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Biomedical subjects

L S Sun

Publications and source records attributed to L S Sun.

At least 19 recordsLinked to original sources
PubMed2000

Perinatal cocaine exposure impairs myocardial beta-adrenoceptor signaling in the neonatal rat.

UNLABELLED: Cardiac dysfunction occurs in infants with prenatal cocaine exposure, and gestational cocaine exposure induces presynaptic and postsynaptic changes in the central monoaminergic receptor pathways. The hypothesis of this study is that prenatal cocaine exposure adversely affects the peripheral adrenergic receptor (betaAR) signaling pathway in the neonatal rat heart. Timed pregnant rats received daily intragastric treatment with saline or cocaine 20 mg/kg or 60 mg/kg from Gestational Day 2 until parturition. After birth, nursing mothers either continued to receive the same treatment or received no treatment. Adenylyl cyclase activity, betaAR density, and the amount of immunoreactive G proteins were measured in myocardial membranes obtained from the offspring on Postnatal Day 1 or 7. On Postnatal Day 1, prenatal cocaine exposure increased the betaAR number but did not affect isoproterenol-stimulated adenylyl cyclase activity. On Postnatal Day 7, perinatal cocaine exposure significantly attenuated isoproterenol-stimulated adenylyl cyclase activity in the absence of betaAR up-regulation. Prenatal cocaine exposure also significantly increased Gi protein and reduced GTP-stimulated adenylyl cyclase activity in Postnatal Day 1 cocaine (20 mg/kg) pups compared with saline (P < 0.05). Therefore, perinatal cocaine exposure impaired the myocardial betaAR-cAMP signaling pathway during the first week of postnatal life in the rat. IMPLICATIONS: This study shows that maternal cocaine use during pregnancy impairs the beta-adrenoceptor signaling pathway in the rat during the first week of life. Abnormal cardiac function in the cocaine-exposed neonate may be related to a defect in beta-adrenoceptors, because they regulate cardiac function.

Adenylyl Cyclases↗
PubMed2000

Incidence of atrial fibrillation after mild or moderate hypothermic cardiopulmonary bypass.

OBJECTIVES: Atrial fibrillation remains a significant source of morbidity after coronary artery bypass grafting (CABG). Whether cardiopulmonary bypass (CPB) temperature influences the occurrence of postoperative atrial fibrillation in CABG patients has not been specifically examined. In the present study, we reviewed postoperative data from patients who were prospectively randomized to mild or moderate hypothermic CPB for elective CABG to determine the incidence of postoperative atrial fibrillation. DESIGN: Randomized, single center, observational study. SETTING: Tertiary university medical center. PATIENTS: Adults undergoing elective CABG surgery. INTERVENTIONS: Enrolled patients were prospectively randomized to mild (34 degrees C [93.2 degrees F]) or moderate (28 degrees C [82.4 degrees F]) hypothermic CPB. MEASUREMENTS AND MAIN RESULTS: The incidence of postoperative atrial fibrillation was determined by review of ICU and hospital records. There was a significantly higher incidence of atrial fibrillation in the moderate compared with the mild hypothermic CPB group. Patients who had postoperative atrial fibrillation were significantly older than those without atrial fibrillation. Furthermore, a significant increase in the relative risk of developing postoperative atrial fibrillation was found for both age and CPB temperature. CONCLUSIONS: Our results indicate that the temperature of systemic cooling during CPB is an important factor in the development of atrial fibrillation after CABG surgery. In addition, this study confirms that increasing age is a significant determinant of postoperative atrial fibrillation.

Adult↗
PubMed1999

Regulation of myocardial beta-adrenergic receptor function in adult and neonatal rabbits.

beta-Adrenergic receptor (betaAR) desensitization is the decrease in response following sustained agonist stimulation by catecholamines. While developmental changes in betaAR response have been well documented in the mammalian heart, much less is known regarding the regulation of betaAR function in immature hearts. The purpose of the present study was to determine whether there are developmental differences in myocardial betaAR desensitization. We used an isolated heart preparation to examine the betaAR-mediated inotropic response before and after sustained exposure to 1 microM isoproterenol in adult and neonatal rabbits. We also assayed the adenylyl cyclase activity and performed radioligand-binding studies to determine betaAR characteristics in adult and neonatal ventricular tissues with and without exposure to isoproterenol. Both adult and neonatal rabbit hearts showed a concentration-dependent increase in systolic function, namely, isovolumic left ventricular developed pressure (LVDP) and maximal positive dP/dt of LVDP (dP/dt(max)) in response to isoproterenol. Adults, however, showed a significantly greater response than neonates. After sustained exposure to isoproterenol, the subsequent betaAR-mediated responses in LVDP and dP/dt(max) were significantly attenuated in adults, but much less so in neonates. The adenylyl cyclase activity in response to isoproterenol was significantly different between adult, but comparable in neonatal tissues both exposed or not to isoproterenol. The total betaAR density was higher in neonatal than in adult tissues without isoproterenol exposure, but there was no significant change in betaAR density in either group following isoproterenol exposure. In addition, isoproterenol exposure increased the amount of the inhibitory G protein in adult, but not neonatal tissues. Our results suggest that there were developmental differences in myocardial betaAR functional responses in betaAR desensitization.

