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Cocaine-enhanced arrhythmogenesis: neural and nonneural mechanisms.

Cocaine abuse increases the susceptibility to cardiovascular complications and sudden cardiac death in man. We used programmed electrical stimulation of the heart to examine the arrhythmogenic influence of cocaine. Twenty-three pentobarbital-anesthetized adult dogs underwent programmed electrical stimulation using one to four extrastimuli before and during cocaine infusion. Autonomic decentralization was performed prior to the protocol in eight dogs. Induced ventricular arrhythmias included single premature ventricular depolarizations, doublets, triplets, ventricular tachycardia, and ventricular fibrillation. Intravenous cocaine, and subsequent adrenergic and muscarinic receptor blockade, or calcium channel blockade were evaluated for their influence on arrhythmogenesis. The incidence of induced ventricular arrhythmias was significantly elevated following cocaine and was reduced following propranolol and atropine. Verapamil, however, did not reduce the incidence of induced arrhythmias. In addition, cocaine significantly increased arrhythmia induction in decentralized animals, but propranolol, atropine, and phentolamine failed to reduce the proarrhythmic effects of cocaine in these animals. Thus, cocaine has a proarrhythmic effect on the heart with multiple mechanisms. The adrenergic mechanism appears to be a result of neurotransmitter uptake blockade, whereas the likely ionic mechanism is a neurally independent, direct effect on the heart.

Adrenergic beta-Antagonists↗

Autonomic nervous system and cellular injury from circumflex ligation in dogs.

The role of the autonomic nerves in the development of irreversible cellular injury (ICI) after circumflex coronary occlusion was examined in dogs with intact, acutely, or chronically decentralized cardiac nerves. Cardiac nerves were chronically decentralized 2 wk before ligation (CD) or acutely at the time of ligation (AD). In one group of AD dogs, the beta-blocker oxprenolol (0.3 mg/kg) was administered before ligation (AD + Ox). Hearts were paced at 160 beats/min to exclude any contribution of rate change secondary to autonomic intervention. The results are expressed in terms of percent of the cross-sectional area of the posterior papillary muscle (PPM) sustaining ICI after 40-min occlusion: intact 64 +/- 4% (SE), 6 +/- 4%, AD 39 +/- 10%, and AD + Ox 2 +/- 2%. Both acute and chronic denervation protect against ICI even in the absence of changes in heart rate. Furthermore, in dogs with intact cardiac nerves, reduction in pacing rate from 160 to 60 beats/min also decreased the extent of ICI from 64 +/- 4 to 34 +/- 10%. Experiments defining the time course of development of ICI in the PPM indicate that protection was only temporary, delaying the onset of injury by 25 min. These findings suggest that 1) neural activity in extrinsic cardiac sympathetic nerves activate beta-receptors, thereby influencing the development of ICI, and 2) differences in protection afforded by acute denervation with and without beta-blockade indicated that intrinsic postganglionic sympathetic nerve terminals can liberate transmitter in response to ischemia even in the absence of extrinsic neural activity.

Animals↗

Activity of in vivo canine cardiac plexus neurons.

The activity of 394 spontaneously active neurons located in the ganglionated plexus of the ventral epicardial fat pad overlying the right atrium and pulmonary veins was recorded. Ganglia that contained various numbers of neurons, many with two or more nucleoli, were identified adjacent to the recording sites. Spontaneous activity was correlated with the cardiac cycle in 39% and with the respiratory cycle in 8% of the identified neurons. Neuronal activity occurred in specific phases of the cardiac cycle when arterial pressure was between approximately 70 and 175 mmHg. During increases in systolic pressure induced by positive inotropic agents or aortic occlusion, responses of neurons that displayed cardiovascular-related activity were enhanced. These responses persisted after acute decentralization. The activity of 14% of all identified neurons was altered when discrete regions of the heart, great thoracic vessels, or lungs were mechanically distorted by gentle touch. Trains of stimuli, but not single stimuli, delivered to the vagosympathetic complexes, stellate ganglia, or cardiopulmonary nerves activated ganglionic neurons in intact or acutely decentralized preparations. It is concluded that the activity of some cardiac ganglion neurons is related to cardiovascular or respiratory dynamics and that some of these neurons receive inputs from sympathetic and parasympathetic efferent axons as well as from cardiac mechanoreceptors.

