Home About us Contact
|
Home About us Contact | ||
|
|
||
Vulnerable Period (vulnerable + period)
Selected AbstractsAtrial Fibrillation Induction and Determination of Atrial Vulnerable Period Using Very Low Energy Synchronized Biatrial Shock in Normal Subjects and in Patients with Atrial FibrillationPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 4 2000HUNG-FAT TSE The atrial vulnerable periods (A VP)for shock induction of atrial fibrillation (AF) in humans have not been clearly defined. Furthermore, the safety and efficacy of using low energy biatrial shock delivered transvenously for AF induction are unknown. We tested the safety and efficacy of using very low energy biatrial shocks, delivered between the right atrium and the coronary sinus for AF induction and used this technique to characterize the A VP in nine controls and nine patients with AF. Thirty-volt and 60-V 3/3-ms biphasic shocks were delivered, starting from 50 ms before the atrial effective refractory period with 20-ms increments until the end of the QRS interval to determine the AVP front, AVP end, and the AVP duration. Successful AF induction could be achieved in eight (89%) of the nine controls and in nine (100%) of the nine patients with AF without any complication. In patients with AF, the AVP front started significantly earlier within the QRS complex, and the AVP duration and the AVP duration/QRS percent ratios were also significantly greater as compared to controls. Furthermore, a higher induction shock energy in patients with AF was associated with an increase in AF inducibility and significantly increased the AVP duration and A VP duration/QRS percent ratio as compared to the controls. This study demonstrated the safe and efficacy of delivering a very low energy biatrial shock during the AVP within the R wave for AF induction. The characteristics of A VP in patients with AF were significantly different from normal subjects. [source] Reentry Site During Fibrillation Induction in Relation to Defibrillation Efficacy for Different Shock WaveformsJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 5 2001Ph.D., RAYMOND E. IDEKER M.D. Reentry Site and Defibrillation Waveform Efficacy.Introduction: Unsuccessful defibrillation shocks may reinitiate fibrillation by causing postshock reentry. Methods and Results: To better understand why some waveforms are more efficacious for defibrillation, reentry was induced in six dogs with 1-, 2-, 4-, 8-, and 16-msec monophasic and 1/1- (both phases 1 msec) 2/2-, 4/4-, and 8/8-msec biphasic shocks. Reentry was initiated by 141 ± 15 V shocks delivered from a defibrillator with a 150- , F capacitance during the vulnerable period of paced rhythm (183 ± 12 msec after the last pacing stimulus). The shock potential gradient field was orthogonal to the dispersion of refractoriness. Activation was mapped with 121 electrodes covering 4 × 4 cm of the right ventricular epicardium, and potential gradient and degree of recovery of excitability were estimated at the sites of reentry. Defibrillation thresholds (DFTs) were estimated by an up-down protocol for the same nine waveforms in eight dogs internally and in nine other dogs externally. DFT voltages for the different waveforms were positively correlated with the magnitude of shock potential gradient and negatively correlated with the recovery interval at the site at which reentry was induced by the waveform during paced rhythm for both internal (DFT = 1719 + 64.5 , V , 11.1RI; R2= 0.93) and external defibrillation (DFT = 3445 + 150 , V , 22RI; R2= 0.93). Conclusion: The defibrillation waveforms with the lowest DFTs were those that induced reentry at sites of low shock potential gradient, indicating efficacious stimulation of myocardium. Additionally, the site of reentry induced by waveforms with the lowest DFTs was in myocardium that was more highly recovered just before the shock, perhaps because this high degree of recovery seldom occurs during defibrillation due to the rapid activation rate during fibrillation. [source] Maturation-Dependent Alcohol Resistance in the Developing Mouse: Cerebellar Neuronal Loss and Gene Expression During Alcohol-Vulnerable and -Resistant PeriodsALCOHOLISM, Issue 8 2008Bahri Karaçay Background:, Alcohol abuse during pregnancy injures the fetal brain. One of alcohol's most important neuroteratogenic effects is neuronal loss. Rat models have shown that the cerebellum becomes less vulnerable to alcohol-induced neuronal death as it matures. We determined if maturation-dependent alcohol resistance occurs in mice and compared patterns of gene expression during the alcohol resistant and sensitive periods. Methods:, Neonatal