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Pseudocholinesterase deficiency

Pseudocholinesterase deficiency is an inherited blood plasma enzyme abnormality. more...

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People who have this abnormality may be sensitive to certain anesthetic drugs, including the muscle relaxants succinylcholine and mivacurium as well as other ester local anesthetics (Maiorana & Roach, 2003). These drugs are normally metabolized by the pseudocholinesterase enzyme. When anesthetists administer standard doses of these drugs to a person with pseudocholinesterase deficiency, the patient experiences prolonged paralysis of his respiratory muscles, requiring an extended period of time during which the patient must be mechanically ventilated. Eventually the muscle-paralyzing effects of these drugs will wear off despite the deficiency of the pseudocholinesterase enzyme. If the patient is maintained on a mechanical respirator until normal breathing function returns, there is little risk of harm to the patient. This enzyme abnormality is a benign condition unless a person with pseudocholinesterase deficiency is exposed to the offending pharmacological agents (Alexander, 2002).


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Acute effects of inhaled and IV cocaine on airway dynamics
From CHEST, 10/1/96 by Donald P. Tashkin

Background: Wheezing has been reported by 32% of habitual smokers of crack cocaine, and several cases of crack-related acute exacerbations of asthma have been reported. Study objective: To compare the acute effects of physiologically active doses of smoked cocaine base and IV cocaine hydrochloride (HCl), a subphysiologic dose of cocaine base (smoked "placebo"), and IV saline solution placebo on bronchomotor tone, subjective level of intoxication, and cardiovascular responses in healthy habitual crack users. Design: A single-blind crossover study in which the order of route of administration (inhaled vs IV was random but placebo always preceded the active drug. Subjects: Fourteen healthy, nonasthmatic current crack-smoking subjects, 34 to 48 years of age, with a history of previous IV cocaine use (1 to 12 times per lifetime). Methods: Heart rate, BP, self-rated level of intoxication (scale of 0 to 10), and measurements of airway resistance (Raw) and specific airway conductance (SGaw) were recorded during separate sessions before and 3 to 5, 10, 15, and 30 min after administration of smoked cocaine base (38.5[+ or -]2.3 [SEM] mg), smoked placebo (2.3[+ or -]0.9 mg cocaine base), IV cocaine HCl (30.0[+ or -]2.0 mg), and IV placebo (saline solution). Results: Both smoked active cocaine and IV cocaine HCl caused comparable, significant (p<0.005) peak levels of acute intoxication (6.7[+ or -]0.7 and 7.3[+ or -]0.8, respectively) and increases in heart rate from baseline (29.6[+ or -]2.9% and 21.4[+ or-]3.7%, respectively, at 5 min.) However, only smoked active cocaine caused significant decreases from baseline in SGaw (25.4[+ or -]6.3% at 5 min), in contrast to nonsignificant changes after IV cocaine HCl (5.6[+ or -]7.0% increase) and smoked placebo (10.2[+ or -]6.0% decrease). Conclusions: Smoked cocaine base, but not systematically administered cocaine HCl, causes acute bronchoconstriction that is probably mediated by local airway irritation and could account for reports of crack-induced wheezing and asthma attacks in nonasthmatic and asthmatic individuals, reports of crack-induced wheezing and asthma attacks in nonasthmatic and asthmatic individuals, respectively.

Key words: airway resistance; bronchomotor tone; cocaine base; cocaine HCl

Abbreviations: ANOVA=analysis of variance; Dco=diffusing capacity of the lung for carbon monoxide; MEG=methylethyl ecgonine; NIDA=National Institute on Drug Abuse; Raw=airway resistance; SGaw=specific airway conductance; TGV=thoracic gas volume

In recent years, smoking of alkaloidal cocaine (freebase or crack cocaine) has replaced nasal insufflation of cocaine hydrochloride (HCl) as the principal mode of cocaine abuse.[1] Unlike cocaine HCl, crack cocaine is resistant to thermal degradation and is lipid soluble. Consequently, it can be smoked and is rapidly absorbed through the extensive network of pulmonary capillaries. These properties yield a euphoric effect as instantaneous and intense as that achieved by IV injection,[2] thus accounting for the increasing popularity of crack cocaine. At the same time, rising use of the smoked form of cocaine has led to increasing reports of a broad spectrum of pulmonary complications of crack cocaine, as recently reviewed by Haim et al.[3] These crack-related complications have included clinical manifestations of airway injury, such as wheezing reported by 32% of habitual crack users during the period of use,[4] several case reports of acute exacerbations of life-threatening and even fatal asthma,[5-7] and recurrent episodes of bronchospasm associated with pulmonary infiltrates and eosinophilia in a nonasthmatic crack smoker.[8] Similar airway complications of nasal insufflation or IV injection of cocaine have not been reported (to our knowledge).