Adipose Tissue↗

Activity of in vivo canine ventricular neurons.

The spontaneous activity of 113 neurons located in the ganglionated plexus in the epicardial fat overlying the cranial portion of the ventral intraventricular groove and the origin of the circumflex coronary artery was recorded in ten anesthetized dogs. Ganglia that contained varying numbers of neurons, some with two or more nucleoli, were subsequently identified anatomically in the vicinity of the recording sites. Spontaneous activity was correlated with the cardiac cycle in 81% and with the respiratory cycle in 17% of the identified neurons. The spontaneous cardiovascular-related activity occurred in relation to specific phases of the cardiac cycle when arterial pressure was between approximately 80 and 175 mmHg. When systolic pressures fell below approximately 80 mmHg or increased above approximately 175 mmHg, neurons displaying cardiovascular-related activity were inactive. The activity of 62% of all identified neurons was altered when discrete regions of the heart or pulmonary tissue were mechanically distorted by gentle touch. In many instances mechanical distortions of tissues were still able to alter neuronal activity following acute decentralization. Single stimuli or trains of stimuli delivered to the vagosympathetic complexes, stellate ganglia, or cardiopulmonary nerves generated bursts of activity in ganglionic neurons. Spontaneous activity occurred whether the ganglia were connected to the central nervous system or acutely decentralized. It is concluded that some neurons located on the canine ventricle display spontaneous activity that is related to cardiovascular or respiratory dynamics. The results also demonstrate that ventricular neurons can be influenced by sympathetic or parasympathetic efferent axons as well as cardiac mechanoreceptors.

Adipose Tissue↗

Activity of canine in situ left atrial ganglion neurons.

The responses of 135 spontaneously active neurons were recorded from ganglionated plexi located in the three epicardial fat pads on the ventral surface of the left atrium of ten dogs. Ganglia, some of which were adjacent to the recording sites, containing varying numbers of neurons were identified throughout these fat pads. Spontaneous activity in 50% of the identified neurons was correlated with specific phases of the cardiac cycle when arterial systolic pressure was between approximately 70 and 180 mmHg and in 28% it was correlated with the respiratory cycle. More neurons displaying cardiovascular-related activity were recorded when systolic pressure was increased after administration of positive inotropic agents or aortic occlusion. However, when systolic pressure increased above approximately 150 mmHg the number of active neurons decreased, and when pressure reached approximately 180 mmHg no activity was recorded. The activity of 36% of identified neurons was altered when discrete regions of the heart, great thoracic vessels, lungs, neck, upper limb, chest wall, or abdominal wall were mechanically distorted by gentle touch. After acute decentralization of the intrathoracic nervous system some neurons still displayed spontaneous cardiovascular- or respiratory-related activity. Single stimuli or trains of stimuli delivered to the vagosympathetic complexes, stellate ganglia, or cardiopulmonary nerves activated neurons in intact or acutely decentralized preparations. It is concluded that ventral left atrial ganglionated plexi neurons display activity related to cardiovascular or respiratory dynamics, and that these neurons are influenced by sympathetic and parasympathetic efferent axons, as well as by cardiac and other mechanoreceptors.

Adipose Tissue↗

Vasoactive intestinal polypeptide enhances automaticity of supraventricular pacemakers in anesthetized dogs.