Adenylyl Cyclases↗
PubMed1998

Characterization of the alpha1-adrenergic chronotropic response in neuropeptide Y-treated cardiomyocytes.

The cardiac alpha1-adrenergic chronotropic response changes from stimulatory to inhibitory post-natally. The mature inhibitory response is mediated by the alpha1B-adrenoceptor and a pertussis toxin sensitive G protein. In vivo and in vitro studies identify sympathetic innervation as critical for the maturation of this inhibitory response. Additional experiments in a culture model indicate the effect of innervation is dependent on neurally released neuropeptide Y. The present study establishes that the individual signaling elements in the neuropeptide Y induced alpha1-adrenergic cascade are the same as those appearing during normal in vivo development. In addition, the data demonstrate that the effect of neuropeptide Y does not result from activation of the putative cardiac Y3 neuropeptide Y receptor subtype, since it is reproduced by the peptide fragment neuropeptide Y-(13-36) but not by [Leu31, Pro34]neuropeptide Y.

Animals↗
PubMed1998

Tracheobronchial anomalies in children with congenital cardiac disease.

OBJECTIVE: To perform preoperative airway evaluations, using radiographic analysis, to review the tracheal anatomy in children with congenital cardiac disease. DESIGN: Prospective. SETTING: A university children's hospital. PARTICIPANTS: One hundred patients. MEASUREMENTS AND MAIN RESULTS: One magnified airway film (high kilovoltage filtered) was performed preoperatively on 100 consecutive children presenting for repair of congenital cardiac disease. Events at intubation, with respect to endotracheal tube size (internal diameter in millimeters) and difficulties with placement of the tube, were recorded. Postoperative morbidity, specifically related to underlying airway anomaly, was documented. Eleven children had positive radiographic findings after review of magnified airway films. Six of 11 patients had evidence of tracheobronchial pathology, and five patients had no tracheal pathology. Difficulties with intubation were noted in two children. No perioperative morbidity was noted in any patient. CONCLUSION: The use of preoperative magnified airway films for tracheal evaluations in children with cardiac disease should be considered.

Child↗
PubMed1998

Exposure to environmental tobacco smoke and the risk of adverse respiratory events in children receiving general anesthesia.

BACKGROUND: Exposure to environmental tobacco smoke is associated with detrimental effects on pulmonary function in children. The authors investigated the relation between airway complications in children receiving general anesthesia and the passive inhalation of tobacco smoke. METHODS: Six hundred two children scheduled to receive general anesthesia were enrolled in this prospective study. The anesthesiologist and the recovery room nurse, unaware of the smoke exposure history, recorded the occurrence of airway complications. A history of passive smoking was assessed by measuring the urinary concentration of the major nicotine metabolite cotinine and by questionnaire. RESULTS: Airway complications occurred in 42% of the patients with urinary concentrations of cotinine > or =40 ng/ml, in 33% of the patients with concentrations of cotinine between 10.0 and 39.9 ng/ml, and in 24% of the patients with concentrations of cotinine < 10 ng/ml (P = 0.01 for the trend among the three groups). The gender of the child (P = 0.001) and the educational level of the child's mother (P = 0.0008) significantly modified the effect of the concentration of cotinine on the incidence of adverse respiratory events. CONCLUSIONS: There is a strong association between passive inhalation of tobacco smoke and airway complications in children receiving general anesthesia. The relationship is greatest for girls and for those whose mothers have a lower level of education. Passive smoking should be regarded as a risk factor in children undergoing general anesthesia.

Anesthesia, General↗
PubMed1998

Gender differences in pain sensitivity and responses to analgesia.

