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C S Lin

Publications and source records attributed to C S Lin.

At least 19 recordsLinked to original sources

Voluntary contraction impairs the refractory period of transmission in healthy human axons.

1. Voluntary contraction of a muscle causes substantial hyperpolarization of the active motor axons due to activation of the electrogenic Na+-K+ pump. The present study was undertaken to determine whether voluntary effort produces a significant impairment in impulse transmission in normal axons and whether mechanisms other than membrane hyperpolarization contribute to the changes in axonal excitability. 2. The compound muscle action potential (CMAP) was recorded after median nerve stimulation at the wrist using sub- and supramaximal stimuli, delivered singly and in pairs at conditioning-test intervals of 2-15 ms. Axonal excitability parameters (threshold, refractoriness, supernormality, and strength-duration time constant (tauSD)) were measured using threshold tracking. Impulse transmission was assessed using supramaximal stimuli. 3. Maximal voluntary contractions of the abductor pollicis brevis for 1 min produced a substantial increase in threshold, an increase in supernormality and a decrease in tauSD, all of which lasted approximately 10 min and indicate axonal hyperpolarization. However, immediately after the contraction there was an unexpected increase in refractoriness. The post-contraction increase in refractoriness could not be mimicked by an imposed ramp of hyperpolarization that produced changes in the other indices to an extent that was similar to voluntary contraction. 4. The contraction had relatively little effect on the size of the unconditioned maximal CMAP. However, there was failure of transmission of supramaximal conditioned volleys when the conditioning-test interval was short. 5. The relationships between axonal excitability and supernormality and tauSD following voluntary contraction differed significantly from those recorded during the hyperpolarization produced by DC current. It is argued that these differences probably result from extra-axonal K+ accumulation with the voluntary contraction but not with the DC polarization. I6. It is concluded that, following maximal voluntary contraction of a normal muscle, the refractory period of transmission is impaired distal to the stimulus site sufficient to cause transmission failure of the second of a pair of closely spaced impulses. The site of transmission failure is likely to be the terminal axon, presumably at branch points, possibly in the unmyelinated pre-terminal segment.

Action Potentials↗

Insulin-like growth factor-I promotes proliferation and migration of cavernous smooth muscle cells.

To better understand the physiology of cavernous smooth muscle cells (CSMC), particularly their regulation by IGF-I, we isolated CSMC from rats of various ages and grew them as cell cultures. CSMC from very young (1 week of age) and very old (28 months of age) rats secreted the least amounts of IGF-I, and those from 16-week-old rats the most. IGF-I stimulated growth of CSMC at an optimal concentration of 12.5 ng/ml. At this concentration, CSMC from 11-week-old rats showed the highest growth rate and CSMC from 28-month-old rats showed the lowest. The optimal IGF-I concentration for migration of CSMC was 10 ng/ml. At this concentration, CSMC from 4-week-old rats showed the highest migratory rate and CSMC from 28-month-old rats showed the lowest. IGF-I also stimulated VEGF secretion from CSMC at an optimal concentration of 10 ng/ml. At this concentration, CSMC from 16-week-old rats secreted VEGF the most and CSMC from 28-month-old rats secreted the least. The expression levels of IGF-IR paralleled the IGF-I-regulated growth rates of these cells. Expression of IGF-IR was identified in the cavernous smooth muscle and the urethra epithelium of the penis.

Aging↗

Identification and regulation of human PDE5A gene promoter.

PDE5A gene encodes type 5 phosphodiesterase (PDE5), the principal cGMP-catalyzing enzyme in the penis and the primary target of sildenafil (Viagra). We have isolated a 3.7-kb DNA fragment that contains the human PDE5A gene promoter. The DNA fragment contains a sequence of 234 nucleotides at its 3' end that corresponds to most of the untranslated region of the PDE5A1 mRNA. The remaining 3.5-kb upstream flanking sequence contains no apparent TATA box but has several sequences that resemble binding sequences for transcription factors such as androgen receptor (AR), AP1, AP2, AP4, Sp1, MyoD, Myc, and CArG. In search of promoter activities, we used a luciferase reporter system to examine 10 DNA fragments that cover various regions of the 3.7-kb fragment. We found that a full basal promoter activity was confined to a 139-bp region that includes 78 bp of the PDE5A1-specific first exon. A lesser basal promoter activity was still detectable in a 94-bp fragment that contains the same 78-bp PDE5A1-specific exon plus 16 bp of upstream sequence. Either the 139-bp or the 94-bp promoter fragment responded minimally to cAMP or cGMP (2 mM) stimulation. Longer fragments that contain either a 308-bp 5' extension (from the 138-bp fragment) or a 156-bp 3' extension (all exon sequence) responded at higher levels to cAMP and cGMP stimulation. The 5' and 3' extensions cooperated with each other to provide the highest level of responses to cAMP and cGMP stimulation. DNase I footprint analysis identified four AP2- and two Sp1-binding sites in the 5' extension and four Sp1-binding sites in the 3' extensions. Cyclic AMP and cGMP had similar stimulatory effects on the PDE5A promoter.