We hypothesized that smoked cocaine base, but not systemically administered cocaine HCI, causes acute airway irritation and bronchoconstriction that might predispose to crack@induced symptoms of wheezing in nonasthmatic individuals and attacks of clinical asthma in patients with hyperreactive airways disease. To test this hypothesis, we compared the short@term effects on specific airway conductance (SGaw) of experimental inhalation of volatilized cocaine base with those of IV injection of cocaine HCI in doses of each form of cocaine that are commonly self-administered recreationally. To control for nondrug-related effects of the experimental procedure on bronchomotor tone, similar studies were performed before and after placebo (a subphysiologic dose of inhaled cocaine base or iv saline solution) using a single-blind experimental protocol.

Materials and Methods


Fourteen healthy current crack-smoking subjects, including 11 men and 3 women, 34 to 48 years of age, without a history of asthma, were recruited for experimental smoking studies from chemical dependency treatment programs in the local community and from a cohort of crack smokers participating in ongoing studies of the pulmonary effects of habitual use of cocaine. Inclusionary criteria included age 25 to 50 years, current smoking of alkaloidal cocaine on a regular basis, and previous occasional use of IV cocaine (from 1 to 12 times per lifetime). Exclusionary criteria included the following: IV drug abuse more than 12 times per lifetime or within the previous year; history of smoking (>20 times per lifetime) other illicit substances (eg, phencyclidine, heroin, opium, methamphetamine) except for cannabis; a history of chronic lung disease (eg, asthma, interstitial lung disease); history or clinical evidence of systemic or pulmonary hypertension, history of coronary artery disease, angina, arrhythmias, or congenital heart disease; abnormal 12-lead ECG; history or official evidence of hyperthyroidism or peripheral vascular disease; history of stroke, seizure disorder, or other neurologic abnormality; history of significant psychiatric disorder; and pseudocholinesterase deficiency. In addition, women of child-bearing potential were not studied if they were pregnant, lactating, or not using a medically acceptable method of contraception. A urine pregnancy test was performed on all female subjects at the beginning of each study day to detect unsuspected pregnancy. Eligible volunteers were studied after signing informed consent forms approved by the UCLA School of Medicine Human Subject Protection Committee and the West Los Angeles VA Medical Center Human Studies Committee.


Preliminary examination procedures included the following: a detailed respiratory and drug use questionnaire modified from the American Thoracic Society/National Heart, Lung, and Blood Institute respiratory questionnaire" and National Institute on Drug Abuse (NIDA) National Survey on Drug Abuse;[10] medical history and physical examination; urine drug screen; 12-lead ECG; spirometry and single-breath diffusing capacity for carbon monoxide (Dco) measurement; and a urine pregnancy test in female subjects. Following completion of these procedures, eligible volunteers were studied on either 4 (n=7; group A) or 2 (n=7; group B) separated days 1 to 2 weeks apart beginning at approximately 8 AM. They were advised to refrain from smoking cocaine or marijuana, taking any prescription or over-the-counter medication, or consuming any caffeine-containing beverage for at least 8 h prior to visiting the laboratory. They were also admonished not to smoke tobacco for at least 2 h before testing or to use any antihistamine preparation for at least 48 h. Experiments were rescheduled for subjects with a history of respiratory tract infection within the preceding 3 weeks. Studies were performed with a physician in attendance and emergency resuscitation equipment nearby.