Effects of the cardiac neuropeptide vasoactive intestinal polypeptide (VIP) and isoproterenol (ISO) were compared on sinus nodal, subsidiary atrial, and atrioventricular junctional pacemaker automaticity in pentobarbital sodium-anesthetized dogs (n = 14). Autonomic cardiac nerves were decentralized by bilateral vagotomy and stellectomy. VIP and ISO (30, 100, and 300 pmol/kg iv) were administered during sinus rhythm and either after crushing the sinus node to unmask a latent subsidiary atrial pacemaker (n = 7 dogs) or after injecting pentobarbital sodium into the sinus node artery to elicit an atrioventricular junctional pacemaker (n = 7). Spontaneous sinus nodal, subsidiary atrial, and atrioventricular junctional pacemaker rates (after autonomic nerve decentralization) were 142 +/- 4, 114 +/- 3, and 79 +/- 4 beats/min (means +/- SE), respectively. Both VIP and ISO dose dependently increased the rates of all three pacemaker sites. Combined muscarinic-cholinergic (atropine; 0.11 mg/kg iv) and beta-adrenergic receptor blockade (nadolol; 0.5 mg/kg iv) abolished the stimulatory effects of ISO on subsidiary atrial and atrioventricular junctional pacemakers but did not affect the responses to VIP. We conclude that exogenous VIP enhances the automaticity of sinus nodal, subsidiary atrial, and atrioventricular junctional pacemakers independently of muscarinic-cholinergic and beta-adrenergic receptors. Based on the previous demonstration of VIP-immunoreactive nerves throughout the heart, our findings also suggest that endogenous VIP may be involved in cardiac pacemaker regulation.

Animals↗

Amino acids modify activity of canine intrinsic cardiac neurons involved in cardiac regulation.

The effects of amino acids on intrinsic cardiac neuronal activity identified in 10 anesthetized dogs were investigated. Local injection of small volumes (1-10 microliters) of the excitatory amino acids, glutamate (100 mM) and aspartate (10 mM), and the inhibitory amino acids, gamma-aminobutyric acid (GABA; 10 mM) and glycine (10 mM), modified the activity of 39 of 50 identified neurons. Spontaneous activity of eight neurons was modified by both excitatory and inhibitory amino acids. Cardiodynamic responses accompanied neuronal activity modification in 15 instances. After acute decentralization, repeat doses of amino acids altered the activity of 21 neurons and elicited cardiovascular responses in 7 instances. Neuronal and cardiovascular responses were elicited after atropine administration. Neuronal but not cardiac responses were elicited after subsequent timolol administration. In other animals, GABA but not other amino acids elicited neuronal and cardiodynamic responses after hexamethonium administration in decentralized preparations, indicating that non-nicotinic synapses were involved in some GABA-induced responses. These results demonstrate that excitatory and inhibitory amino acids can modify intrinsic cardiac neuronal activity such that, as a consequence, cardiac variables can be modified.

Amino Acids↗

Differing sympathetic and vagal effects on atrial fibrillation in dogs: role of refractoriness heterogeneity.

Although sympathetic activation is believed to promote atrial fibrillation (AF), the effects of sympathetic stimulation on AF have not been systematically studied. In seven morphine-chloralose-anesthetized dogs, autonomic decentralization increased atrial effective refractory period (ERP) and reentrant wavelength (WL) and decreased the duration of AF induced by burst atrial pacing. Graded bilateral stellate ansa stimulation decreased ERP and WL to values similar to those before decentralization but did not return AF duration to predecentralization values. Sympathetic and bilateral vagal stimulation were adjusted in six additional dogs to produce similar effects on ERP and WL. Despite comparable effects on mean WL, the duration of AF was increased by vagal stimulation from 14 +/- 5 (control) to 372 +/- 96 s (P < 0.001) but was not altered significantly (26 +/- 10 s) by sympathetic stimulation. Vagal stimulation increased the variability in atrial refractoriness, as indicated by the standard deviation of ERP at seven atrial sites and of activation frequency during AF at 112 recording sites, whereas sympathetic stimulation had no significant effect on these indexes of ERP heterogeneity. We conclude that sympathetic stimulation is much less effective than vagal stimulation in promoting AF and that heterogeneity in atrial ERP may be important in determining the ability to sustain AF.