3',5'-Cyclic-GMP Phosphodiesterases↗

Regulation of human PDE5A2 intronic promoter by cAMP and cGMP: identification of a critical Sp1-binding site.

PDE5A gene encodes type 5 phosphodiesterase (PDE5), the principal cGMP-catalyzing enzyme in the penis and the primary target of sildenafil (Viagra). We have previously reported the isolation of three alternatively spliced PDE5A isoforms in humans. We also reported the identification of three corresponding alternative first exons and an intronic promoter in the human PDE5A gene. The intronic promoter is situated upstream from the PDE5A2-specific first exon but downstream from the PDE5A1- and A3-specific first exons. In the current study we showed that the intronic promoter could be upregulated by either cAMP or cGMP. In order to identify possible regulatory elements in the promoter, we created deletion and base-substitution mutants targeting one AP2- and four Sp1-binding sequences. Loss of function of these mutants to bind to the respective transcription factors was verified by DNase I footprint analysis, and changes in promoter function were analyzed with a luciferase reporter system. Mutation of the AP2-binding sequence and deletion of the 3'-most Sp1-binding site (within the exon) had little effects on the basal or the cyclic nucleotide-inducible promoter functions. Mutation of the 5'-most Sp1-binding site had much more severe effects on the basal and the cyclic nucleotide-inducible promoter functions. Mutation of a neighboring site that contains two overlapping Sp1-binding sequences completely nullified the basal and cyclic nucleotide-inducible promoter activities. Thus, the PDE5A2 intronic promoter depends on the overlapping Sp1-binding site for basal and cyclic nucleotide-inducible functions.

3',5'-Cyclic-GMP Phosphodiesterases↗

Differences in accommodative properties of median and peroneal motor axons.

OBJECTIVES: To investigate whether accommodation to depolarising and hyperpolarising currents differs for motor axons of human upper and lower limb nerves. METHODS: The threshold tracking technique was used to measure threshold electrotonus for median and peroneal motor axons. The threshold current that produced a compound muscle action potential 50% of maximum was measured, and membrane potential was altered using subthreshold polarising currents of 330 ms duration but of variable intensity, from +40% (depolarising) to -100% (hyperpolarising) of the unconditioned threshold. RESULTS: The maximal threshold changes (the peak of the S1 phase of threshold electrotonus) were significantly greater in median axons for both depolarising and hyperpolarising currents. The subsequent phases of accommodation to depolarising currents (S2) and to hyperpolarising currents (S3) were also significantly greater in median axons. These findings raised the possibility that greater accommodation (S2 and S3) in median axons resulted from greater changes in membrane potential. However, regression of S2 against S1 to depolarising currents disclosed significantly greater accommodation (27.8%) for median axons, suggesting that slow K(+) conductances may be more prominent on median than peroneal axons. By contrast, the relation between S3 and S1 to hyperpolarising currents was similar for the two nerves, suggesting that the difference in inward rectification was merely because the conductance varies with the extent of hyperpolarisation. CONCLUSIONS: Slow K(+) conductances are more prominent for median motor axons than for peroneal axons. It would therefore be expected that axons innervating the lower limbs have less protection from depolarising stress and could develop ectopic activity more readily.

Action Potentials↗

Accommodation to depolarizing and hyperpolarizing currents in cutaneous afferents of the human median and sural nerves.