On each study day, the amount of daily drug use (crack cocaine, marijuana, tobacco, other drugs) during the preceding week and the time of last use were ascertained by self-report using a standard questionnaire, and a urine sample was obtained for determination of cocaine metabolite (benzoylecgonine). A 12-lead ECG was obtained and, on days when cocaine was administered IV, a catheter was inserted in an arm vein for injection of cocaine HCI or saline solution. Baseline measurements of heart rate, BP, and whole-body plethysmographic, measurements of airway resistance (Raw) and thoracic gas volume (TGV) at functional residual capacity[11,12] were then performed using a constant-volume body plethysmograph (model 2800; Sensormedics; Yorba Linda, Calif). In addition, other physiologic measurements were performed, including Dco and its components (membrane diffusion and pulmonary capillary blood volume), respiratory pattern (tidal volume and breathing frequency), and Doppler echocardiographic assessment of pulmonary artery pressure and stroke volume index, the results of these additional physiologic measurements will be reported separately.

Group A subjects were studied on 4 separate days; on 2 days, they received 3 IV injections of either cocaine HCl or saline solution (placebo) and on 2 other days, they received either 3 physiologically active or 3 inactive ("placebo") doses of inhaled cocaine base (see below). The 3 doses were administered at 45- to 60-min intervals to allow multiple physiologic measurements to be performed before and immediately after drug administration. Airway measurements were performed before and 3, 5, 10, 15, and 30 min following the third dose. Heart rate and systemic BP were also measured at these same times (except at 3 min) just prior to the plethysmographic measurements. Prior to drug administration, subjects were asked to indicate their level of cocaine intoxication using a scale of 0 to 10, "0" representing "not at all high" and "10" "extremely high," respectively; 30 min following drug admmistration, subjects were asked to recall their maximum level of "high" during the preceding 30 min. Days on which saline solution placebo or inactive base (placebo) was administered always preceded days on which active cocaine was administered.

Airway measurements were performed in group B subjects on two separate days, one devoted to IV administration and the other to inhalation. On each of the days, after baseline measurements, a placebo dose was administered, followed by heart rate, BP, and airway measurements at 3 (airway only), 5, 10, 15, 30, and at additional times up to 60 min, if necessary, until Raw returned to baseline predrug levels. When Raw had returned to baseline, the active dose was administered, followed by a second set of measurements. Subjective level of intoxication ("high") was also assessed prior to administration of both placebo and active drug (predrug baseline) and over the 30-min interval after each drug was administered. A 2-day protocol was used in group B subjects in place of the 4-day protocol in group A subjects for logical reasons.

For both groups subject, the order of the days on which the study drug was administered by the IV vs the inhaled route was randomized. On IV days, group A subjects received 23.0[+ or -]0.0 mg cocaine HCl in 3 mL saline solution, group B subjects received 0.5 mg/kg body weight (mean dose, 37.[+ or -]0.9 [SEM] mg), and both groups received a volume of saline solution (placebo) equivalent to the volume of cocaine HCl. On inhaled days, subjects inhaled either a physiologic dose of volatilized cocaine base (mean active dose delivered) group A, 39.1[+ or -]4.9 mg or 0.62[+ or -]0.087 mg/kg; and group B, 38.0[+ or -]1.0 mg or 0.56[+ or -]0.019 mg/kg) or a physiologically inactive dose of cocaine base or placebo (mean dose delivered: group A, 2.8[+ or -]1.6 mg or 0.04[+ or -]0.025 mg/kg; and group B, 2.0[+ or -]0.9 mg or 0.03[+ or -]0.015 mg/kg) using the delivery device of Hatsukami et al.[13]

