Maxillofacial injuries associated with domestic violence.

PURPOSE: The purpose of this study was to report the incidence, causes, and patterns of maxillofacial injury associated with domestic violence. PATIENTS AND METHODS: A retrospective review of patients treated for domestic violence injuries at an inner-city hospital over a 5-year period was done, and data were collected on type and location of injury, mechanism of injury, alcohol involvement, and treatment. RESULTS: The sample consisted of 236 emergency room admissions. The majority (81%) of victims presented with maxillofacial injuries. The fist was a favorite means for assaults (67%). The middle third of the face was most commonly involved (69%). Soft tissue injuries were the most common type of injury (61%). Facial fractures were present in 30% of victims. The average number of mandible fractures per patient was 1.32. The majority of facial fractures (40%) were nasal fractures. Left-sided facial injuries were more common than right sided. CONCLUSIONS: These data confirm that most victims of domestic violence sustain maxillofacial injuries. Midface injuries predominate. The preponderance of facial injuries makes it very likely that oral and maxillofacial surgeons will be involved in the care of these patients.

Manual differential cell counts help predict bacterial infection. A multivariate analysis.

We developed logistic regression models that combine information from the automated CBC and manual 100-cell differential counts to predict bacterial infection. The logistic models were fitted from a case group of 116 patients with proven bacterial infection and a control group of 930 presumably uninfected outpatients. A 4-variable, 15-parameter model, which includes automated absolute neutrophil, manual band, and manual immature granulocyte counts, performed best with a receiver operating characteristic (ROC) curve area of 89%. A more practical 2-variable model including automated absolute neutrophil and manual band counts performed almost as well with an ROC curve area of 86%. The automated neutrophil count-only model is less informative with an ROC curve area of 78%. The combined information from automated and manual differential cell counts more accurately predicts bacterial infection than automated counting alone. Despite these modest improvements, the high cost of manual differential cell counts dictates careful patient selection. The supplemental information gained from manual differential counts is most useful for patients with low to normal neutrophil counts (8,000/microL [8.0 x 10(9)/L] or less). Further studies are indicated to determine the characteristic patient populations deriving maximal benefit from this information.

Lipopolysaccharide transport from the peritoneal cavity to the blood: is it controlled by the vagus nerve?

Vagotomy suppresses fever and hyperalgesia caused by intraperitoneal lipopolysaccharide (LPS) but has little effect on the febrile response to intravenous or intramuscular LPS. This suggests that some vagus-mediated mechanisms are recruited only when LPS is administered via the intraperitoneal route. We hypothesized that such mechanisms are associated with LPS transport from the peritoneal cavity to the circulation. Adult Wistar rats underwent total subdiaphragmatic, bilateral selective celiac, or sham vagotomy. On day 28-32 after surgery, they were injected IP with Escherichia coli LPS (5, 20, or 100 microg/kg) or saline and decapitated 90 min thereafter. Their plasma levels of LPS and their plasma interleukin-6, adrenocorticotropin, and corticosterone responses to LPS were measured. Success of intraperitoneal administration of LPS was verified by increased interleukin-1beta and interleukin-6 concentrations in the peritoneal lavage fluid. Effectiveness of vagotomies was confirmed by increased stomach mass (food retention) and pancreas mass (hypertrophy). In the shams, LPS caused a dose-dependent endotoxemia and increased plasma levels of interleukin-6, adrenocorticotropin, and corticosterone. Neither celiac nor total vagotomy affected any of these responses. LPS escapes from the peritoneal cavity by two primary routes, viz., the hematogenous (via the portal vein) and lymphogenous (via the lymphatic system). The design of the present study did not allow for evaluating the rapid, hematogenous transport. The results obtained suggest that the abdominal vagus does not control the slow. lymphogenous escape of LPS from the peritoneal cavity.

A model of extravascular bubble evolution: effect of changes in breathing gas composition.