Animals↗

Beta 1- and beta 2-adrenoceptor subtypes in canine intrathoracic efferent sympathetic nervous system regulating the heart.

The augmentation of cardiac inotropism induced by electrical stimulation of acutely decentralized efferent preganglionic sympathetic axons is reduced after the administration of timolol into the major ipsilateral intrathoracic ganglia. Thus it has been proposed that, in addition to nicotinic synapses, beta-adrenergic ones exist in intrathoracic ganglia that are involved in the efferent sympathetic regulation of the mammalian heart. Whether these are beta 1- as opposed to beta 2-adrenoceptor subtypes is unknown. In the present series of experiments, acutely decentralized canine efferent preganglionic sympathetic axons were stimulated before and after the administration of beta 1 (atenolol)- or beta 2 (ICI 118551)-selective adrenoceptor antagonists into the ipsilateral stellate and middle cervical ganglia to determine whether beta 1- or beta 2-adrenoceptors exist in intrathoracic ganglia that are involved in cardiac regulation. Augmentations of right and left ventricular inotropism induced by efferent preganglionic sympathetic axon stimulation were attenuated when either agent was administered into the major ipsilateral intrathoracic sympathetic ganglia. Myocardial liberation of norepinephrine evoked by these stimulations was also reduced after intraganglionic administration of either agent. These data indicate that canine intrathoracic neurons contain beta 1- and beta 2-adrenoceptors that are involved in the efferent sympathetic regulation of the heart.

Adrenergic beta-Antagonists↗

Cardiovascular responses of heart transplant recipients to graded exercise testing.

A group of orthotopic heart transplant (OHT, n = 28) and heart surgery (n = 19) patients, with similar ejection fractions and left ventricular end-diastolic pressures, were exercised to symptom-limited maximum to describe differences in cardiovascular and gas exchange responses. Testing was performed at a mean of 3 and 6 mo after surgery, respectively (P less than 0.05). OHT patients have a greater resting systolic and diastolic blood pressure (P less than 0.01) and a significantly greater (P less than 0.01) heart rate (HR) at rest in the supine and standing positions and during minutes 2 through 7 of supine recovery. Peak treadmill time was significantly less (P less than 0.01) in OHT patients. No significant differences were found for systolic blood pressure (SBP) during recovery, peak HR, ventilation, relative O2 uptake (VO2), body weight, ventilatory equivalents for O2 and CO2, O2 pulse, and HR-SBP product (peak HR x peak SBP). Peak pulse pressure, heart rate reserve, total VO2, and absolute VO2 at ventilatory threshold were significantly lower (P less than 0.01) in the OHT patients. We concluded that 1) complete cardiac decentralization is evident, 2) the significantly reduced VO2 at ventilatory threshold should be considered when activities of daily living are prescribed, and 3) SBP response is more appropriate than HR for assessing recovery of the decentralized heart after maximal exercise.

Blood Pressure↗

Cardiovascular control during voluntary static exercise in humans with tetraplegia.

The purpose of the present study was 1) to investigate whether an increase in heart rate (HR) at the onset of voluntary static arm exercise in tetraplegic subjects was similar to that of normal subjects and 2) to identify how the cardiovascular adaptation during static exercise was disturbed by sympathetic decentralization. Mean arterial blood pressure (MAP) and HR were noninvasively recorded during static arm exercise at 35% of maximal voluntary contraction in six tetraplegic subjects who had complete cervical spinal cord injury (C(6)-C(7)). Stroke volume (SV), cardiac output (CO), and total peripheral resistance (TPR) were estimated by using a Modelflow method simulating aortic input impedance from arterial blood pressure waveform. In tetraplegic subjects, the increase in HR at the onset of static exercise was blunted compared with age-matched control subjects, whereas the peak increase in HR at the end of exercise was similar between the two groups. CO increased during exercise with no or slight decrease in SV. MAP increased approximately one-third above the control pressor response but TPR did not rise at all throughout static exercise, indicating that the slight pressor response is determined by the increase in CO. We conclude that the cardiovascular adaptation during voluntary static arm exercise in tetraplegic subjects is mainly accomplished by increasing cardiac pump output according to the tachycardia, which is controlled by cardiac vagal outflow, and that sympathetic decentralization causes both absent peripheral vasoconstriction and a decreased capacity to increase HR, especially at the onset of exercise.

