Biomedical subjects

M K Patel

Publications and source records attributed to M K Patel.

At least 19 recordsLinked to original sources

PubMed2001

Adenosine exerts multiple effects in dorsal horn neurones of the adult rat spinal cord.

In the present study, we have examined the effects of adenosine and its analogues on the electrophysiological properties of dorsal horn neurones in the rat adult spinal cord. Adenosine and the A1 receptor agonist R-phenylisopropyl adenosine (RPIA) reversibly hyperpolarised these neurones via the generation of an outward current at -60 mV that was inhibited by pre-application of barium or Rp-adenosine 3', 5'-cyclic monophosphothioate triethylamine. In contrast, the A2a receptor agonist 2-[p-(2-carboxyethyl)phenylethylamino]-5'-N-ethylcarboxamidoadenosine (CGS21680) had no effect on the resting membrane properties of these neurones. Stimulation of the dorsal root evoked non-NMDA receptor-mediated excitatory postsynaptic currents (EPSCs) at -60 mV that were completely abolished by 2,3-dihydroxy-6-nitro-7-sulophamoyl-benzo(F)quinoxalone (NBQX). Bath application of adenosine or RPIA reversibly inhibited these EPSCs in a concentration-dependent manner via a presynaptic action. In contrast, CGS21680 increased the amplitude of the EPSC in 20% of neurones tested and decreased the EPSC amplitude in 30% of neurones tested. It is concluded that adenosine exerts multiple effects upon the electrophysiological properties of dorsal horn neurones in the adult spinal cord via interaction with multiple receptors. These findings have important implications in the understanding of adenosine action in preclinical models of pain.

Adenosine↗

PubMed2001

Smoking cessation in patients with chronic obstructive pulmonary disease: a double-blind, placebo-controlled, randomised trial.

BACKGROUND: Tobacco smoking is associated with chronic obstructive pulmonary disease (COPD) in more than 80% of cases. Our aim was to investigate the effect of sustained-release bupropion (amfebutamone) (SR) in promoting abstinence from smoking in patients with COPD. METHODS: In a double-blind, randomised, placebo-controlled trial 404 individuals with mild or moderate COPD who smoked 15 or more cigarettes per day, were assigned bupropion SR (150 mg twice daily) or placebo for 12 weeks. All patients received smoking cessation counselling. Study medication was taken for 1 week before patients attempted to stop smoking. The primary efficacy endpoint was the complete and continuous abstinence from smoking from the beginning of week 4 to the end of week 7. Participants were followed up at month 6. Analysis was by intention to treat. FINDINGS: All patients were chronic smokers with a smoking history of about 51 pack-years. Continuous smoking abstinence rates from week 4 to 7 were significantly higher in participants receiving bupropion SR than in those receiving placebo (28% [57/204] vs 16% [32/200], p=0.003). Continuous abstinence rates from weeks 4 to 12 (18% [36/204] vs 10% [20/200]) and weeks 4 to 26 (16% [32/204] vs 9% [18/200]) were also higher in participants receiving bupropion SR than in those taking placebo (p<0.05). Furthermore, symptoms of tobacco craving and withdrawal were attenuated in those receiving bupropion SR. Seven individuals discontinued study medication because of adverse events. INTERPRETATION: Bupropion SRis a well-tolerated and effective aid to smoking cessation in people with mild to moderate COPD.

Adult↗

PubMed2001

Properties of native P2X receptors in rat trigeminal mesencephalic nucleus neurones: lack of correlation with known, heterologously expressed P2X receptors.

Trigeminal mesencephalic nucleus (MNV) neurones express functional P2X receptors. In order to determine the molecular identity of the P2X receptors in this nucleus we have used whole cell patch clamp recording of P2X receptor-mediated currents to determine the pharmacological properties of the receptors, and have compared them with those of cloned P2X receptor subunits. The purine nucleotides ATP (300 microM), ATP-gamma-S (30 microM) and alphabetameATP (300 microM) evoked inward currents in all MNV neurones whereas alphabetameADP (300 microM) did not. betagammame-L-ATP (300 microM) evoked only a small ( approximately 20 pA) current in 3 out of 6 MNV neurones. The P2X receptor antagonist TNP-ATP (10 nM-10 microM) and raised extracellular Ca(2+) (8 and 30 mM) reduced, but did not abolish, the current evoked by ATP-gamma-S. The current remaining in TNP-ATP was insensitive to blockade by raised Ca(2+). These properties suggest that MNV neurones do not express homomeric P2X(3), P2X(4) or P2X(6) receptors. Whilst the TNP-ATP-insensitive ATP-gamma-S-evoked current has many characteristics similar to both homomeric P2X(2) and P2X(5) receptors, its insensitivity to blockade by raised Ca(2+) is difficult to reconcile with the receptor being a P2X(2) or P2X(5) homomeric channel. More likely, the receptor is a heteromer that comprises either or both of these subunits. The TNP-ATP-sensitive component of the ATP-gamma-S-evoked current is dissimilar to known cloned homomeric or heteromeric P2X receptors.

