The first twitch depression (T1) of neuromuscular blockade was maintained within 11% to 25% (atracurium 0.3 mg/kg) or 0% to 10% (atracurium 0.5 mg/kg) of control during the entire session of MMECT. Patients pretreated with atracurium 0.5 mg/kg had significantly fewer ECT-induced moderate and vigorous convulsions when compared with patients receiving atracurium 0.3 mg/kg (16.7% vs. 78.4%, moderate; 0% vs. 8.3%, vigorous). However, patients pretreated with atracurium 0.5 mg/kg took a longer time to attain a T4 ratio of 0.5 than did patients receiving atracurium 0.3 mg/kg (9.2 +/- 0.8 minutes vs. 4.3 +/- 0.4 minutes). There was no significant difference between the two groups with respect to cumulative seizure duration or frequency of bradycardia, sialorrhea, postseizure myalgia, nausea, headache, or confusion. No patient in either group recalled any event concerning electroconvulsive shock. CONCLUSIONS: Whereas full neuromuscular blockade by atracurium 0.5 mg/kg i.v. is very effective in the modification of tonic-clonic convulsions induced by ECT, we suggest that a lower dose of atracurium (0.3 mg/kg i.v.) be used if one needs to ascertain the occurrence of ECT-induced seizures as indicated by minimum peripheral muscle activity at the time of EEG recording during MMECT.

Incidence and risk factors of guidewire-induced arrhythmia during internal jugular venous catheterization: comparison of marked and plain J-wires.

STUDY OBJECTIVES: To compare the incidence and risk factors of guidewire-induced arrhythmia (GIA) during internal jugular venous catheterization (IJV). DESIGN: Prospective study. SETTING: Operating rooms at a medical center. PATIENTS: 303 ASA physical status I, II, III, and IV patients undergoing elective surgery. INTERVENTIONS: All patients were cannulated with the central venous catheters placed via the right internal jugular vein after induction of anesthesia. They were randomly divided into two groups. In one group, we used a marked J-wire and inverted up to, but not beyond 20 cm (Group M, n = 127). In the other group, a plain unmarked J-wire was used and inserted at will (Group UM, n = 176). All IJV catheterizations were performed by residents, and the length of J-wire inserted was then measured. MEASUREMENTS AND MAIN RESULTS: Types of arrhythmia [eg, premature atrial contraction (PAC) or premature ventricular contraction (PVC)] were interpreted by attending anesthesiologists on lead II ECG. Patients in Group UM had a significantly greater incidence of GIA than those in Group M (28.4% vs. 3.9%; p < .005). However, in both groups, PAC occurred more frequently than PVC. Factors such as the inserted length of guidewire longer than 20 cm, body height less than 170 cm, and female gender were significantly associated with GIA (p < 0.005). CONCLUSIONS: Limiting the length of the guidewire insertion to less than or equal to 20 cm for right IJV catheterization by using a marked J-wire will reduce the incidence of GIA. We recommend the use of a marked J-wire for IJV catheterization.