Variations in pain sensitivity between men and women have been reported in numerous studies. Women have more severe and longer lasting pain than men. The goal of this review is to summarize the current state of knowledge with respect to the sexual dimorphism of surgical pain and its management. This assessment excludes gender-specific pain conditions that are exclusively found in women (e.g., labor pain and surgical pain related to gynecologic procedures), focusing instead on those pain conditions that are common to men and women.

Analgesics, Opioid↗
PubMed1997

Plasma neuropeptide Y and catecholamines in pediatric patients undergoing cardiac operations.

OBJECTIVE: Our objective was to assess the sympathoadrenal response in pediatric patients undergoing repair of congenital cardiac defects. METHODS: Plasma catecholamine (norepinephrine and epinephrine) and neuropeptide Y concentrations were quantified before and after cardiopulmonary bypass to assess the response to cardiopulmonary bypass. To determine the response to aortic occlusion, levels of plasma catecholamines and neuropeptide Y were measured at the time of and immediately after release of the aortic crossclamp. RESULTS: During cardiopulmonary bypass, no significant change in levels of plasma norepinephrine (n = 43), epinephrine (n = 37), or neuropeptide Y (n = 46) was observed. Aortic occlusion induced a significant increase in plasma neuropeptide Y, but not in catecholamines. There was a greater increase in plasma neuropeptide Y in children older than age 1 year than in those younger than 1 year. CONCLUSIONS: Plasma neuropeptide Y may be a useful marker of sympathetic nervous system activity. Children younger than age 1 year showed a lesser sympathetic response compared with the response in older children.

Adolescent↗
PubMed1997

Sympathetic response during cardiopulmonary bypass: mild versus moderate hypothermia.

OBJECTIVE: To determine the sympathetic response during cardiopulmonary bypass at mild (34 degrees C) and moderate (28 degrees C) hypothermia. DESIGN: A randomized study. SETTING: Tertiary university hospital. PATIENTS: Adults undergoing elective coronary artery bypass graft surgery. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Plasma norepinephrine, epinephrine, and neuropeptide Y concentrations were measured. Moderate, but not mild, hypothermic cardiopulmonary bypass evoked a significant sympathetic response with increases in plasma norepinephrine and neuropeptide Y concentrations. A significantly higher incidence of postoperative atrial fibrillation was also observed in the moderate hypothermic compared with the mild hypothermic group. CONCLUSIONS: Our results indicate that the degree of hypothermia significantly influences the sympathetic response during cardiopulmonary bypass. The higher incidence of postoperative atrial fibrillation in the moderate hypothermic group suggests that the enhanced sympathetic response might be one contributing factor in the development of atrial fibrillation.

Aged↗
PubMed1997

Right ventricular infundibular beta-adrenoceptor complex in tetralogy of Fallot patients.

Patients with tetralogy of Fallot may have episodes of paroxysmal hypoxic spells ("tet spells") or could be asymptomatic. In patients who have these episodes, treatment with a beta-adrenoceptor (betaAR) blocking agent can often ameliorate or attenuate the severity of the symptoms. Additionally, excitement, crying, and situations associated with increased sympathetic activity could provoke the occurrence of these hypoxic spells. We hypothesized that altered myocardial betaAR function may contribute to the development of paroxysmal hypoxic spells in the symptomatic tetralogy patient. Surgically excised right ventricular infundibular myocardial specimens from symptomatic (patients with spells) and asymptomatic patients were used to determine total beta1 and beta2 betaAR density and betaAR adenylyl cyclase activity. Symptomatic patients had a significantly greater number of total betaAR. The relative proportion of beta1 and beta2 receptors was comparable in both patient groups. betaAR-stimulated adenylyl cyclase activity was found to be more enhanced in the symptomatic patient group. Our results indicate that infundibular betaARs may play a role in the development of paroxysmal hypoxic spells.

Adenylyl Cyclases↗
PubMed1996

The association of tracheal anomalies and tetralogy of Fallot.

OBJECTIVE: To determine the incidence of tracheal anomalies in children with tetralogy of Fallot. DESIGN: Retrospective. SETTING: A university children's hospital. PARTICIPANTS: Forty-four children with the diagnosis of tetralogy of Fallot who underwent either primary or palliative cardiac surgery. MEASUREMENTS AND MAIN RESULTS: Three criteria were used to identify tracheal abnormalities: (1) direct laryngoscopic evidence; (2) radiographic evidence; and/or (3) inability to intubate the trachea with an endotracheal (ET) tube of appropriate size for age, followed by insertion of a 2.5-mm ET tube. An 11% incidence (5/44) of tracheal anomalies was noted. These could be separated into two categories: isolated upper airway pathology (either glottic or subglottic stenosis) and lower tracheal pathology. None of the five children identified with tracheal abnormalities manifested any preoperative signs or symptoms suggestive of airway problems. Four of the children experienced significant perioperative complications resulting directly from the underlying tracheal pathology. This represented a 9% morbidity (4/44) for patients presenting for repair of tetralogy of Fallot. CONCLUSIONS: A significant incidence of tracheal anomalies is associated with tetralogy of Fallot, leading to potential perioperative complications.