Adaptation, Physiological↗

Role of sympathetic postganglionic neurons in synovial plasma extravasation induced by bradykinin.

1. Plasma extravasation through the endothelium of blood vessels is an integral component of the inflammatory response and is dependent to a large extent on the inflammatory mediator bradykinin (BK). We studied plasma extravasation induced by BK perfusion (BK-induced PE) of the rat knee joint before and after various interventions that affect the sympathetic supply to the knee joint. We tested the hypothesis that plasma extravasation is dependent on the local sympathetic terminal supply to the synovia but not directly dependent on more proximal activity in the sympathetic neurons. As a control we used plasma extravasation induced by platelet activating factor (PAF), which acts directly on the endothelium of the blood vessels, that is, its action is independent of any innervation. Plasma extravasation into the knee joint cavity was determined spectrophotometrically by measuring, over time, the concentration of Evans blue dye extravasation into the joint perfusate following intravenous injection of the dye. 2. Surgical sympathectomy at the lumbar level (L2-L4), performed 4 and 14 days previously, reduced BK-induced PE by approximately 55-70%. 3. Decentralization of the lumbar sympathetic chain (cutting the preganglionic axons that innervate the postganglionic neurons to the hindlimb), interruption of the lumbar sympathetic chain during infusion of BK, or coperfusion of tetrodotoxin into the knee joint cavity did not reduce BK-induced PE. All three interventions abolish the activity in the sympathetic neurons but leave the peripheral postganglionic terminals in the joint capsule intact. 4. Surgical sympathectomy and decentralization did not affect plasma extravasation induced by the intra-articular perfusion with PAF. 5. Electrical stimulation of the lumbar sympathetic chain at frequencies of 0.25-5 Hz, which probably also significantly decreases blood flow through the joint capsule, reduced basal plasma extravasation, BK-induced PE and PAF-induced PE. This reduction was frequency dependent and was almost maximal at a stimulation frequency of 1 Hz. 6. In conclusion, BK-induced PE into the rat knee joint is dependent on the presence of intact sympathetic postganglionic nerve terminals innervating the joint capsule and not directly dependent on excitation of these neurons. However, electrical stimulation of the sympathetic neurons reduces the level of plasma extravasation, presumably because of vasoconstriction and decrease of blood flow through the joint capsule. These results indicate that peripheral action of inflammatory mediators on terminals of sympathetic neurons produces a facilitative effect on vascular permeability, whereas centrally generated excitation of these neurons, which depresses blood flow (vasoconstrictor function), decreases plasma extravasation. The effect on blood flow is presumed to occur at the precapillary resistance vessels by vesicular release of transmitter(s). The facilitative effect on permeability occurs at the venules and includes inflammatory-mediator-stimulated, non-vesicular-dependent production and release of a chemical substance (probably prostaglandin E2). Whether both functions are represented in the same class of sympathetic postganglionic neuron or in distinct ones remains to be elucidated.

Animals↗

[Evaluation of the pilot programme for the descentralization of control of oral anticoagulant treatment in the Osasunbidea Healthcare Service (Navarra, Spain)].