Observations of bubble evolution in rats after decompression from air dives (O. Hyldegaard and J. Madsen. Undersea Biomed. Res. 16: 185-193, 1989; O. Hyldegaard and J. Madsen. Undersea Hyperbaric Med. 21: 413-424, 1994; O. Hyldegaard, M. Moller, and J. Madsen. Undersea Biomed. Res. 18: 361-371, 1991) suggest that bubbles may resolve more safely when the breathing gas is a heliox mixture than when it is pure O(2). This is due to a transient period of bubble growth seen during switches to O(2) breathing. In an attempt to understand these experimental results, we have developed a multigas-multipressure mathematical model of bubble evolution, which consists of a bubble in a well-stirred liquid. The liquid exchanges gas with the bubble via diffusion, and the exchange between liquid and blood is described by a single-exponential time constant for each inert gas. The model indicates that bubbles resolve most rapidly in spinal tissue, in adipose tissue, and in aqueous tissues when the breathing gas is switched to O(2) after surfacing. In addition, the model suggests that switching to heliox breathing may prolong the existence of the bubble relative to breathing air for bubbles in spinal and adipose tissues. Some possible explanations for the discrepancy between model and experiment are discussed.

Risks associated with 72- and 96-hour peripheral intravenous catheter dwell times.

BACKGROUND: The risk of complications in peripheral intravenous therapy is higher on the second day of therapy and may continue to increase with time, making routine restarts after 3 days a common practice. The objective of the study was to determine whether the risks of complications after a peripheral i.v. catheter restart after 72 hours are less than the risks of complications if the therapy is continued to 96 hours. METHODS: A retrospective chart review was completed for 722 patients in a community hospital with peripheral i.v. catheters for i.v. fluids or saline locks. Measurements collected were i.v. therapy start date, number of restarts, termination date, and reason for termination; the data were analyzed using risk models. RESULTS: There were 596 uncomplicated therapies. Complications prompted termination in 188 cases. The average duration of therapy was 1.8 days. The probability of complications was least in the first 24 hours, (0.074; standard deviation [SD], 0.013), and increased to 0.176 (SD, +/- 0.026) in the 24- to 48-hour period. The probability of a complication in the 48- to 72-hour period and the 72- to 96-hour period was 0.130 (SD, 0.026). A restarted catheter has a significantly higher risk of complication in its first 24 hours than does an initial catheter. CONCLUSIONS: From these results, the authors conclude that restarting catheters at 72 hours does not reduce the risk of complication in the next 24 hours when compared with simply continuing the therapy with the original catheter. Additional studies should be conducted to justify a policy of automatically restarting therapy after 72 hours.

Signaling the brain in systemic inflammation: which vagal branch is involved in fever genesis?

Recent evidence has suggested a role of abdominal vagal afferents in the pathogenesis of the febrile response. The abdominal vagus consists of five main branches (viz., the anterior and posterior celiac branches, anterior and posterior gastric branches, and hepatic branch). The branch responsible for transducing a pyrogenic signal from the periphery to the brain has not as yet been identified. In the present study, we address this issue by testing the febrile responsiveness of male Wistar rats subjected to one of four selective vagotomies: celiac (CBV), gastric (GBV), hepatic (HBV), or sham (SV). In the case of CBV, GBV, and HBV, only the particular vagal branch(es) was cut; for SV, all branches were left intact. After the postsurgical recovery (26-29 days), the rats had a catheter implanted into the jugular vein. On days 29-32, their colonic temperature (Tc) responses to a low dose (1 microg/kg) of Escherichia coli lipopolysaccharide (LPS) were studied. Three days later, the animals were subjected to a 24-h food and water deprivation, and the effectiveness of the four vagotomies to induce gastric food retention, pancreatic hypertrophy, and impairment of the portorenal osmotic reflex was assessed by weighing the stomach and pancreas and measuring the specific gravity of bladder urine, respectively. Stomach mass, pancreas mass, and urine density successfully separated the four experimental groups into four distinct clusters, thus confirming that each type of vagotomy had a different effect on the indexes measured. The Tc responses of SV, CBV, and GBV rats to LPS did not differ and were characterized by a latency of approximately 40 min and a maximal rise of 0.7 +/- 0.1, 0.6 +/- 0.1, and 0.9 +/- 0.2 degrees C, respectively. The fever response of the HBV rats was different; practically no Tc rise occurred (0.1 +/- 0.2 degrees C). The HBV appeared to be the only selective abdominal vagotomy affecting the febrile responsiveness. We conclude, therefore, that the hepatic vagus plays an important role in the transduction of a pyrogenic signal from the periphery to the brain.

Lower decompression sickness risk in rats by intravenous injection of foreign protein.