Humans↗
PubMed1996

Perioperative lymphocyte adenylyl cyclase function in the pediatric cardiac surgical patient.

OBJECTIVE: To examine intraoperative and postoperative lymphocyte adenylyl cyclase activities in children undergoing repair of congenital cardiac defects with hypothermic cardiopulmonary bypass. DESIGN: A prospective study. SETTING: Tertiary university pediatric hospital. PATIENTS: Twelve children were enrolled into the study to examine intraoperative lymphocyte adenylyl cyclase activities and 12 children were enrolled to examine postoperative lymphocyte adenylyl cyclase activities. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Basal (unstimulated), isoproterenol, and prostaglandin E-1 stimulated adenylyl cyclase activities, and plasma norepinephrine and epinephrine concentrations were measured. Intraoperative basal (unstimulated), beta-adrenergic receptor-stimulated (in response to isoproterenol), and prostaglandin E1 (PGE1)-stimulated lymphocyte adenylyl cyclase activities all increased during cardiopulmonary bypass, then decreased immediately after cardiopulmonary bypass. In the postoperative group, a significant decrease in basal (unstimulated), beta-adrenergic receptor- and PGE1-stimulated adenylyl cyclase activities were observed on postoperative day 1 as compared with precardiopulmonary bypass values. CONCLUSIONS: In the pediatric cardiac surgical patient, there was an intraoperative enhancement of lymphocyte adenylyl cyclase activities. This increase in adenylyl cyclase activities was followed by reduced lymphocyte adenylyl cyclase activities, including beta-adrenergic receptor desensitization, postoperatively, as we have previously documented in adults.

Adenylyl Cyclases↗
PubMed1996

Muscarinic receptor heterogeneity in neonatal rat ventricular myocytes in culture.

Carbachol increased ventricular automaticity in a concentration-dependent fashion from a control rate of 72 +/- 5 (mean +/- SEM) to 86 +/- 4 beats per minute at 10(-4) M carbachol. Pirenzepine, an M1-selective antagonist, and AFDX 116, an M2-selective antagonist, both at 10(-7) M, did not block the carbachol-induced positive chronotropic response. In contrast, 10(-7) M HHSiD, an M3-selective antagonist, completely blocked the positive chronotropic effect of carbachol. Carbachol stimulated the accumulation of IP1 in a concentration-dependent manner at concentrations > or = 3 x 10(-6) M. AFDX 116 had no effect on carbachol-induced IP1 accumulation. HHSiD significantly inhibited IP1 accumulation at concentrations > or = 3 x 10(-8) M, while pirenzepine inhibited IP1 accumulation only at concentrations > or = 10(-5) M. McN A343 and methacholine, two muscarinic receptor agonists with minimal M2 activities, and carbachol did not alter basal cAMP concentration, but all three agonists significantly attenuated the increase in cAMP accumulation in response to isoproterenol. Carbachol inhibited isoproterenol-mediated cAMP accumulation at concentrations > or = 10(-7) M. AFDX 116, HHSiD, and pirenzepine blocked the carbachol-induced inhibition of isoproterenol-stimulated cAMP accumulation. At equimolar concentrations, the inhibitory effects of HHSiD and AFDX-116 were similar, while that of pirenzepine was much less. Pretreatment with pertussis toxin for 24 h did not prevent the carbachol-mediated positive chronotropic response or accumulation of IP1 but completely abolished the inhibition of isoproterenol-stimulated cAMP accumulation. These results indicate that (a) neonatal ventricular myocytes in culture have a heterogeneous population of muscarinic (M2 and M3) receptors, (b) the M3 receptor is coupled to pertussis toxin-sensitive and pertussis toxin-insensitive G proteins, (c) M3 receptor stimulation activates phosphoinositide hydrolysis and increases automaticity via a pertussis toxin-insensitive G protein-dependent pathway, and (d) both M2 and M3 receptors couple to pertussis toxin-sensitive G protein(s) to mediate the inhibition of intracellular cAMP accumulation in response to isoproterenol stimulation.