To determine whether accommodation to depolarizing and hyperpolarizing stimuli differs for cutaneous afferents in the median and sural nerves, studies were performed in normal human subjects using threshold electrotonus. The changes in threshold for compound sensory action potentials of 50 % of maximum were recorded when the nerves were subjected to long-lasting depolarizing and hyperpolarizing DC. The premise was that the threshold changes largely mirror the underlying electrotonic changes in membrane potential. The maximal threshold changes produced by depolarizing and hyperpolarizing currents were greater for median afferents, suggesting that the DC produced greater changes in membrane potential in these afferents. Median afferents underwent greater accommodation to depolarizing currents than sural afferents and a greater threshold undershoot at the end of the currents, suggesting greater activity of a slow K+ conductance. Median afferents also underwent greater accommodation to hyperpolarizing currents, suggesting greater inward rectification. These conductances are voltage dependent, and the differences in accommodation could be due to greater changes in membrane potential for the median nerve. The changes in threshold produced by long-lasting depolarizing and hyperpolarizing currents of graded intensity were therefore measured. When the threshold changes were matched for the two nerves, median afferents underwent 22.4 % more accommodation to depolarizing currents and 28.7 % more accommodation to hyperpolarizing currents. We conclude that there is greater expression of two internodally located conductances responsible for accommodation on median afferents. The biophysical differences identified in this study might contribute to the finding that sural afferents have a greater tendency to dysfunction than median afferents.

Action Potentials↗

Epstein-barr virus nuclear antigen 2 retards cell growth, induces p21(WAF1) expression, and modulates p53 activity post-translationally.

The Epstein-Barr virus (EBV) nuclear antigen 2 (EBNA2) has been shown to be required for promotion of cell-cycle progression in EBV-immortalized B-lymphocytes. However, other studies have indicated that EBNA2 alone, in the absence of other EBV genes, may retard cell growth. To resolve this discrepancy, we investigated the effect of EBNA2 on the growth of various cells, including EBV target nasopharyngeal carcinoma cells, NPC-TW01 and NPC-TW04. We found that EBNA2 could retard cell growth, in stable Vero, HEp-2, and U2OS cell clones expressing EBNA2, and in Vero, 293, NPC-TW01, and NPC-TW04 cells transiently transfected with EBNA2. While investigating the mechanism underlying the growth-retarding function of EBNA2, we found that EBNA2 induced p21(WAF1) expression in these cells. This induction of p21(WAF1) expression was mediated through p53. EBNA2 was found to stimulate p53 to bind to the p53-response element within the p21(WAF1) promoter, possibly by promoting p53 phosphorylation. This enhancement of p53 sequence-specific DNA-binding activity may be the mechanism through which EBNA2 activates the expression of p53-regulated genes, including p21(WAF1) and mdm-2. Together, these studies reveal a possible intrinsic function of EBNA2 in cell-growth regulation and elucidate a novel mechanism by which EBNA2 modulates transcription.

Animals↗

Ischaemic changes in refractoriness of human cutaneous afferents under threshold-clamp conditions.

1. A technique was developed to counteract the changes in threshold to electrical stimuli of large myelinated cutaneous afferents in the human median nerve induced by ischaemia for 13 min. Intermittent application of polarizing currents was used in five subjects, in whom refractoriness, supernormality and the strength-duration time constant (tauSD) were tracked to determine whether compensating for the ischaemia-induced changes in threshold also controlled the ischaemic changes in these excitability parameters. 2. The threshold compensation prevented the ischaemic changes in tauSD, an excitability parameter dependent on nodal Na+ channels. Threshold compensation did not prevent the changes in refractoriness and supernormality, whether the compensation began 10, 100 or 200 ms prior to the test stimuli. 3. In three subjects, continuous polarizing current was injected for 13 min to compensate for the ischaemic change in threshold, thus clamping threshold at the pre-ischaemic level. Again, tauSD was effectively controlled, but there were still ischaemic changes in refractoriness and supernormality. 4. The effective control of tauSD suggests that both the intermittent threshold compensation and the continuous threshold clamp effectively controlled membrane potential at the node of Ranvier. 5. The ischaemic increase in refractoriness when threshold was kept constant could be due to interference with the processes responsible for refractoriness by a metabolic product of ischaemia. The ischaemic change in supernormality during effective compensation probably results from the intrusion of refractoriness into the conditioning-test intervals normally associated with maximal supernormality. 6. The present results indicate that ischaemia has effects on axonal excitability that cannot be readily explained by changes in membrane potential. Specifically, it is suggested that ischaemic metabolites interfere with the recovery of Na+ channels from inactivation.

Adaptation, Physiological↗

Identification of three alternative first exons and an intronic promoter of human PDE5A gene.