Drug Preparation and Administration

Cocaine Base: The cocaine base was obtained from the National Institute on Drug Abuse in crystalline form. Dry cocaine base (2.5 mg) was dissolved in 25 mL 95% ethanol (100 mg cocaine base per milliliter) and stored in a stoppered flask. Prior to each experiment, microliter pipettes were used to drip 15 [mu]L or 150 [mu]L of the stock solution of cocaine base (yielding 1.5 or 15 mg cocaine base, respectively) onto each of 3 separate preweighed 5x18-mm wire coils, resulting in a total dose of 4.5 or 45 mg, respectively; sufficient time (overnight) was allowed for all the ethanol solvent to evaporate, leaving a fine coating of crystalline cocaine on the wire coils, which were then reweighed. The same inhaled doses of active cocaine were administered to both group A and group B subjects. Just prior to smoking, one of the coils was inserted into the cocaine smoking device (Fig 1), as described by Hatsukami et al.[13] After insertion of the coil, the subject was instructed to exhale nearly completely and then to slowly inhale from the smoking device through a 15x75-mm glass cylinder mouthpiece. Inspiratory flow was restricted to approximately 0.3 to0.4 L/s using a resistance connected to the air intake port of the device, resulting in a total duration of inhalation of more than 10 s. Immediately after the subject began to inhale, the electrical power supply for the device was manually triggered for approximately 4 s to allow the cocaine to be completely volatilized by heat (temperature regulated at approximately 200 [degrees]C) and inhaled under continuous-flow conditions. Following complete inhalation, subjects were instructed to hold their breath for 14 s before exhaling to emulate the long breathhold that is common in recreational use. The same procedure was repeated after insertion of each of the other two wire coils. After the cocaine had been inhaled from all three wire coils, the glass mouthpiece was removed and reweighed, along with each of the wire coils, to confirm that the cocaine on the coils was completely volatilized and to determine the amount of cocaine vapor that reprecipitated on the cooler glass mouthpiece; subtraction of residual cocaine in the smoking device and mouthpiece from the total amount initially added to the coils yielded the total dose of cocaine that was actually delivered to the mouth. Hatsukami and colleagues[13] have shown that cocaine base smoked under these conditions yields highly reproducible blood cocaine concentrations with repeated doses. These authors have also documented that a dose of 5 mg cocaine base (similar to the 4.5-mg dose we used for placebo), when delivered using their smoking device, had no significant physiologic effect.[14]

Cocaine HCl: For IV injection, a 7.67-mg/mL solution of cocaine HCl in saline solution was prepared. Group A subjects received 3 mL of this solution (23 mg cocaine HCl) or 3 mL of saline solution (placebo) injected over 30 s via an indwelling IV catheter. Group B subjects received 0.5 mg/kg body weight of a 5-mg/mL solution of cocaine HCl in saline solution or an equivalent volume of saline solution injected over 30 s. Each dose of cocaine HCl or placebo was followed by a flush of 6 mL saline solution.

The doses of smoked cocaine base and IV cocaine HCl were selected since they have been shown to yield euphoric effects comparable to those achieved during recreational use of cocaine[15] and to be below the dose levels associated with significant cocaine toxicity, according to unpublished NIDA guidelines for experimental cocaine administration (personal communication; 1994; Peter Bridge, MD; Clinical Trials Branch, Medication Development Division, NIDA). Higher doses of smoked cocaine base than IV cocaine HCl were administered since the potency of the smoked base has been shown to be less than that of IV cocaine HCl due to variable efficiency in delivery of alkaloidal cocaine by smoking.[15]

A physician was present at all times during the cocaine smoking experiments. Following cocaine administration, subjects were carefully monitored for evidence of acute cocaine toxic reactions, such as systemic hypertension, tachycardia, clinically significant arrhythmias, chest pain, or headache.

Data Analysis

Baseline values for each physiologic parameter were compared across the four treatment conditions (inhaled cocaine, inhaled placebo, IV cocaine, and IV saline solution [placebo]) using analysis of variance (ANOVA). Responses to cocaine or placebo by each route at each measurement time after drug administration were compared with the corresponding baseline value using Student's paired t tests. Paired t tests were also used to compare changes from baseline in response to active doses of cocaine vs placebo delivered by the same route and of smoked vs IV administration. Two-way ANOVA with repeated measures was also performed using drug (cocaine vs placebo) and route as the two factors; however, an independent effect of active cocaine by either route could not be assessed because of an interaction between drug and route of administration. p values <0.05 were considered statistically significant.


Demographic, smoking, and baseline screening physiologic characteristics of the study participants are shown in Table 1. Subjects were young to middle-aged adults who, on the average, were heavy smokers of cocaine base (mean, 2.6 gm/wk). Most also smoked tobacco, but only five were current smokers of marijuana. Baseline spirometry was well within expected normal limits, while Dco was mildly reduced (<75% predicted) in most subjects.