BACKGROUND AND OBJECTIVE: The objective of this study was the evaluation of the pilot programme of decentralization of oral anticoagulant therapy (OAT) in eight basic health zones (ZBS) for the first six months and then a year after the programme was put into practice. PATIENTS AND METHOD: Descriptive transversal study. It includes all patients aged 14 years or older in the OAT (540 in the initial period and then 640 more) in eight ZBS (five urban and three rural). The evaluation was done including: prevalence of INR in control (2-3 or 2.5-3.5, according to indications), clinically suitable INR (INR in control +/- 0.2) and INR in control +/- 0.5, accumulated thrombosis and bleeding incidence. Source data: ANTICOAGN computer programme. RESULTS: Comparison of INR control between both periods: 59% against 63.9% of INR in the range of INR in control (p < 0.001), 72.8% against 78.8% for clinically suitable INR (p < 0.001), and 86.6% against 91.4% for INR in control +/- 0.5 (p < 0.001). Accumulated incidence of bleeding episodes in 6 months: Pilot: 1.1% (0.7% majors and 0.4% minors). Subsequent period: 3.6% (0.6% majors and 3% minors). CONCLUSIONS: The decentralization of control of the OAT with adequate resources implies a greater accessibility for the patient. The control of INR is acceptable and has improved significantly over the second period. We have detected an improvement in the increase of the INR below that of the range of the control INR. The incidence of minor hemorrhages has increased, owing probably to a better recording.

Administration, Oral↗

Long-term results with Iogel IOLs.

130 single piece hydrogel Iogel intraocular lenses (IOL) were implanted in the capsular bag after planned extracapsular cataract extraction. Anterior capsulotomy was performed by capsulorhexis in 59 patients while the envelope technique was used in 71 cases. The mean follow-up was 22 months and the average visual acuity was more than 8/10 in 78.5% of cases. In the capsulorhexis group a higher percentage of IOL was placed right into the capsular bag. No significant inflammatory and noninflammatory postoperative complications occurred. Lens decentration, observed in 5 cases, was due to asymmetric lens placement with one flange in the bag and the other in the ciliary sulcus. In both groups endothelial cell loss was about 7%. Results of the study indicate the safety and the efficacy of the Iogel lens as an intraocular implant. To prevent postoperative decentration and deformation of the IOL unnecessary intraocular manipulation and 'in-out' positioning should be avoided.

Aged↗

Cardiac sympathetic afferent cell bodies are located in the peripheral nervous system of the cat.

Studies of the stellate ganglion and middle cervical ganglion indicate that sympathetic efferent nerve activity can be modified by peripheral excitatory inputs and that these neural connections may function as pathways for a peripheral reflex at the level of the thoracic sympathetic ganglia. This excitatory synaptic input could have a soma in either the central or the peripheral nervous system. A study was designed to determine whether chronic decentralization (3 weeks) of the stellate ganglion in cats would 1) abolish sympathetic cardiac afferent nerve activity recorded at the stellate cardiac nerve and 2) abolish local thoracic reflexes that are generated by stimulation of peripheral nerves. The ansae subclaviae, T3 and T4 rami, and stellate ganglion were also examined by electron microscopy for the extent of Wallerian degeneration. Afferent cardiac activation of the axon collaterals arising from cell bodies located in the dorsal root ganglia was abolished due to degeneration. However, sympathetic afferent nerve activity from the left ventricular receptors was still present and was recorded from the stellate cardiac nerve in all cats. Cardiac receptors were sensitive to mechanical distortion, increases in the left ventricular pressure, and epicardial application of veratrine hydrochloride. These data imply that 1) cardiovascular afferent input to the stellate ganglion persists following chronic decentralization and 2) the sensory neurons are located in the peripheral sympathetic nervous system. Thus, we find that regulation of the heart occurs in part via thoracic ganglia, independently of the central nervous system.

Afferent Pathways↗

Shifting the responsibility for payment for state hospital services to community mental health agencies.