We have identified a novel means of reducing the risk of decompression sickness (DCS) in rats. A substantial reduction in DCS, from 55% in untreated animals to 24% in animals injected intravenously with a hydrogenase of bacterial origin, was documented for animals breathing a mixture of oxygen and hydrogen. However, this reduction was clearly not a function of metabolic elimination of H2; injections of proteins lacking hydrogenase activity also elicited a lower DCS incidence, and animals breathing hyperbaric helium had the same protective advantage as animals breathing H2. The reduction in DCS risk was shown to be caused by intravenous injection of a foreign protein. The magnitude of the effect varied: two foreign proteins tested did not induce a statistically significant response. We speculated that the foreign protein elicited an immune reaction pre-dive, which diminished the subsequent response of the immune system in DCS. Identifying the underlying mechanism may be important to understanding the pathophysiology of this malady, and may ultimately lead to a therapy applied pre-decompression for reducing DCS risk in human diving.

Experimental design and estimation of parameters in complex radioligand binding systems.

A computer was used to simulate data from typical radioligand binding experiments with a 2-site competitive-allosteric model of a receptor. The 4 equilibrium parameters of this model cannot be estimated by fitting the model to equilibrium data. Data from simulations of association experiments give satisfactory estimates of the 9 competitive-allosteric model parameters. From the kinetic parameters, equilibrium constants may be calculated. Combining data from equilibrium simulations with data from association simulations provided estimates of the model parameters with smaller standard deviations. A further improvement in design was shown possible by including simulated experiments in which receptor was preincubated with inhibitor before adding ligand. This improvement was documented using Monte Carlo replications of parameter estimates using competing experimental designs. Replications also revealed certain biases in the parameter estimates and could provide a means of estimating those biases when parameter estimates are made using experimental rather than simulated data. Simulations offer a powerful tool in planning experiments designed to estimate kinetic parameters of a receptor system. This is especially true with complex systems that may require pooling data from different kinds of experiments in order to estimate the kinetic parameters.

Development and interactions of two inert gas bubbles during decompression.

A mathematical model has been developed to simulate the evolution of two inert gas bubbles in tissue. This is useful for understanding the dynamics of bubbles that presumably arise during decompression. It is assumed that they are spherical and that the tissue volume surrounding them is infinite. The total pressure in each bubble is determined by the barometric and metabolic gas pressures as well as the pressure due to surface tension. Bipolar coordinates are employed to determine the inert gas pressure distribution. Two coupled governing equations for bubble radii are then derived and solved numerically. The results demonstrate how bubble evolution is affected by the distance between bubbles and the initial bubble radii. The existence time and bubble surface flux of two equal-sized bubbles are calculated and compared with those of a single gas bubble model. The results indicate that when two bubbles are very close, it takes 20% more time for two bubbles to dissolve than for a single one, and the total surface flux of two bubbles is nearly 20% less than twice of a single bubble. When the center-to-center distance is 10 times of bubble radius, the effect of bubble interaction on bubble existence time and surface flux are about 6 and 9% changes, respectively. We conclude that if bubbles are not too small, the interactions among bubbles should be included in inert gas bubble models predicting bubble evolution.

Does the time course of bubble evolution explain decompression sickness risk?

A probabilistic model of decompression sickness (DCS) risk based on linear-exponential (LE) kinetics has given the best fit of the human air and nitrox DCS database. To test the hypothesis that its success may be due to the formation of a gas phase during decompression, we developed a physiologically based bubble evolution model using a numerical solution of a partial differential equation system. Because of the computational intensity of this method, it could not be used to fully explore our hypothesis. Consequently, we compared the solution with that of a computationally simpler approximation that was previously published by Van Liew and found the two approaches gave similar results. Using the simpler model, assuming bubble densities of 1 and 1,000 bubbles/cm3, we found a tissue time constant of at least 80 min (equivalent to perfusion of 1/80 ml.g-1.min-1) was required to achieve a delay in bubble dissolution comparable to the prolonged risk of DCS predicted by the LE model. We suggest that the persistence of single bubbles in a uniformly perfused homogeneous tissue alone is unlikely to explain persistent DCS risk.

A model for predicting central nervous system oxygen toxicity from hyperbaric oxygen exposures in humans.

