O período da contaminação com petróleo influencia a rebrota de Echinochloa polystachya (H.B.K.) Hitchcock em solo de várzea da Amazônia central?

Several factors may influence the impact of oil on the environment. However, although it is understood that the effect of pollutants may change throughout the year according to seasonal variations in environmental parameters, this effect is poorly studied in the tropical region. The effects of Urucu's crude oil on the vegetative propagation and growth of Echinochloa polystachya were evaluated in a 63 days period, in two experiments, "A" (July-September) and "B" (September-November) planting the species in a greenhouse. In both experiments parts of stems were placed in 2 L of várzea soil contaminated by 6 oil doses, ranging from 0 to 0.231 L oil m-2 soil. In response to dosage increase there was a decrease of total biomass, ratio of live /total biomass, the leaf length and number of leaves. The period of planting influenced the response of plants to the dosage applied due to climate change, with negative effects in the "B" period of higher temperatures. We concluded that the exposure period influence the vegetative propagation and growth of the seedlings, being a spill in the period of the higher temperatures more dangerous for this specie

Prenatal nicotine exposure alters central cardiorespiratory responses to hypoxia in rats: implications for Sudden Infant Death Syndrome.

Maternal cigarette smoking and prenatal nicotine exposure are the highest risk factors for sudden infant death syndrome (SIDS). During hypoxia, respiratory frequency and heart rate transiently increase and subsequently decrease. These biphasic cardiorespiratory responses normally serve to prolong survival during hypoxia by reducing the metabolic demands of cardiac and respiratory muscles. However, exaggerated responses to hypoxia may be life threatening and have been implicated in SIDS. Heart rate is primarily determined by the activity of brainstem preganglionic cardioinhibitory vagal neurons (CVNs) in the nucleus ambiguus. We developed an in vitro rat brainstem slice preparation that maintains rhythmic inspiratory-related activity and contains fluorescently labeled CVNs. Synaptic inputs to CVNs were examined using patch-clamp electrophysiological techniques. Hypoxia evoked a biphasic change in the frequency of both GABAergic and glycinergic IPSCs in CVNs, comprised of an initial increase followed by a decrease in IPSC frequency. Prenatal exposure to nicotine changed the GABAergic response to hypoxia from a biphasic response to a precipitous decrease in spontaneous GABAergic IPSC frequency. This study establishes a likely neurochemical mechanism for the heart rate response to hypoxia and a link between prenatal nicotine exposure and an exaggerated bradycardia during hypoxia that may contribute to SIDS

Respiratory sinus arrhythmia: endogenous activation of nicotinic receptors mediates respiratory modulation of brainstem cardioinhibitory parasympathetic neurons

The heart rate increases during inspiration and decreases during expiration. This respiratory sinus arrhythmia (RSA) occurs by modulation of premotor cardioinhibitory parasympathetic neuron (CPN) activity. However, RSA has not been fully characterized in rats, and despite the critical role of CPNs in the generation of RSA, little is known about the mechanisms that mediate this cardiorespiratory interaction. This study demonstrates that RSA in conscious rats is similar to that in other species. The mechanism of RSA was then examined in vitro. Rhythmic inspiratory-related activity was recorded from the hypoglossal rootlet of 700- to 800-μm medullary sections. CPNs were identified by retrograde fluorescent labeling, and neurotransmission to CPNs was examined using patch-clamp electrophysiological techniques. During inspiratory bursts, the frequency of both spontaneous γ-aminobutyric acidergic (GABAergic) and spontaneous glycinergic synaptic events in CPNs was significantly increased. Focal application of the nicotinic antagonist dihydro-β-erythroidine in an α4β 2-selective concentration (3 μmol/L) abolished the respiratory-evoked increase in GABAergic frequency. In contrast, the increase in glycinergic frequency during inspiration was not altered by nicotinic antagonists. Prenatal nicotine exposure exaggerated the increase in GABAergic frequency during inspiration and enhanced GABAergic synaptic amplitude both between and during inspiratory events. Glycinergic synaptic frequency and amplitude were unchanged by prenatal nicotine exposure. This study establishes a neurochemical link between neurons essential for respiration and CPNs, reveals a functional role for endogenous acetylcholine release and the activation of nicotinic receptors in the generation of RSA, and demonstrates that this cardiorespiratory interaction is exaggerated in rats prenatally exposed to nicotine

Hydrogen peroxide in exhaled air: A source of error, a paradox and its resolution.

The concentration of hydrogen peroxide (H2O2) in exhaled air has been reported to be elevated in asthma and chronic obstructive pulmonary disease (COPD), but results are inconsistent and difficult to reproduce. As H2O2 occurs in ambient air, we examined its association with exhaled H2 O2 in human subjects. Exhaled breath condensate (EBC) of 12 COPD patients and nine healthy control subjects was collected either with an inhalation filter (efficiency 81%) or without. Ambient air condensate (AAC) was collected in parallel and samples were analysed for H2O2. Additionally, ambient H2O2 was recorded by an atmospheric measuring device (online fluorometric measurement). H2 O2 concentration in AAC was significantly higher (p<0.001) than in EBC. AAC variations were concordant with the data from the atmospheric measuring instrument. In both subjects’ groups, the inhalation filter reduced H2O2 values (p<0.01). Despite generally low levels in exhaled air, analysis by a mathematical model revealed a contribution from endogenous H2O2 production. The low H2O2 levels in exhaled air are explained by the reconditioning of H2O2-containing inhaled air in the airways. Inhaled H2O2 may be one factor in the heterogeneity and limited reproducibility of study results. A valid determination of endogenous H2 O2 production requires inhalation filters