OBJECTIVE: In 1990 the state of Arkansas shifted financial responsibility for state hospital services to community mental health centers; through a policy known as "bed buy-back," centers now authorize all state hospital admissions and prospectively purchase bed days for their patients. Characteristics of patients hospitalized before and after implementation of the policy were examined to determine how the policy affected hospital admission rates, types of patients admitted, and the amount of contact between CMHC and hospital staff about admitted patients, as well as how these elements were affected differently in rural and urban areas. METHODS: Changes in the types of patients admitted over the 13 months before and 14 months after the change in financing were studied through retrospective chart review of 648 patients. Administrative data were used to examine changes in numbers of admissions for 30 months before and 26 months afterward. Data were analyzed by piecewise regression, least-squares, and logistic regression analyses. RESULTS: After financial decentralization, state hospital use was reduced in both urban and rural areas, although the reduction in urban areas was proportionally greater. Contrary to expectation, admissions were not limited to the most severely ill, disruptive, or substance-abusing patients, nor were they more likely to be readmitted. For patients who were admitted, communication between the community and the state hospital was greater than before financial decentralization. CONCLUSIONS: Shifting financial responsibility for patient care significantly reduced state hospital use, did not affect patient mix, and apparently increased coordination of care between community and hospital. Whether bed buy-back has affected the kind or quality of services delivered in the community awaits further study.

Adolescent↗

Managing diverse occupational therapy resources in a creative, corporate model.

Two occupational therapy departments were amalgamated into a corporate whole and charged with the development of a workable, corporate structure. The departmental model which was developed served to enhance the concepts of quality of working life, employee autonomy, management team and quality circle theory. This paper provides a background from business and organizational literature, and outlines the development of the departmental model, in concert with the adoption of the client-centred model of occupational performance as a department basis for practice. This development was taking place concurrently with larger, institutional changes into a decentralized clinical programme management model. Discussion highlights the level of staff satisfaction with the changes, areas of concern during the development of the system and plans for the future growth. During this period of massive and critical change in the delivery of health care services, there has been a trend in restructuring health care institutions towards decentralized models. This paper will describe the experience of one occupational therapy department in developing an innovative departmental structure involving participatory management amalgamation. It is believed that the experience of the past occupational therapy work units with one viable option for a renewed management model. Staff skill sets can be maximized and optimal potential realized while faced with inevitable resource shrinkage and service reorganization.

Health Facility Merger↗

Posterior chamber lens implantation techniques in posterior capsular rupture.

PURPOSE: To evaluate posterior chamber lens implantation techniques and their results in patients in whom posterior capsular rupture and zonular dialysis arose during cataract operation. METHODS: Forty-three cataractous eyes of 43 consecutive patients with complicated cataract operations such as posterior capsular rupture or zonular dialysis were accepted into this prospective study between November 1999 and January 2001. Intraocular lens implantation to ciliary sulcus was achieved without sutures in 19 cases (Group 1), with one suture from 12 o'clock quadrant in 14 cases (Group 2), and with two sutures from 3 to 9 o'clock quadrants in 10 cases (Group 3). Patients were followed up for 3 months after operation and evaluated for best-corrected visual acuity, refractive astigmatism, corneal edema, anterior chamber depth and inflammation, synechia at angle, intraocular pressure, lens tilt and decentration, intraocular hemorrhage, cystoid macular edema, and retinal detachment. RESULTS: There was no difference among groups in best-corrected visual acuity, refractive astigmatism, corneal edema, anterior chamber depth and inflammation, intraocular pressure, lens tilt and decentration, cystoid macular edema, or retinal detachment. Anterior chamber and vitreous hemorrhage and peripheral anterior synechia were significantly higher in Group 3 when compared with Group 1 (p = 0.009, p = 0.009, and p = 0.004). CONCLUSIONS: In all cases with posterior capsular rupture and zonular dialysis, different posterior chamber lens implantation techniques could be performed, beginning with the least invasive procedure suitable for the conditions with the least complications.

Aged↗