mice received alcohol daily over postnatal day (PD) 2 to 4 or PD8 to 10. Purkinje cells and granule cells were quantified on PD25. The temporal expression patterns of 4 neuro-developmental genes and 3 neuro-protective genes in the cerebellum were determined daily over PD0 to 15 to determine how gene expression changes as the cerebellum transitions from alcohol-vulnerable to alcohol-resistant. The effect of alcohol on expression of these genes was determined when the cerebellum is alcohol sensitive (PD4) and resistant (PD10). Results:, Purkinje and granule cells were vulnerable to alcohol-induced death at PD2 to 4, but not at PD8 to 10. Acquisition of maturation-dependent alcohol resistance coincided with changes in the expression of neurodevelopmental genes. The vulnerability of cerebellar neurons to alcohol toxicity declined in parallel with decreasing levels of Math1 and Cyclin D2, markers of immature granule cells. Likewise, the rising resistance to alcohol toxicity paralleled increasing levels of GABA ,-6 and Wnt-7a, markers of mature granule neurons. Expression of growth factors and genes with survival promoting function (IGF-1, BDNF, and cyclic AMP response element binding protein) did not rise as the cerebellum transitioned from alcohol-vulnerable to alcohol-resistant. All 3 were expressed at substantial levels during the vulnerable period and were not expressed at higher levels later. Acute alcohol exposure altered the expression of neurodevelopmental genes and growth factor genes when administered either during the alcohol vulnerable period or resistant period. However, the patterns in which gene expression changed varied among the genes and depended on timing of alcohol administration. Conclusions:, Mice have a temporal window of vulnerability in the first week of life, during which cerebellar neurons are more sensitive to alcohol toxicity than during the second week. Expression of genes governing neuronal maturation changes in synchrony with the acquisition of alcohol resistance. Growth factors do not rise as the cerebellum transitions from alcohol-vulnerable to alcohol-resistant. Thus, a process intrinsic to neuronal maturation, rather than rising levels of growth factors, likely underlies maturation-dependent alcohol resistance. [source] Temporal Vulnerability of Fetal Cerebellar Purkinje Cells to Chronic Binge Alcohol Exposure: Ovine ModelALCOHOLISM, Issue 10 2007Jayanth Ramadoss Background: Human magnetic resonance imaging (MRI) and autopsy studies reveal abnormal cerebellar development in children who had been exposed to alcohol prenatally, independent of the exposure period. Animal studies conducted utilizing the rat model similarly demonstrate a broad period of vulnerability, albeit the third trimester-equivalent of human brain development is reported to be the most vulnerable period, and the first trimester-equivalent exposure produces cerebellar Purkinje cell loss only at high doses of alcohol. However, in the rat model, all 3 trimester-equivalents do not occur prenatally, requiring the assumption that intrauterine environment, placenta, maternal interactions, and parturition do not play an important role in mediating the damage. In this study, we utilized the ovine model, where all 3 trimester-equivalents occur in utero, to determine the critical window of vulnerability of fetal cerebellar Purkinje cells. Methods: Four groups of pregnant sheep were used: first trimester-equivalent pair-fed saline control group, first trimester-equivalent alcohol group (1.75 g/kg), third trimester-equivalent pair-fed saline control group, and third trimester-equivalent alcohol group (1.75 g/kg). The alcohol exposure regimen was designed to mimic a human binge pattern. Alcohol was administered intravenously on 3 consecutive days beginning on day 4 and day 109 of gestation in the first and third trimester-equivalent groups, respectively, and the alcohol treatment was followed by a 4-day inter-treatment interval when the animals were not exposed to alcohol. Such treatment episodes were replicated until gestational day 41 and 132 in the first and third trimester-equivalent groups, respectively. All fetal brains were harvested on day 133 and processed for stereological cerebellar Purkinje cell counting. Results: Significant deficits were found in the fetal cerebellar Purkinje cell number and density in the first and third trimester-equivalent alcohol exposed fetuses compared with those in the saline controls. However, there was no difference between the first and third trimester-equivalent alcohol administered groups. When comparing the present findings to those from a previous study