Nitrous oxide emission from riparian buffers in relation to vegetation and flood frequency.

The nitrate (NO(3)(-)) removal capacity of riparian zones is well documented, but information is lacking with regard to N(2)O emission from riparian ecosystems and factors controlling temporal dynamics of this potent greenhouse gas. We monitored N(2)O fluxes (static chambers) and measured denitrification (C(2)H(2) block using soil cores) at six riparian sites along a fourth-order stretch of the White River (Indiana, USA) to assess the effect of flood regime, vegetation type, and forest maturity on these processes. The study sites included shrub/grass, aggrading (<15 yr-old), and mature (>80 yr) forests that were flooded either frequently (more than four to six times per year), occasionally (two to three times per year), or rarely (every 20 yr). While the effect of forest maturity and vegetation type (0.52 and 0.65 mg N(2)O-m(-2) d(-1) in adjacent grassed and forested sites) was not significant, analysis of variance (ANOVA) revealed a significant effect ( < 0.01) of flood regime on N(2)O emission. Among the mature forests, mean N(2)O flux was in this order: rarely flooded (0.33) < occasionally flooded (0.99) < frequently flooded (1.72). Large pulses of N(2)O emission (up to 80 mg N(2)O-m(-2) d(-1)) occurred after flood events, but the magnitude of the flux enhancement varied with flood event, being higher after short-duration than after long-duration floods. This pattern was consistent with the inverse relationship between soil moisture and mole fraction of N(2)O, and instances of N(2)O uptake near the river margin after flood events. These results highlight the complexity of N(2)O dynamics in riparian zones and suggest that detailed flood analysis (frequency and duration) is required to determine the contribution of riparian ecosystems to regional N(2)O budget.

A controlled trial to investigate whether the orientation of the bevel and angle of approach determine the side of endobronchial intubation in an adult manikin.

One of the commonest complications of endotracheal intubation occurs when the tip of the endotracheal tube passes distal to the carina and enters one of the main bronchi. The perioperative practitioner may observe high airway pressures, hypoxia or even pneumothorax. The most common reason given for the high incidence of right endobronchial intubation is that the right main bronchus comes off the trachea at a more acute angle from the midline. We sought, however, to explore two other factors which may explain this phenomenon ­ the angle of the tube's bevel and its trajectory of approach. We conducted a prospective controlled trial in which doctors from our department intubated the trachea of an adult manikin in three distinct sets using standard tube, reversed tubes and reversed laryngoscope blades. We found that the angle of the bevel and trajectory of approach determines the side of endobronchial intubation in an adult manikin.

Electrophysiological effects of remodeling cardiac gap junctions and cell size: experimental and model studies of normal cardiac growth.

The increased incidence of arrhythmias in structural heart disease is accompanied by remodeling of the cellular distribution of gap junctions to a diffuse pattern like that of neonatal cardiomyocytes. Accordingly, it has become important to know how remodeling of gap junctions due to normal growth hypertrophy alters anisotropic propagation at a cellular level (V(max)) in relation to conduction velocities measured at a macroscopic level. To this end, morphological studies of gap junctions (connexin43) and in vitro electrical measurements were performed in neonatal and adult canine ventricular muscle. When cells enlarged, gap junctions shifted from the sides to the ends of ventricular myocytes. Electrically, normal growth produced different patterns of change at a macroscopic and microscopic level. Although the longitudinal and transverse conduction velocities were greater in adult than neonatal muscle, the anisotropic velocity ratios were the same. In the neonate, mean V(max) was not different during longitudinal (LP) and transverse (TP) propagation. However, growth hypertrophy produced a selective increase in mean TP V(max) (P<0.001), with no significant change in mean LP V(max). Two-dimensional neonatal and adult cellular computational models show that the observed increases in cell size and changes in the distribution of gap junctions are sufficient to account for the experimental results. Unexpectedly, the results show that cellular scaling (cell size) is as important (or more so) as changes in gap junction distribution in determining TP properties. As the cells enlarged, both mean TP V(max) and lateral cell-to-cell delay increased. V(max) increased because increases in cell-to-cell delay reduced the electric current flowing downstream up to the time of V(max), thus enhancing V(max). The results suggest that in pathological substrates that are arrhythmogenic, maintaining cell size during remodeling of gap junctions is important in sustaining a maximum rate of depolarization.

Threshold variability in fibers with field stimulation of excitable membranes.

The central focus of this report is the evolution of transmembrane potentials following initiation of a point-source field stimulus, particularly when the stimulus is short and the stimulating electrode is close to the fiber. The transmembrane voltage threshold in response to a point-source field stimulus was determined in a numerical model of a single unmyelinated fiber. Both nerve (Hodgkin-Huxley) and cardiac (Ebihara-Johnson [1]) models of the fiber membrane were evaluated. A central question is whether it is possible to know in advance whether a stimulus of specific magnitude, duration, and location will result in a subsequent action potential. Such determination can be based on the membrane's "voltage threshold." In contrast to the commonly held view, the voltage threshold was found to vary markedly depending on the duration and location of the field stimulus. Voltage thresholds ranged from about 8 mV above baseline to more than 100 mV above baseline, the higher thresholds occurring with shorter stimuli and electrode locations closer to the membrane. A related question is whether the passive membrane response can be used as a tool in determining whether a subsequent action potential is elicited. If the answer is affirmative, this finding can be very useful, since passive properties are linear and thereby much simpler to evaluate than active ones. The results show that the passive response tracks active responses long enough to be a good estimator of subsequent action potential development. Examples show that the evaluation of Vm at 0.2-0.5 msec after stimulus initiation, times chosen on the basis of membrane characteristics, was a better predictor of subsequent excitation than was either initial transmembrane current or Vm at the time when the stimulus ends. Most of the circumstances analyzed here with electric field stimulation also appear likely to be valid with magnetic field stimulation.