In the accompanying paper we present evidence for the existence of three PDE5A isoforms that differed only in the 5' end of the mRNAs. In this paper we present evidence that the three isoform-specific 5' ends were encoded by three alternative first exons that were arranged in the order of A1-A3-A2. Because the isoform-specific mRNAs could be transcribed from individual promoters, DNA fragments of the two intronic regions (A1-A3 and A3-A2) were tested for possible promoter activities. The intron between A1- and A3-specific exons did not exhibit any promoter activities even in smooth muscle cells that expressed the A3 isoform (see accompanying paper). In contrast, the intron between A3- and A2-specific exons had promoter activities in PDE5A2-expressing COS-7 and smooth muscle cells. This intronic promoter was bound by transcription factors AP-2 and Sp1, but not by AP-1, as shown by DNase I footprint analysis. However, the sequence bound by AP-2 (5'-GGGAAACGCTCGCGGGAGAGTTGG) is unusual in that it bears little resemblance to the consensus AP-2-binding sequence.

3',5'-Cyclic-GMP Phosphodiesterases↗

Expression of three isoforms of cGMP-binding cGMP-specific phosphodiesterase (PDE5) in human penile cavernosum.

Inhibition of cGMP-specific phosphodiesterase type V (PDE5) has been shown to improve penile erection in patients with erectile dysfunction. We report here the cloning of three PDE5 isoforms from human penile tissues. Two of the isoforms were identical to PDE5A1 and PDE5A2, respectively, which had been isolated from nonpenile tissues. The third isoform was novel and hence called PDE5A3. The deduced amino acid sequence of PDE5A3 was the same as the C-terminal 823-residue sequence of PDE5A1 and PDE5A2. While PDE5A1 and A2 isoforms were expressed in all tissues examined, the A3 isoform was confined to tissues with a smooth muscle or cardiac muscle component. When expressed in COS-7 cells, PDE5A1, A2, and A3 isoforms had similar cGMP-catalytic activities with K(m) of 6.2, 5.75, and 6.06 microM, respectively. Their cGMP-catalytic activities were inhibited by zaprinast with IC(50) values of 3.2 microM, 1.3 microM, and 1.6 microM, respectively, and by sildenafil with IC(50) of 28, 14, and 13 nM, respectively.

3',5'-Cyclic-GMP Phosphodiesterases↗

Recovery of excitability of cutaneous afferents in the median and sural nerves following activity.

In acquired polyneuropathies, symptoms and signs are typically distal and symmetrical, more prominent in the lower limbs than the upper limbs. This study was undertaken to measure the extent of the decrease in excitability produced by single impulses and by impulse trains in cutaneous afferents in the median and sural nerves, and to compare the resulting changes in excitability of these afferents. Threshold tracking was used in 10 healthy subjects to measure the changes in threshold for a compound sensory action potential of 50% maximum produced by conditioning stimuli. Following a single supramaximal conditioning stimulus, the threshold changes occurring during the refractory and supernormal periods were identical for the two nerves, but there was a greater increase in threshold during the late subnormal period for median afferents. Following a train of 10 supramaximal conditioning stimuli, threshold increased by approximately 40% for median afferents and by approximately 20% for sural afferents. These differences are consistent with differences in a slow K(+) conductance. It is suggested that the hypo-excitability produced by brief trains of impulses may be sufficient to disturb conduction in diseased nerve fibers, and that the lesser expression of slow K(+) conductances on cutaneous afferents in the sural nerve could render them more sensitive to depolarizing stresses than median afferents. This could be a factor in the ease with which sural afferents become ectopically active in polyneuropathies.

Action Potentials↗

2D CSI proton MR spectroscopy of human spinal vertebra: feasibility studies.

This report focuses on proton magnetic resonance spectroscopy (1H MRS) of spine vertebra acquired with two-dimensional chemical shift imaging (2D CSI), utilizing the stimulated echo acquisition mode (STEAM) sequence. Both validity and reproducibility studies were performed. To validate the 2D CSI method, its spectra were compared with those obtained with the single-voxel (SV) method. Five normal volunteers were scanned. The reproducibility of 2D CSI was examined by performing spectroscopy on two different occasions, on three normal volunteers. Data show that the STEAM 2D CSI technique results in MRI spectra comparable to those obtained with the STEAM SV method. 2D CSI offers significant time savings and convenient multi-voxel spectral analysis at a substantially higher signal-to-noise ratio. The 2D CSI method was then applied to a patient with a small vertebral hemangioma. The results demonstrated that the voxels containing the hemangioma exhibit different spectra than the neighboring voxels of the same vertebra. Additionally, a case of vertebral osteoporosis was investigated. Results showed a significant increase in the lipid-to-water ratio (LWR). It is suggested that 2D CSI may be powerful in identifying physiological as well as pathological changes of the bone marrow. Furthermore, covering a more extensive area of the vertebral body will maximize the chances of depicting a small focus of pathologic tissue. A more detailed bone marrow pattern was noticed in on one subject whose spectra show more lipid peaks.