Under certain circumstances, Navy divers breathe 100% O2 when working underwater. Serious symptoms of central nervous system (CNS) O2 toxicity can develop from hyperbaric O2 exposure; immersion and exercise are also known to exacerbate toxicity. We developed risk models for quantitative prediction of the probability of developing symptoms using a large set of human data in which occupational exposure conditions were simulated. Exposures were 5 to 265 min at PO2 levels from 20 to 50 feet of sea water (fsw) (1 fsw = 3.06 kPa). Approximately half of the exposures were to a single PO2, while the remainder were more complicated consisting of exposures to multiple levels of hyperbaric O2. In 688 trials, there were 42 exposure-stopping symptoms. We used maximum likelihood to estimate parameters, likelihood ratios to compare model fits, and chi 2 tests to judge goodness-of-fit of model predictions to observations. The modeling shows that risk has a steep PO2 dependence. A model with autocatalytic features fits the data as well as a simpler model: when PO2 is elevated beyond 34 fsw, risk accumulates rapidly without bound while accumulating toward an asymptote at lower PO2 levels. This autocatalytic feature of risk accumulation implies a testable hypothesis that substantial protection from human CNS O2 toxicity can be obtained from intermittent exposure (periodic exposure to lower PO2). The models predict that the probability of O2 toxicity is less than 7% with current Navy limits while breathing 95% O2. Probability of symptoms is < 1% if FIO2 is maintained at the United States Navy recommended level of 75%.

A test for variations in individual sensitivity to hyperbaric oxygen toxicity.

It has been suggested that some individuals have above-average sensitivity to hyperbaric oxygen toxicity. An extensive human study completed at the Naval Experimental Diving Unit (NEDU) tested human tolerance to HBO and raised the possibility of assessing this hypothesis. In a group of 113 subjects given multiple exposures, some developed no symptoms of O2 toxicity while others developed symptoms on several occasions. The subjects in this study received unequal numbers of exposures of different depths and durations however, and it was not obvious how to determine unusual sensitivity. To assess the influences of chance vs. differences in sensitivity on the outcome of this experimental series, we performed a Monte Carlo simulation in which the experimental design was duplicated and the sensitivity hypothesis was evaluated statistically. The number of subjects giving rise to any symptoms and the distribution of individuals having symptoms on multiple occasions were evaluated. The simulation showed that the NEDU results were not unusual: nearly one quarter of the time the observed pattern of multiple symptoms could have been expected due to chance alone. The power of this simulation would have permitted detection of sensitivity factors 10 times (or greater) normal in 20% of the subjects at least half of the time.

Hydrogen gas is not oxidized by mammalian tissues under hyperbaric conditions.

Mammalian tissues, including heart, lung, liver, kidney, spleen, and skeletal muscle of guinea pig, rat, or pig, were exposed to tritium (T2) and high pressures of H2. Incorporation of the tritium label was measured to test for a latent capacity by mammalian tissues to oxidize H2 under conditions such as those experienced by deep divers breathing H2. Tissues were removed aseptically, and either minced, homogenized, or prepared as live cell cultures. The tissues were placed in a chamber to which 8 mCi T2, 1 MPa He, and either 1 or 5 MPa H2 were added. After 1 h the chamber was decompressed. The tissues were spun briefly in a vortex mixer to facilitate elimination of T2 in the gas phase. Samples were analyzed by scintillation counting for tritium incorporation in the liquid phase or in the tissues. Saline and distilled water were used as negative controls. Palladium (Pd) beads immersed in water, and cultures of the H2-metabolizing bacterium Alcaligenes eutrophus were used as positive controls. The tissues incorporated on the order of 10 nCi T2.ml-1, which implied a H2 incorporation of 10-50 nmol H2.g-1.min-1. However this incorporation was not different from that found in the water controls and was attributed to radioisotope effects. The Pd and bacterial samples incorporated over 1,000-fold more T2 than the mammalian tissues. We concluded that the mammalian tissues did not oxidize H2 under hyperbaric conditions, with a limit of detection of 100 nmol H2.g-1.min-1.

Effect of lipid on inert gas kinetics.