Adenosine Diphosphate↗

PubMed2001

Prognostic significance of periodic acid-Schiff-positive patterns in primary cutaneous melanoma.

The patterns of periodic acid-Schiff (PAS) staining of extracellular matrix in histological sections of certain melanomas may be predictive of outcome. Recent in vitro and molecular genetic data suggest that the appearance of these patterns in both uveal and cutaneous melanoma is a function of aggressive tumor cells. We studied 96 patients with primary cutaneous melanomas treated at the University of Illinois at Chicago who were monitored for disease-free survival. Survival probabilities were determined by Kaplan-Meier estimates, and prognostic factors were evaluated by multivariate analysis. By univariate analysis, there was a significant decrease in disease-free survival among patients whose tumors contained parallel with cross-linking or network patterns (PXNs; P = 0.0070). Stepwise regression with Cox models that included the combinations of the PAS-positive patterns, tumor thickness, female gender, ulceration, and age yielded a model with thickness and the PAS-positive parallel with cross-linking or networks. Despite the relatively small sample size in this study, the detection of the PAS-positive parallel with cross-linking or networking in cutaneous melanoma was associated with a decrease in disease-free outcome. Additional studies of the prognostic significance of these patterns is warranted on larger data sets.

Adolescent↗

PubMed2000

Contributions of charged residues in a cytoplasmic linking region to Na channel gating.

Na channels inactivate quickly after opening, and the very highly positively charged cytoplasmic linking region between homologous domains III and IV of the channel molecule acts as the inactivation gate. To test the hypothesis that the charged residues in the domain III to domain IV linker have a role in channel function, we measured currents through wild-type and two mutant skeletal muscle Na channels expressed in Xenopus oocytes, each lacking two or three charged residues in the inactivation gate. Microscopic current measures showed that removing charges hastened activation and inactivation. Macroscopic current measures showed that removing charges altered the voltage dependence of inactivation, suggesting less coupling of the inactivation and activation processes. Reduced intracellular ionic strength shifted the midpoint of equilibrium activation gating to a greater extent, and shifted the midpoint of equilibrium inactivation gating to a lesser extent in the mutant channels. The results allow the possibility that an electrostatic mechanism contributes to the role of charged residues in Na channel inactivation gating.

Animals↗

PubMed2000

A ligand of peroxisome proliferator-activated receptor gamma, retinoids, and prevention of preneoplastic mammary lesions.

BACKGROUND: Chemoprevention of breast cancer is an active area of investigation. Recent in vivo and in vitro studies have shown that thiazolidinediones (e.g., troglitazone) and retinoids are able to inhibit the growth of breast cancer cells. Troglitazone mediates its action via peroxisome proliferator-activated receptor gamma (PPARgamma). We evaluated the ability of troglitazone, alone or in combination with retinoids, to prevent the induction of preneoplastic lesions by 7,12-dimethylbenz[a]anthracene (DMBA) in a mouse mammary gland organ culture model. METHODS: Mammary glands of BALB/c mice were treated with DMBA (2 microg/mL) to induce preneoplastic lesions in organ culture. Effects of troglitazone, all-trans-retinoic acid (retinoic acid; ligand for retinoic acid receptor [RAR] alpha), and LG10068 (ligand for retinoid X receptors [RXRs]), singly or in combination, on the development of lesions were evaluated. Expression of retinoid receptors (RARalpha and RXRalpha) and PPARgamma was determined by western blot analysis. Statistical significance was determined by generalized chi-squared analysis using the GENCAT software program and Bonferroni correction. All P values are two-sided. RESULTS: Troglitazone (at 10(-5) M) or retinoic acid (at 10(-6) M) markedly inhibited the development of mammary lesions (both P values <.05); however, together they did not enhance the effectiveness of the other. In contrast, LG10068 (at 10(-7) M or 10(-8) M) alone had very little ability to inhibit development of these lesions, but a combination of LG10068 (at 10(-8) M) and troglitazone (at 10(-5) M or 10(-6) M) almost completely inhibited (by 85% and 100%, respectively; both P values <. 05) the development of mammary lesions. The expression of PPARgamma and RXRalpha remained unchanged with the various treatments, whereas the expression of RARalpha was substantially reduced after treatment with the combination of retinoic acid and troglitazone. CONCLUSIONS: To our knowledge, this is the first report showing the possibility of a PPARgamma ligand having chemopreventive activity. Furthermore, an RXR-selective retinoid, LG10068, appears to enhance this activity.

