Objective-We have observed consistent hemodynamic patterns after restoration of spontaneous circulation (ROSC) after ventricular fibrillation (VF) cardiac arrest. We sought to characterize the time-course of these patterns, and to determine whether these differed based on duration of the VF insult.Methods-We performed a retrospective review of data from a randomized animal experiment that was conducted in an AAALAC-approved animal laboratory. We used mixed-breed domestic swine of either sex. Animals were anesthetized and instrumented for continuous recording of ECG and blood pressures. VF was induced electrically and allowed to progress for various times ranging from brief (22s) to moderate (less than 3 minutes) to prolonged (3 to 10 minutes). All animals were initially shocked (150J) up to three times. If ROSC was not achieved on the 3 initial shocks, a standardized treatment protocol was followed. We defined cardiovascular collapse as a SBP < 90 mmHg sustained for one minute. For statistical purposes, we classified animals as having VF of <3 minutes, or >3minutes duration. Data were analyzed with Fisher's exact test and survival analysis.Results-A hyperdynamic phase, consisting of very high blood pressures and tachycardia, was seen in all animals immediately after ROSC. This lasts from 1 to 4 minutes. Post-resuscitation cardiovascular collapse occurred in 2/7 (29%) animals in the <3 minute group and 13/14 in the >3 minute group (93%) p=0.006. Onset of cardiovascular collapse was highly related to duration of VF (log-rank p=0.004).Conclusions-There are two distinct phases of hemodynamic change after resuscitation of VF. The first phase is a brief hyperdynamic phase. The second phase is either stabilization or cardiovascular collapse. When VF is brief, blood pressures often return to normal without exogenous support. When VF was prolonged animals were rescued with exogenous pressor. Healthcare providers should be prepared to provide pressor support for patients having ROSC after prolonged VF.

The researchers performed experiments to evaluate whether the effects of bombesin are selective for the satiation of ingestive behaviors related to energy balance or if ingestive behaviors associated with sodium balance are also suppressed by bombesin. Injections of 4 and 8 micrograms/kg bombesin reliably reduced need-free and sodium deficiency-induced NaCl intake in male rats. The effects of bombesin on the sodium-deficiency-induced change in taste reactivity was assessed. Injections of 4 micrograms/kg and 8 micrograms/kg bombesin had no effect on the sodium deficiency-induced shift in taste reactivity. These data indicate that bombesin suppresses NaCl intake and that bombesin does not appear to interact with gustatory sensibility in exerting its behavior-controlling action.

Increased brain-derived neurotrophic factor (BDNF) levels and extracellular-signal regulated kinase (ERK) signaling are associated with reduced brain injury after cerebral ischemia. In particular, mild hypothermia after cardiac arrest increases BDNF and ERK signaling. This study tested whether intracerebroventricular infusions (0.025 µg/ hr × 3 days) of BDNF also improved recovery of rats resuscitated from cardiac arrest and maintained at 37°C. BDNF infusions initiated at the time of cardiac arrest did not alter survival, neurological recovery, or histological injury. Separate experiments confirmed that BDNF infusions increased tissue levels of BDNF. However, these infusions did not increase ERK activation in hippocampus. These data suggest that increased BDNF levels are not sufficient to explain the beneficial effects of mild hypothermia after cardiac arrest, and that exogenous BDNF administration does not increase extracellular ERK signaling. KeywordsIschemia; Heart Arrest; Hippocampus; Brain-derived Neurotrophic Factor Brain derived neurotrophic factor (BDNF) is a eurotrophic factor that binds to the neurotrophin receptor tyrosine kinase receptor B (TrkB). BDNF signaling can increase neuronal survival in some model systems [11]. The beneficial effects of BDNF have been associated with increased activation of p42/p44 mitogen-activated protein kinase (extracellular signal-related kinase, ERK) [2].In vivo, the effect of exogenous BDNF on ischemic brain injury is unclear. BDNF infusions [3,15,22,27] or pretreatment of brain with BDNF-producing cells [9] decrease neuronal injury after both focal and global cerebral ischemia. Conversely, inhibition of BDNF activity worsens recovery from forebrain ischemia [16]. However, intracranial BDNF infusion does not improve recovery or reduce histological damage in rat brain after resuscitation from ventricular fibrillation cardiac arrest [21].In other studies of cardiac arrest, BDNF signaling is associated with improved neuronal survival after ischemia. Therapeutic hypothermia (33-34°C) for 12-24 hours improves neurological recovery and survival after resuscitation from cardiac arrest [4,10]. In rats,

Hipertensión arterial en población pediátrica, sus efectos en la dispersión de la onda P y el área auricular izquierda. Resumen:Antecedentes: Entre los factores descritos para desarrollar fibrilación auricular se encuentra el mayor tamaño de la aurícula izquierda; esto lleva a cambios en sus propiedades eléctricas y a mayores valores de dispersión de la onda P del electrocardiograma.Objetivo: Determinar la dispersión de la onda P con relación al área de la aurícula izquierda en niños entre 8 a 11 años.Métodos: Se estudiaron 400 niños aparentemente sanos de ese rango de edad. Se les realizó electrocardiograma de superficie de 12 derivaciones para medir los valores de P máxima, P mínima y se calculó la dispersión de la onda P; se les midió 4 veces la presión arterial. Se realizó además, ecocardiograma para medición del área auricular izquierda.Resultados: Los valores de media de dispersión de la onda P aumentan desde normotensos a hipertensos (32.5 a 38.5 ms, respectivamente), existiendo diferencias significativas intergrupos, encontrando la mayor significación al comparar los normotensos con el grupo de prehipertensos (p=0.001). Un estudio de regresión demostró la dependencia de la dispersión de la onda P del electrocardiograma en el grupo de normotensos y prehipertensos con r=0,22 y p<0.05. Una regresión lineal para la muestra de niños hipertensos muestra una correlación positiva para la dependencia de la onda P con el área auricular izquierda.Conclusiones: Existe dependencia de la dispersión de la onda P del electrocardiograma con el área auricular izquierda, así como diferencias significativas entre valores medios de dispersión de la onda P en los subgrupos de niños normotensos, prehipertensos e hipertensos. Background: left atrial size is a recognized factor increasing the risk of atrial fibrillation. Left atrial electrical properties are modified, with a greater dispersion of the P wave on the electrocardiogram. Aim: to determine the relation between left atrial area and P wave dispersion in children. Methods: 400 healthy children from 8 to 11 years of age had a 12 lead ECG. Maximum and minimum voltages of the P wave and P wave dispersion were measured. Blood pressure was recorded in 4 separate measurements. Echocardiography was used to determine left atrial area. Results: Compared to normotensive children, mean dispersion of the P wave was higher in hypertensives (38.5 vs 32.5 ms, respectively). The most significant difference was observed between normotensives and pre-hypertensive children (regression analysis, p=0.001). Linear regression analysis showed a positive correlation of P wave dispersion and left atrial area Conclusion: P wave dispersion and left atrial area are positively correlated in groups of normal, prehypertensive and hypertensive children. The corresponding mean values of dispersion follow the same tendency. Key Words: P wave, children, arterial hypertension.Hypertension in pediatric patients: effects upon P wave dispersion and left atrial area Introducción:En los últimos años se ha descr...

No abstract