where the duration of alcohol exposure was all 3 trimester-equivalents of gestation, we did not detect a difference in fetal cerebellar Purkinje cell number. Conclusions: We conclude that the fetal cerebellar Purkinje cells are sensitive to alcohol exposure at any time during gestation and that women who engage in binge drinking during the first trimester are at a high risk of giving birth to children with cerebellar damage even if drinking ceases after the first trimester. Our findings also support the hypothesis that only a certain population of Purkinje cells are vulnerable to alcohol-induced depletion irrespective of the timing or duration of alcohol exposure. [source] Assessment of metabolic and immune changes in postspawning Pacific oyster Crassostrea gigas: identification of a critical period of vulnerability after spawningAQUACULTURE RESEARCH, Issue 9 2010Yan Li Abstract This study investigates the vulnerable period in postspawning Pacific oysters (Crassostrea gigas) through physiological and immunological assessments. After spawning, the oyster condition index reduced by 50% and required 70 days to recover to the prespawning level. The mantle glycogen reduced quickly while the reduction in tissue protein occurred slowly. The mantle tissue also lost more protein than gills. The analysis of adenylate energy charge indicated that oysters were stressed in the first 8 days after spawning. As a result of spawning, haemocyte phagocytosis was reduced and remained at a low level for 3 days. In contrast, the reduction of haemolymph antimicrobial activity did not occur until 3 days after spawning and continued to decline until day 8. This immunesuppression was not directly correlated to the changes in haemocyte density. Our study suggests that the first 8 days after spawning are a critical period for oyster survival due to the loss of energy and low immunity. This study further improves our understanding of the coincidence between spawning and summer mortality in oyster aquaculture. [source] Effect of prenatal exposure to fine particulate matter on ventilatory lung function of preschool children of non-smoking mothersPAEDIATRIC & PERINATAL EPIDEMIOLOGY, Issue 5 2010Wieslaw A. Jedrychowski Summary Jedrychowski WA, Perera FP, Maugeri U, Mroz E, Klimaszewska-Rembiasz M, Flak E, Edwards S, Spengler JD. Effect of prenatal exposure to fine particulate matter on ventilatory lung function of preschool children of non-smoking mothers. Paediatric and Perinatal Epidemiology 2010. Impaired fetal development is associated with a number of adult chronic diseases and it is believed that these associations arise as a result of the phenomenon of prenatal programming, which involves persisting changes in structure and function of various body organs caused by ambient factors during critical and vulnerable periods of early development. The main goal of the study was to assess the association between lung function in early childhood and prenatal exposure to fine particulate matter (PM2.5), which represents a wide range of chemical compounds potentially hazardous for fetal development. Among pregnant women recruited prenatally to the study, personal measurements of PM2.5 were performed over 48 h in the second trimester of pregnancy. After delivery, infants were followed for 5 years; the interviewers visited participants in their homes to record children's respiratory symptoms every 3 months in the child's first 2 years of life and every 6 months thereafter. In the fifth year of the follow-up, children were invited for standard lung function testing of levels of forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1) and forced expiratory volume in 0.5 s (FEV0.5). There were 176 children of non-smoking mothers, who performed at least two acceptable spirometry measurements. Multivariable linear regression showed a significant deficit of FVC at the highest quartile of PM2.5 exposure (beta coefficient = ,91.9, P = 0.008), after adjustment for covariates (age, gender, birthweight, height and wheezing). Also FEV1 level in children was inversely correlated with prenatal exposure to PM2.5, and the average FEV1 deficit amounted to 87.7 mL (P = 0.008) at the higher level of exposure. Although the effect of PM2.5 exposure on FEV0.5 was proportionally weaker (,72.7, P = 0.026), it was also statistically significant. The lung function level was inversely and significantly associated with the wheezing recorded over the follow-up. The findings showed that significant lung function deficits in early childhood are associated with prenatal exposure to fine particulate matter, which may affect fetal lung growth. [source] | ||||||||||