9,10-Dimethyl-1,2-benzanthracene↗

PubMed2000

Sodium channel isoform-specific effects of halothane: protein kinase C co-expression and slow inactivation gating.

The modulatory effect of protein kinase C (PKC) on the response of Xenopus oocyte-expressed Na channel alpha-subunits to halothane (2-bromo-2-chloro-1,1,1-trifluroethane) was studied. Na currents through rat skeletal muscle, rat brain and human cardiac muscle Na channels were assessed using cell-attached patch clamp recordings. PKC activity was increased by co-expression of a constitutively active PKC alpha-isozyme. Decay of macroscopic Na currents could be separated into fast and slow exponential phases. PKC co-expression alone slowed Na current decay in neuronal channels, through enhancement of the amplitude of the slower phase of decay. Halothane (1.0 mM) was without effect on any of the three isoforms expressed alone but, after co-expression of PKC, there was enhancement of Na current decay with reduction in charge movement through skeletal muscle and neuronal channels. Cardiac channels were relatively insensitive to halothane. Enhanced Na current decay resulted from suppression of the slow phase, without effect on the faster phase or on either decay tau. Suppression of Na current through skeletal muscle channels was concentration-dependent over the therapeutic range and was described by third order reaction kinetics, with an IC(50) of 0.55 mM. We conclude that the halothane suppresses skeletal muscle and brain Na channel activity in this preparation through a reduction in the slow mode of inactivation gating, but only after PKC co-expression. Cardiac Na channels were relatively insensitive to halothane. The mechanism is likely to involve phosphorylation of the channel inactivation gate, although phosphorylation of other sites in the channel may account for the isoform specific differences.

Animals↗

PubMed2000

Gabapentin inhibits excitatory synaptic transmission in the hyperalgesic spinal cord.

In the present study we tested the effects of the antihyperalgesic compound gabapentin on dorsal horn neurones in adult spinal cord. Slices were taken from control and hyperalgesic animals suffering from streptozocin-induced diabetic neuropathy. At concentrations up to 100 microM, bath application failed to affect the resting membrane properties of dorsal horn neurones taken from both groups of animal. In contrast, bath application of gabapentin dramatically reduced the magnitude of the excitatory postsynaptic current (EPSC) in neurones taken from hyperalgesic animals without altering the magnitude of the EPSC in control animals. Using a paired pulse stimulation protocol, together with analysis of miniature EPSC's, it was possible to demonstrate that gabapentin mediated these effects via a pre-synaptic site of action.

Acetates↗

PubMed2000

Cyanide increases reduction but decreases sequestration of methylene blue by endothelial cells.

The mechanisms of endothelial cell transplasma membrane electron transport (TMET) have not been completely identified. Redox probes such as methylene blue (MB) can be useful tools, but the complexity of their disposition upon exposure to the cells can hinder interpretation. For example, MB is reduced on the cell surface by TMET, but after entering the cell in reduced form, it is reoxidized and sequestered within the cell. We developed a method to separately quantify the reduction and reoxidation rates such that it can be determined whether a metabolic inhibitor such as cyanide affects the reduction or oxidation process. MB was introduced at the inlet to a column filled with endothelial cell covered beads either as a short 12 s injection (bolus) or a long 45 min infusion (pulse), and its effluent concentration was measured as a function of time. The cells extracted 56% of the MB from the bolus, but only 41% during the pulse steady state. In the presence of cyanide, these extractions increased to 70% and decreased to 4%, respectively. Mathematical model results support the interpretation that these paradoxical effects on bolus and pulse extractions reflect the differential effects of cyanide on extracellular reduction and intracellular oxidation, i.e., cyanide increased the reduction rate from 7.3 to 13.0 cm s-1 X 10(-5) and decreased the oxidation rate from 1.09 to 0.02 cm s-1 X 10(-3). Cyanide also increased intracellular NADH by almost eight times, suggesting that TMET is sensitive to the cell redox status, i.e., NADH is a direct or indirect electron source. The cyanide-induced decrease in sequestration indicates a cyanide-sensitive intracellular oxidation mechanism. The results also demonstrate the potential utility of this approach for further evaluation of these endothelial redox mechanisms.