Adult↗

Excitability properties of median and peroneal motor axons.

Threshold tracking was used to compare excitability properties (stimulus-response curves, strength-duration properties, recovery cycle, and threshold electrotonus) of median motor axons at the wrist and peroneal motor axons at the ankle in 12 healthy subjects. Stimulus-response curves and strength-duration properties were similar, though higher stimulus intensities were required for peroneal axons. However, there were significant differences in the recovery cycle of excitability following a conditioning stimulus and in threshold electrotonus. In the recovery cycle, median axons had significantly greater supernormality and late subnormality. In threshold electrotonus, the initial slow threshold changes in response to subthreshold depolarizing and hyperpolarizing currents (S1) were significantly greater in median axons, and there was also greater accommodation to depolarizing currents (S2) and greater threshold undershoot after depolarization. Similar differences in supernormality and the S1 phase of threshold electrotonus were found between peroneal axons at ankle and knee, suggesting that these properties may be dependent on nerve length. When median motor axons at the wrist were compared with peroneal motor axons at the knee, there were no differences in refractoriness and supernormality and only small differences in S1, but the late subnormality and undershoot were significantly greater in the median axons. These findings suggest that, in addition to any length-dependent differences, peroneal axons have a less prominent slow K(+) conductance. We conclude that the properties of different motor axons are not identical and their responses to injury or disease may therefore differ.

Adult↗

Strength-duration properties and their voltage dependence as measures of a threshold conductance at the node of Ranvier of single motor axons.

In a number of clinical studies, measurement of axonal strength-duration properties has been used to provide indirect insight into conductances at the node of Ranvier, particularly persistent Na(+) conductance. However, the specificity of any changes is limited because other factors can affect strength-duration behavior. The present study was undertaken to define the relationship between different strength-duration measures at rest and at different membrane potentials, and also to determine the limits within which strength-duration behavior can be used as a measure of nodal conductances. The strength-duration time constant (tau(SD)) and rheobase of 20 single motor units in the flexor carpi ulnaris were calculated from thresholds defined using threshold tracking. "True" rheobase and rheobasic latencies were measured using test stimuli of 100-ms duration. For ten units, the technique of latent addition was used to measure threshold changes directly attributable to nodal conductances, and for six units these were compared with strength-duration properties at different membrane potentials. The data indicate that measurements of tau(SD) and rheobase can provide sensitive indicators of conductances present at the node of Ranvier when membrane potential changes. There is a reciprocal relationship between tau(SD) and rheobase for single motor units at different membrane potentials, and this relationship may allow changes in tau(SD) due to depolarization and demyelination to be differentiated.

Action Potentials↗

Magnetic resonance spectroscopy to detect lecithin in amniotic fluid and fetal lung.

BACKGROUND: Proton magnetic resonance spectroscopy is a noninvasive technique that detects molecules within a specified region in vivo. Lecithin, the major component of surfactant, has a characteristic magnetic resonance signal, but to our knowledge, it has never been reported in fetal lung or amniotic fluid (AF). The objective of this study was to characterize the lecithin signal in utero, which could lead to a noninvasive fetal lung maturity test. METHOD: Human fetal lung and AF pockets can be identified and studied with magnetic resonance spectroscopy with the use of a 1.5-tesla Vision whole-body magnetic resonance scanner (Siemens Medical Systems; Erlangen, Germany). Spectroscopy data are collected with a single-voxel-point-resolved spectroscopy sequence. After identification of fetal anatomy with the use of scout magnetic resonance images, magnetic resonance spectroscopy of human fetal lung and AF identifies a lecithin peak. EXPERIENCE: Three healthy gravidas near term were studied and lecithin peaks were identified in all. CONCLUSION: Lecithin can be identified in vivo with the use of volume-selected proton magnetic resonance spectroscopy. Patient comfort and extremely short scan times suggest that refined magnetic resonance spectroscopy might be a safe, quick, and comfortable test of fetal lung maturity.