Ironically, cocaine was once used as a constituent of proprietary sprays for the relief of asthma.[29,30] Although to our knowledge no objective evidence of the putative brochodilator properties of inhaled cocaine exists, another topical anesthetic, lidocaine, has been shown to have a relaxant effect on guinea pig tracheal smooth muscle in vitro.[31] Moreover, lidocaine has also been demonstrated to produce delayed bronchodilation (45 min) and to inhibit methacholine-induced bronchospasm when administered as an aerosol to some asthmatic patients.[32] In contrast, nebulized lidocaine more consistently induced bronchoconstriction in asthmatic subjects within 2 to 5 min following nebulization and the bronchospasm lasted as long 30 min in some patients.[32,33] Although the reason for these divergent responses to lidocaine is unclear, the initial bronchospasm could be mediated by vagal reflex pathways since the bronchospastic response was blocked by atropine in the two patients studied.[32] The inconsistent late bronchodilator effect appeared to be dose related, and binding of intracellular calcium ion by higher delivered doses of lidocaine has been hypothesized." Since we measured airway resistance up to only 30 min following cocaine base inhalation, we cannot exclude the possibility of a similar late bronchodilator response to inhaled cocaine.

In summary, experimental inhalation of an intoxicating dose of alkaloidal cocaine, but not IV administration of an equally intoxicating dose of cocaine HCl caused acute bronchoconstriction of prompt onset and a duration of at least 15 min in healthy, nonasthmatic subjects. This finding is likely attributable to a local airway irritant effect of the alkaloidal cocaine causing reflex bronchospasm and may explain clinical reports of wheezing in nonasthmatic persons following cocaine smoking and near-fatal or fatal bronchospasm in crack@using patients with preexisting asthma. In view of these findings, asthmatic patients should be warned of the potentially serious pulmonary complications of cocaine smoking.

If local crack-induced airway irritation is responsible for the bronchoconstriction associated with cocaine smoking, repeated episodes of such irritation and bronchospasm do not appear to result in sufficient injury to the lower airways of nonasthmatic users to cause persistent airways narrowing or hyperresponsiveness because heavy, habitual crack smoking has not been found to be associated with either chronic obstructive ventilatory abnormality[4,19,34,35] or nonspecific airways hyperreactivity.[36]