Animals↗

PubMed2000

Heart rate variability in preterm brain-injured and very-low-birth-weight infants.

Heart rate variability (HRV) reflects the complex interplay of the sympathetic and parasympathetic innervation of the heart. Developmental maturation of the fetus and newborn results in predictable alterations in the neural cardiac control of heart rate. Furthermore, patterns of HRV are closely correlated to clinical outcome in several pathologic situations. The first aim of this study was to characterize the maturational patterns of HRV in a group of developmentally at-risk newborns (those with severe hemorrhagic or ischemic brain injury and extremely immature, low-birth-weight infants). Secondly, we sought to determine whether a correlation exists between HRV and length of hospital stay, diagnosis of cerebral palsy, and neurodevelopmental test scores at 1-year corrected age. Time domain indices of HRV were computed longitudinally from 32 to 37 weeks of corrected gestational age in 19 very low birth weight, preterm infants. Among the 19 infants studied, 7 infants had no evidence of brain injury, 7 infants had periventricular leukomalacia (PVL), 3 infants had grade III/IV intraventricular hemorrhage (IVH), and 2 infants had both IVH and PVL. Neurologic injuries were documented using ultrasound and neurodevelopmental progress was followed through 1 year of corrected gestational age. A multivariate repeated measures analysis was performed to determine the relationship between the type of perinatal brain injury and neurodevelopmental status at 1 year of corrected gestational age. The type of perinatal brain injury was highly correlated to specific patterns of HRV with multivariate regression models producing adjusted r(2) values ranging from 0.63 to 0.99. The type of perinatal brain injury was highly correlated to the developmental outcome measures (p < 0.0000) with PVL patients having the lowest neurodevelopmental scores, IVH patients having the highest scores, and noninjured infants having midrange, grossly normal values. Using ANOVA, HRV was correlated to outcome, but individual comparisons revealed statistical significance only for the noninjured group (p < 0.04). However, multivariate models, which characterized outcome within each brain injury group, were highly significant (adjusted r (2) ranged from 0.23 to 0.89). In summary, the type of perinatal brain injury determined the pattern of HRV and HRV was highly correlated to length of hospital stay and neurodevelopmental function assessed at 1 year of corrected gestational age.

Cerebral Hemorrhage↗

PubMed1999

Modulation of Xenopus oocyte-expressed phospholemman-induced ion currents by co-expression of protein kinases.

Phospholemman (PLM), the major sarcolemmal substrate for phosphorylation by cAMP-dependent kinase (PKA) protein kinase C (PKC) and NIMA kinase in muscle, induces hyperpolarization-activated anion currents in Xenopus oocytes, most probably by enhancing endogenous oocyte currents. PLM peptides from the cytoplasmic tail are phosphorylated by PKA at S68, by NIMA kinase at S63, and by PKC at both S63 and S68. We have confirmed the phosphorylation sites in the intact protein, and we have investigated the role of phosphorylation in the regulatory activity of PLM using oocyte expression experiments. We found: (1) the cytoplasmic domain is not essential for inducing currents in oocytes; (2) co-expression of PKA increased the amplitude of oocyte currents and the amount of PLM in the oocyte membrane largely, but not exclusively, through phosphorylation of S68; (3) co-expression of PKA had no effect on a PLM mutant in which all putative phosphorylation sites had been inactivated by serine to alanine mutation (SSST 62, 63, 68, 69 AAAA); (4) co-expression of PKC had no effect in this system; (5) co-expression of NIMA kinase increased current amplitude and membrane protein level, but did not require PLM phosphorylation. These findings point to a role for phosphorylation in the function of PLM.

Amino Acid Sequence↗

PubMed1999

Characterization of [3H]-heparin binding in human vascular smooth muscle cells and its relationship to the inhibition of DNA synthesis.