Amniotic Fluid↗

The effect of pregnancy and delivery on the function and ultrastructure of the rat bladder and urethra.

OBJECTIVE: To examine the effect of pregnancy and delivery on the function and ultrastructure of the bladder and urethra in rats. Material and methods The study comprised six virgin and 18 pregnant rats; both groups underwent cystometry (at the 19th day of gestation, and 2 days and 6 weeks after parturition). Tissues from the bladder and urethra were collected for electron microscopy, western blotting and immunostaining for caveolin-1 and caveolin-3. RESULTS: The bladder capacity was greater and the modified leak-point pressures lower in pregnant and 2-day postpartum rats than in virgin and 6-week postpartum rats. The residual volume was significantly higher in the pregnant group. Electron microscopy showed more sarcolemmal caveolae in the smooth muscle cells of both the bladder and urethra of virgin rats than in the other groups. Lipid droplets and subsarcolemmal mitochondria accumulated in pregnant and 2-day postpartum rats. Caveolin-1 protein was detected in the cytoplasmic membrane of urethra and bladder smooth muscle cells. Caveolin-3 was detected in the membrane of striated muscle in the intrinsic sphincter. Western blotting showed increased caveolin-1 protein expression in the bladder and urethra of 2-day postpartum rats; in contrast, levels of caveolin-1 were lower in pregnant rats than in virgin and 6-week postpartum rats. CONCLUSION: s During pregnancy there was a significant decrease in sarcolemmal caveolae and caveolin-1 in the smooth muscle cells of the rat bladder and urethra. The changes in caveolae and the membrane protein caveolin may play a role in the functional changes associated with pregnancy and after delivery.

Animals↗

Upregulation of L-plastin gene by testosterone in breast and prostate cancer cells: identification of three cooperative androgen receptor-binding sequences.

L-Plastin is normally a leukocyte-specific actin-binding protein; it is also expressed in the majority of human cancer cell lines that are derived from many types of solid tumors. We have previously reported the isolation of the L-plastin gene promoter, in which we identified several potential steroid receptor-binding sequences. We now obtained evidence that L-plastin gene expression was positively regulated by testosterone in androgen receptor (AR)-positive prostate and breast cancer cells. DNase I footprint analysis identified three AR-binding elements (ARE) located in a 545-bp region approximately 1.1 kb upstream from the transcription initiation site. However, each of these three AREs exhibited very little testosterone/AR-responsive enhancer activities toward a test promoter (of the thymidine kinase gene) when tested in MCF-7 breast cancer cells. Their testosterone/AR responsiveness became evident only when two or three of them were combined. In PC-3 prostate cancer cells, cooperation among L-plastin AREs was still evident although individually they had moderate levels of testosterone/AR responsiveness. Thus, the three L-plastin AREs, despite their imperfect sequences compared with the consensus ARE, could cooperate with each other to become a potent testosterone/AR-responsive unit, which was likely responsible for the inducibility of the L-plastin gene by testosterone.

Base Sequence↗

Prophylactic intravenous ondansetron reduces the incidence of intrathecal morphine-induced pruritus in patients undergoing cesarean delivery.

UNLABELLED: Pruritus is a common side effect of intrathecal morphine injection for postoperative pain control. Its incidence is especially high in patients undergoing cesarean delivery. We investigated the effectiveness of ondansetron in preventing intrathecal morphine-induced pruritus in such patients. We included 60 consecutive nonbreastfeeding women who were scheduled for elective cesarean delivery. After the administration of spinal anesthesia with bupivacaine and intrathecal morphine 0.15 mg injection, the patients were randomly divided into three groups. Group 1 received placebo (normal saline) IV injection, Group 2 diphenhydramine 30 mg IV injection, and Group 3 ondansetron 0.1 mg/kg IV injection. The incidence of pruritus was significantly lower in the ondansetron group (25%) when compared with that in the placebo group (85%) and in the diphenhydramine group (80%) (both P < 0.05). The postoperative pain score and time to flatus passage were not significantly different among the three groups. There were no headache or extrapyramidal signs associated with ondansetron use. In conclusion, ondansetron prophylaxis significantly reduced the incidence of intrathecal morphine-induced pruritus in patients undergoing cesarean delivery. IMPLICATIONS: Ondansetron prophylaxis significantly decreases the incidence of pruritus, a common side effect of intrathecal morphine used to treat postcesarean delivery pain.

Adolescent↗