[1] Schnoll SH, Kartigan J, Kitchen SB, et al. Characteristics of cocaine abusers presenting for treatment. In: NJ Kozel EH Adams, eds. Cocaine use in America: epidemiolgic and clinical perspectives: NIDA research monograph 61. Rockville, Md: NIDA, 1985 [2] Siegel RK. Cocaine smoking. J Psychoactive Drugs 1982; 14:277-359 [3] Haim DY, Lippmann ML, Goldberg SK, et al. The pulmonary complications of crack cocaine: a comprehensive review. Chest 1995; 107:233-40 [4] Suhl J, Gorelick DA. Pulmonary function in male freebase cocaine smokers [abstract]. Am Rev Respir Dis 1988; 137(suppl):A488 [5]Rebhun J. Association of asthma and freebase cocaine. Ann Allergy 1988; 60;339-42 [6]Rubin RB, Neugarten J. Cocaine-associated asthma. Am J Med 1990; 88:438-39 [7] Rao AN, Polos PG, Walther FA. Crack abuse and asthma: a fatal combination. NY State J Med 1990; 90:511-12 [8] Kissner DG, Lawrence WD, Selis JE, et al. Crack lung: pulmonary disease caused by cocaine abuse. Am Rev Respir Dis. 1987; 136:1250-52 [9] Ferris BG. Epidemiology standardization project. Am Rev Respir Dis 1978; 118/6(pt 2):1-88 [10] Fishburne PM, Abelson HI, Cisin I. National survey on drug abuse: main findings: 1979; DHHS publication No (ADM) 80-976. Rockville, Md. NIDA, 1980 [11] Dubois AB, Botelho SY, Comroe JH Jr. A new method for measuring airway resistance in man using a body plethysmograph: values in normal subjects and in patients with respiratory disease. J Clin Invest 1956; 35:327-35 [12] Dubois AB, Botelho SY, Bedell GN, et al. A rapid plethysmographic method for measuring thoracic gas volume: a comparison with a nitrogen washout method for measuring functional residual capacity in normal subjects. J Clin Invest 1956; 35:322-26 [13] Hatsukami DK, Keenan R, Carroll M, et al. A method for delivery of precise doses of smoked cocaine-base to humans. Pharmacol Biochem Behav 1990; 36:1-7 [14] Hatsukami DK, Pentel PR, Glass J, et al. Methodological issues in the administration of multiple doses of smoked cocaine-base in humans. Pharmacol Biochem Behav 1994; 47:531-40 [15] Foltin RW, Fischman MW. Smoked and intravenous cocaine in humans: acute tolerance, cardiovascular and subjective effects. J Pharmacol Exp Ther 1991; 257:247-61 [16] Luparello T, Lyons HA, Bleecker ER, et al. Influences of suggestion on airway reactivity in asthmatic subjects. Psychosom Med 1968; 30:819-825 [17] Ritchie JM, Greene NM. Local anesthetics. In: Gilman AG, Goodman LS, Rall TW, et al, eds. The pharmacologic basis of therapeutics. 7th ed. New York: Macmillan, 1985; 309-10 [18] Widdicombe JG. Regulation of tracheobronchial smooth muscle. Physiol Rev 1963; 43:1-37 [19] Tashkin DP, Khalsa M-E, Gorelick D, et al. Pulmonary status of habitual cocaine smokers. Am Rev Respir Dis 1992; 145:92-100 [20] Roth M, Tashkin DP. Effects of cocaine on lung inflammation and immunity. Presented at an NIDA workshop on crack cocaine-associated pulmonary and cardiovascular manifestations and underlying physiological mechanisms, Bethesda, Md, August 30-31, 1995 [21] Chen LC, Wood RW, Zhong MH, et al. Bronchoconstriction following exposure to cocaine test atmospheres: NIDA research monograph. DHHS, NIH publication No. 94-3789, proceedings of the 55th annual scientific meeting (1993), the College of Problems of Drug Dependence, 1994, 141:320 [22] Warner EA. Cocaine abuse. Ann Intern Med 1993; 119:226-35 [23] Greenbaum E, Copeland A, Grew R. Blackened bronchoalveolar lavage fluid in crack smokers: a preliminary study. Am J Clin Pathol 1993; 100:481-87 [24] Klinger JR, Bensadoun E, Carrao WM. Pulmonary complications from alveolar accumulation of carbonaceous material in a cocaine smoker. Chest 1992; 101:1171-73 [25] Martin BR, Lue LP, Boni JP Pyrolysis and volatilization of cocaine. J Anal Toxicol 1989; 13:158-62 [26] Nakahara Y, Ishigami. A Inhalation efficiency of free-base cocaine by pyrolysis of `crack' and cocaine hydrochloride. J Anal Toxicol 1991; 15:105-09 [27] Chen LC, Graefe JF, Shojaie J, et al. Pulmonary effects of the cocaine pyrolysis product, methylecgonidine, in guinea pigs. Life Sci 1995; 56:PL 7-12 [28] Waldbott GL. Asthma due to a local anesthetic. JAMA 1932; 99:1942 [29] Vaughan WT, Black JH. Practice of allergy. 3rd ed. St. Louis: Mosby, 1954; 963-64 [30] Ziment I. Respiratory pharmacology and therapeutics. Philadelphia: WB Saunders, 1978; 137 [31] Weiss EB, Anderson WH, O'Brien KP. The effect of a local anesthetic, lidocaine, on guinea pig trachealis muscle in vitro. Am Rev Respir Dis 1975; 112:393 [32] Weiss EB, Patwardhan AV. The response to lidocaine in bronchial asthma. Chest 1977; 72:429-38 [33] McAlpine LG, Thomson NC. Lidocaine-induced bronchoconstriction in asthmatic patients: relation to histamine airway responsiveness and effect of preservative. Chest 1989; 96:1012-15 [34] Itkonen J, Scholl S, Glassroth J. Pulmonary dysfunction in freebase cocaine users. Arch Intern Med 1984; 144:2195-97 [35] Dean NC, Clark HW, Doherty JJ, et al. Pulmonary function in heavy users of `freebase' cocaine [abstract]. Am Rev Respir Dis 1988; 137(suppl):A489 [36] Tashkin DP, Simmons MS, Chang P, et al. Effect of smoked substance abuse on airways hyperresponsiveness. Am Rev Respir Dis 1993; 147:97-103

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