1. The glycosaminoglycan heparin inhibits vascular smooth muscle cell (VSMC) proliferation and migration, but the mechanism of its antiproliferative action remains unclear. Heparin has been reported to bind to high affinity cell surface sites on animal VSMC before undergoing receptor mediated endocytosis resulting in signal transduction into the cytoplasm and modulation of genes involved in proliferation. In this study, we have characterized the binding of [3H]-heparin to human saphenous vein-derived VSMC and examined whether there is any relationship between the affinity of [3H]-heparin binding and the inhibitory effect of heparin and its structural analogues on DNA synthesis. 2. At 4 degrees C [3H]-heparin binding to human VSMC occurred in a specific, time and concentration-dependent manner and was not influenced by the removal of calcium ions. Binding of the ligand appeared to occur to the cell surface and was both saturable and reversible. Kinetic and steady state data indicated a single class of binding sites. 3. The pharmacology of [3H]-heparin binding was examined in displacement studies using unlabelled heparin and structural analogues. A comparison of the rank potencies of heparin, heparan sulphate fraction II, low molecular weight heparin and trehalose octasulphate showed that there was a marked discrepancy between their estimated affinities in the binding assays and their effect on DNA synthesis. 4. In summary, we have characterized the heparin binding site on human saphenous vein-derived VSMC. Our findings suggest that the action of heparin and its analogues on DNA synthesis does not simply reflect an interaction with the cell-associated heparin binding site defined in these studies, but may also be determined by the internalization and metabolism of the glycosaminoglycan(s).

Anticoagulants↗

PubMed1999

Protein kinase C co-expression and the effects of halothane on rat skeletal muscle sodium channels.

1. Voltage-gated Na channels, which are potential targets for general anaesthetics, are substrates for PKC, which phosphorylates a conserved site in the channel inactivation gate. We investigated the idea that PKC modulates the effect of volatile anaesthetics on Na channels via phosphorylation of this inactivation gate site. 2. Na currents through rat skeletal muscle Na channel alpha-subunits expressed in Xenopus oocytes were measured by two-microelectrode voltage clamp in the presence of the volatile anaesthetic agent halothane (2-bromo-2-chloro-1,1,1-trifluroethane). PKC activity was modulated by co-expression of a constitutively active PKC alpha-isozyme. 3. Halothane (0.4 mM) had no effect on Na currents. With co-expression of PKC, however, halothane dose-dependently enhanced the rate of Na current decay and caused a small, but statistically significant reduction in Na current amplitude. 4. The enhancement of Na current decay was absent in a Na channel mutant in which the inactivation gate phosphorylation site was disabled. Effects of halothane on amplitude were independent of this mutation. 5. Co-expression of a PKC alpha-isozyme permits an effect of halothane to hasten current decay and reduce current amplitude, at least in part through interaction with the inactivation gate phosphorylation site. We speculate that the interaction between halothane and Na channels is direct, and facilitated by PKC activity and by phosphorylation of a site in the channel inactivation gate.

Anesthetics, Inhalation↗

PubMed1999

Coeliac disease in adults: variations on a theme.

In childhood, coeliac disease (gluten enteropathy) tends to show itself with failure to thrive and growth retardation; in adult life with malabsorption syndromes. We report six cases in adults who presented atypically, with features including clotting disorder, hypoglycaemia, weight loss, anaemia and angina pectoris, all of which responded to gluten withdrawal.

Aged↗

PubMed1998

Vein graft stenosis and the heparin responsiveness of human vascular smooth muscle cells.

BACKGROUND: Vascular smooth muscle cell (VMSC) proliferation is an essential component of myointimal hyperplasia, which is implicated in the failure of 30% to 50% of vascular interventions, such as coronary angioplasty and peripheral vein grafting. We have shown that cells derived from stenotic lesions in infrainguinal vein grafts were significantly more resistant than controls to growth inhibition by heparin. METHODS AND RESULTS: In a prospective study, we correlated antiproliferative responses to heparin in vitro with graft patency after 1 year. Sixty-two patients with infrainguinal vein grafts were entered into a graft surveillance program for > or = 1 year. At operation, saphenous vein segments were explanted for VSMC culture. Cell proliferation in response to fetal calf serum was later determined in the presence and absence of heparin. In 35 cell cultures, including 13 from the above-mentioned patients, [3H]heparin binding was also estimated. VSMCs from patients with patent grafts were significantly more sensitive to growth inhibition by heparin than cells from patients with stenoses (median, 54% versus 20.9%, P<0.001), and [3H]heparin binding was strongly correlated with inhibition of proliferation (r=0.81). CONCLUSIONS: Responsiveness to heparin in cultured VSMCs is a strong predictor of outcome for infrainguinal vein grafts, and reduced sensitivity to heparin is correlated with decreased heparin binding. Relative resistance to the antiproliferative action of heparin may be a marker for aberrant regulation of VSMC growth.