Electric field stimulation of excitable tissue.

This paper examines the transmembrane voltage response of an unmyelinated fiber to a stimulating electric field from a point current source. For subthreshold conditions, analytic expressions for the transmembrane potential, vm, are developed that include the specific effects of fiber-source distance, h, and time from the onset of the stimulus, T. Suprathreshold effects are determined for two examples by extending the analytical results with a numerical model. The vm response is a complex evolution in time, especially for small h, that differs markedly from the "activating function." In general, the subthreshold response is a good predictor of the wave shape of the suprathreshold vm, but a poor predictor of its magnitude. The subthreshold response also is a good (but not a precise) predictor of the region where excitation begins.

Computer simulations of activation in an anatomically based model of the human ventricular conduction system.

Simulations of the electrical activity during excitation were performed in an anatomically based model of the human ventricular conduction system. Each of the 33,000 elements of this model represented a unit bundle of Purkinje or atrioventricular nodal tissue. The Ebihara-Johnson model for sodium defined the active membrane characteristics. Using a combination of new and existing modeling techniques, simulations of excitation were completed in approximately 5 min CPU time on an IBM 3090 at the Cornell National Supercomputer Facility. Activation times at sites in the model were compared to experimental measurements for the excitation of the ventricular myocardium on the endocardial surface. These "literature-based" times were estimated from a number of reported human heart mapping studies. Initially, the times fit poorly. The major factor for the discrepancy was the conduction velocities of the elements, which were a result of the physical and electrical parameters derived from a review of histologic and electrical properties studies. In addition, there was a latency between activation of the system in the left ventricle of the model and that in the right ventricle when compared to the experimental work. When the times were scaled to adjust for the conduction velocity and ventricular latency effects, the match between the simulation and literature-based times was much improved. Quantitative comparison between normalized times resulted in correlation coefficients CCF = 0.76 for the right ventricle and CCF = 0.64 for the left ventricle.

The construction of an anatomically based model of the human ventricular conduction system.

The ventricular conduction system is a complicated network of specialized muscle cells responsible for the transmission of electrical activity between the atria and the ventricles of the human heart. It has been the focus of numerous electrical and anatomical studies at both the microscopic and macroscopic levels. An understanding of its behavior at both levels is considered important, because it is primarily responsible for the spread of excitation in the ventricles. Previous computer models have been very simple ones that have been primarily adjuncts to models of the ventricles. This paper describes a strategy for the construction of conduction system models which is based on real microscopic and macroscopic features, although the model still is much simpler than reality. The model contains almost 35,000 individual cylindrical elements, each of whose physical dimensions approximate unit bundles of Purkinje and atrioventricular nodal cells. The model, whose physical appearance closely resembles that of the conduction system, was generated from limited anatomical data in less than 2 min CPU time on an IBM 3090 at the Cornell National Supercomputer Facility.

Electrocardiographic inverse solution for ectopic origin of excitation in two-dimensional propagation model.

Inverse calculations were examined that sought the origin of a cardiac ectopic excitation sequence. Cardiac anatomy and its geometric relationships to sites on the body surface were adapted from human cross-sectional images to form a two-dimensional model, which included ventricular muscle and a primitive conduction system. The surrounding volume conductor was modelled in a simplified way as unbounded, homogeneous and isotropic. In a series of tests, one ectopic origin was designated the 'true' origin. The ECG for this true origin was compared to ECGs for 197 ectopic 'trial' origins, and differences between the wave forms for true versus trial origins were determined. Core issues were the magnitudes of changes in ECG wave forms as a function of the site of origin, whether these changes were sufficient to imply uniqueness, and what spatial resolution might be expected, in the presence of realistic noise levels. For a noise level of 10 microV RMS, the origin of excitation was localised to a single region of the muscle using one wave form from the body surface, with a resolution of 10 mm. The resolution was not improved significantly with a second electrode on the body surface, but was substantially improved with an endocardial electrode.

Propagation model using the DiFrancesco-Noble equations. Comparison to reported experimental results.

Propagation, re-entry and the effects of stimuli within the conduction system can be studied effectively with computer models when the pertinent membrane properties can be represented accurately in mathematical form. To date, no membrane models have been shown to be accurate representations during repolarisation and recovery of excitability, although for the Purkinje membrane the DiFrancesco-Noble (DN) model has become a possibility. The paper examines the DN model, restates its equations and compares simulated waveforms in a number of propagation contexts to experimental measurements reported in the literature. The objective is to determine whether or not the DN model reproduced phenomena such as supernormality, shortening in action potential duration during pacing rate increases, alternation of duration with changes in rhythm, graded responses and 'all-or-none' repolarisation in a quantitatively realistic way, as each of these come from time and space dependencies not directly a part of the ionic current measurements on which the DN model is based. The results show that the DN equations correctly simulate these situations and support the goal of having a model that is broadly applicable to Purkinje tissue, including refractory period properties and response to electrical stimulation.

One-dimensional model of cardiac defibrillation.

The response of a single strand of cardiac cells to a uniform defibrillatory shock assuming steady-state linear conditions is examined. It is argued that the effect of this current is quantitatively described by the induced transmembrane potential even under passive conditions. The characteristics of the single strand are those that would exist if the heart was a system of equivalent parallel pathways from apex to base. It is shown that essentially every cell is both hyperpolarized and depolarised from the shock by an amount proportional to the stimulus intensity and the intercellular junctional resistance. For physiological values of model parameters the evaluated depolarisations are consistent with levels necessary to affect electrophysiological behaviour.