Animals↗
PubMed1996

Effect of procainamide on pulmonary thromboembolism and platelet malondialdehyde in mice.

AIM: To study the effect of procainamide (PA) on pulmonary thromboembolism, platelet malondialdehyde (MDA) level and platelet aggregation induced by collagen and adrenaline. METHODS: Pulmonary thromboembolism, 2-thiobarbituric acid fluorescence micro-determination, conventional microscopic counting, and platelet aggregation test were used. RESULTS: PA (10-20 mg.kg-1) and mannitol (200 mg.kg-1) reduced thrombosis by 30%-75% and 75%, respectively. Thrombocytopenia followed thrombosis increased after the pretreatment of PA and mannitol. MDA decreased by both of them in vivo. In vitro, PA inhibited platelet aggregation and MDA production induced concentration-dependently by collagen and adrenaline. CONCLUSION: Inhibition of PA on pulmonary thromboembolism is involved in the decrease of platelet aggregation and MDA production.

Animals↗
PubMed1995

Influence of 3,4',5-trihydroxystibene-3-beta-mono-D-glucoside on vascular endothelial epoprostenol and platelet aggregation.

AIM: To study the relationship between the inhibiting effect on platelet aggregation and the enhancing effect on epoprostenol (PGI2) released from vascular endothelium with 3,4',5-trihydroxystibene-3-beta-mono-D-glucoside (polydatin, Pol). METHODS: After having been incubated with Pol, the incubating medium was withdrawn from the bottles with newborn umbilical vein endothelial cells (VEC group, trypsin digesting method) and added to the platelets (washing method). The medium withdrawn from the bottles without VEC was designated as control group. Reduction of platelet aggregation rates (PAR, turbidity method) and changes of 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha) and thromboxane B2 (TXB2) (radioimmunoassay method) in the supernatant of the aggregated platelets induced by thrombin were scrutinized. RESULTS: PAR in the control group showed no reduction, whereas PAR reduction (-10 +/- 10) and 6-keto-PGF1 alpha increase (108 +/- 30 ng.L(-1)) in the VEC group treated 10 min with Pol 0.41 mmol.L(-1) (vs that of distilled water, ie, 2 +/- 12 and 54 +/- 20 ng.L(-1)) occurred. CONCLUSION: Increase of PGI2 from VEC by Pol was involved in its (Pol's) inhibition effect of platelet aggregation.

6-Ketoprostaglandin F1 alpha↗
PubMed1994

An excitatory muscarinic response in neonatal rat ventricular myocytes and its modulation by sympathetic innervation.

Previously, we demonstrated that low concentrations of acetylcholine (< or = 10(-9) M) increased automaticity in neonatal but not in adult rat ventricular myocardium. In the present study, we used cultured neonatal rat ventricular myocytes grown alone or in the presence of dissociated sympathetic neurons as an experimental model to study the ontogeny of the muscarinic response. McN A343 (< or = 10(-9) M), an M1 selective agonist, increased spontaneous rate from 51 +/- 4 to 56 +/- 5 beats per minute (bpm), and this excitatory response was blocked by 10(-9) M pirenzepine, an M1 selective antagonist, but not by the M2 selective antagonist AFDX-116, nor by the alpha 1 adrenergic antagonist prazosin and the beta adrenergic antagonist propranolol (all 10(-7) M) In innervated myocytes, McN A343 also increased rate from 48 +/- 6 to 55 +/- 6 bpm. However, this effect was blocked by either 10(-9) M pirenzepine or 10(-7) M propranolol. After pretreatment with 10 ng/ml of pertussis toxin, the McN A343-induced excitatory response in non-innervated myocytes was absent, thus suggesting that this response involved a pertussis toxin-sensitive G protein dependent pathway. McN A343 failed to stimulate inositol phosphate or cAMP accumulation in non-innervated myocytes. These results demonstrate the following. (1) The muscarinic excitatory response is mediated via direct stimulation of a post-synaptic M1 receptor in non-innervated myocytes. (2) The excitatory response after innervation is related to the release of catecholamines, possibly through activation of muscarinic receptors located at the pre-synaptic sympathetic nerve terminals. (3) Sympathetic innervation prevents the functional expression of the post-synaptic myocardial M1 receptor. (4) The intracellular pathway for the post-synaptic M1 excitatory response involves a pertussis toxin-sensitive G protein, but does not depend on obvious changes in cAMP or phosphoinositide hydrolysis.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