Adult↗

PubMed1998

Gene therapy with HSP72 is neuroprotective in rat models of stroke and epilepsy.

Brain areas damaged by stroke and seizures express high levels of the 72-kd heat shock protein (HSP72). Whether HSP72 represents merely a marker of stress or plays a role in improving neuron survival in these cases has been debated. Some induced tolerance experiments have provided correlative evidence for a neuroprotective effect, and others have documented neuroprotection in the absence of HSP72 synthesis. We report that gene transfer therapy with defective herpes simplex virus vectors overexpressing hsp72 improves neuron survival against focal cerebral ischemia and systemic kainic acid administration. HSP72 overexpression improved striatal neuron survival from 62.3 to 95.4% in rats subjected to 1 hour of middle cerebral artery occlusion, and improved survival of hippocampal dentate gyrus neurons after systemic kainic acid administration, from 21.9 to 64.4%. We conclude that HSP72 may participate in processes that enhance neuron survival during transient focal cerebral ischemia and excitotoxin-induced seizures.

Animals↗

PubMed1998

Low-dose heparin appears safe and can eliminate protamine use for carotid endarterectomy.

OBJECTIVE: To determine the morbidity associated with carotid endarterectomy (CEA) when low doses of heparin (30 U/kg) are used for anticoagulation. This technique eliminates the need for protamine and its potentially deleterious effects on some patients. DESIGN: A retrospective chart review. SETTING: A large academic medical center. PARTICIPANTS: The records of 420 consecutive CEAs in 337 patients (83 bilateral procedures). INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: The amount of heparin used was less than that used in most reported studies. Eighty-two percent of patients received only 2,000 U of heparin for their entire operation (range, 500 to 3,000 U). Complication rates were low. Neurologic complications included a 0.95% incidence of nonfatal stroke and a 2.1% incidence of transient neurologic deficits that resolved in the first day. There was no mortality. The wounds were described in the postoperative period as dry (96%), swollen (3%), or bloody (1%). No patients received protamine. CONCLUSION: The use of 5 to 10,000 U of heparin will provide anticoagulation for more than an hour. In CEA surgery, anticoagulation for this duration is often unnecessary. A smaller dose of heparin (30 U/kg) can provide adequate anticoagulation for this procedure while eliminating the potentially deleterious effects of protamine use. No additional morbidity was attributed to this technique.

Anticoagulants↗

PubMed1998

Intravenous lidocaine speeds the return of bowel function, decreases postoperative pain, and shortens hospital stay in patients undergoing radical retropubic prostatectomy.

UNLABELLED: Postoperative ileus is a concern among surgical patients. Epidural anesthesia and analgesia with local anesthetics can decrease the duration of ileus. Significant systemic absorption of local anesthesia occurs during epidural use. In this study, we examined whether many of the beneficial effects on bowel function seen with epidural lidocaine are also present when the drug is given parenterally. Forty patients undergoing radical retropubic prostatectomy were studied with one half of the patients receiving a lidocaine bolus (1.5 mg/kg) and infusion (3 mg/min, unless weight <70 kg, then 2 mg/min); the other half received a saline infusion. A blind observer recorded the patient's daily pain score, the time the patient first experienced flatulence and had the first bowel movement, and the total use of analgesics. Lidocaine-treated patients first experienced flatulence in a significantly shorter time (P < 0.01) than control patients. Lidocaine patients' hospital stay was also significantly shorter (P < 0.05); on average, they spent 1.1 fewer days in the hospital. I.V. lidocaine initiated before anesthesia and continued 1 h postoperatively significantly sped up the return of bowel function. Lidocaine patients were also more comfortable postoperatively. Many of the bowel function benefits attributed to epidural lidocaine are also present when the drug is administered parenterally. Additionally, the length of hospital stay was reduced in lidocaine-treated patients. IMPLICATIONS: This study prospectively examined whether I.V. lidocaine could affect the return of bowel function after radical prostate surgery. Lidocaine-treated patients had shorter hospital stays, less pain, and faster return of bowel function. In this population, lidocaine infusion can be a useful adjunct in anesthetic management.

Gastrointestinal Motility↗