A Monte Carlo simulation of inert gas transit through skeletal muscle has been extended to include regions of increased gas solubility to simulate regions of high lipid content. Position of the regions within the simulation module was varied, as was the muscle-lipid partition coefficient (lambda). The volume percentage of the lipid regions (alpha) was varied from 0 to 25% while lambda covered the range from 1 to 50. The effects of alpha and lambda on mean transit time and on relative dispersion (RD; ratio of SD to the mean) were examined for a single lipid volume and compared with expected values under the assumption that the tissue is composed of two well-stirred compartments. Mean transit times varied from approximately 0.80 to 1.20 times the values predicted by a simple parallel two-compartment model, whereas RD varied from 0.9 to 3.6. For fixed lambda, RD as a function of lipid fraction passes through a maximum that is shifted and was also smaller than expected from a simple two-compartment model. For fixed alpha, RD approaches an asymptotic value for large lambda, but the asymptote is smaller than that expected from the two-compartment model. When lipid is distributed in only two regions, RD decreases with increasing separation of the regions and with increasing surface area of the fat regions. A model of two well-stirred compartments that allows mixing between the compartments yields results similar to those from the simulation.

Changes in triiodothyronine (T3) mononuclear leukocyte receptor kinetics after T3 administration and multiple cold-air exposures.

Repeated cold-air exposures increase human triiodothyronine (T3) plasma clearance rates. To study the response of the nuclear T3 receptor (NT3R) in this condition, binding characteristics were analyzed in human mononuclear leukocytes (MNL). In addition, we supplemented one group of individuals with a daily oral replacement dose of T3 to isolate the influence of serum thyroxine (T4) and thyrotropin (TSH) levels on receptor kinetics. The subjects were exposed to cold air (4 degrees C) twice/d, 30 min/exposure, for a total of 80 exposures. The T3-subjects received placebo [n = 8] and the T3 + subjects received T3 (30 micrograms/d) [n = 8] in a double-blind fashion. Mononuclear leukocytes were isolated from peripheral blood before the cold exposure and drug regimen began, and then after every 20 exposures. The dissociation constant (Kd) and maximum binding capacity (MBC) of the NT3R values were log transformed to minimize between-subject variability. In the T3+ group, serum total thyroxine (TT4), free T4 (FT4), and TSH were approx 50% lower than both basal and T3-values. The log10Kd increased 0.304 +/- 0.139 (p < 0.04) and the log10MBC increased 0.49 +/- 0.10 (p < 0.001) in the T3+ subjects compared to baseline. This change in MBC represents a 311% increase in the MBC over baseline and a fivefold increase over placebo-treated subjects. The T3- group showed no change in MBC over the study. These results describe for the first time the rapid modulation of the NT3R in response to the combined influence of cold exposure and reduced circulating T4 and TSH.

Contribution of tissue lipid to long xenon residence times in muscle.

Experiments demonstrate that the mean residence time of an inert gas in tissue is longer than that predicted by a single-compartment model of gas exchange. Also the relative dispersion (RD, the standard deviation of residence times divided by the mean) is 1 according to this model, but RDs in real tissues are closer to 2, suggesting that a multiple-compartment model might be more accurate. The residence time of a gas is proportional to its solubility in the tissue. Although the noble gases in particular are 10 times more soluble in lipid than in nonlipid tissues, models of gas exchange generally do not incorporate measurements of the lipid in tissue, which may lead to error in the predicted gas residence times. Could a multiple-compartment model that accounts for the lipid in tissue more accurately predict the mean and RD of gas residence times? In this study, we determined the mean and RD of Xe residence times in intact and surgically isolated muscles in a canine model. We then determined the lipid content and the perfusion heterogeneity in each tissue, and we used these measurements with a multiple-compartment model of gas exchange to predict the longest physiologically plausible Xe residence times. Even so, we found the observed Xe mean residence times to be twice as long as those predicted by the model. However, the predicted RDs were considerably larger than the observed RDs. We conclude that lipid alone cannot account for the residence times of Xe in tissue and that a multiple-compartment model is not an accurate representation of inert gas exchange in tissue.(ABSTRACT TRUNCATED AT 250 WORDS)

Quantifying the effect of intravascular perfluorocarbon on xenon elimination from canine muscle.

Intravenous infusions of perfluorocarbon (PFC) may improve decompression sickness outcome in animals by accelerating inert gas elimination from tissue, but any such effect has not been quantified experimentally. In this study we used an animal model of tissue Xe kinetics to test this hypothesis and to quantify the effect of PFC. Eight dogs were ventilated with dilute 133Xe in air for 4 h of Xe uptake. Four dogs were then given an infusion (20 ml/kg iv) of a 40% (vol/vol) perfluorodecalin-glycerol emulsion, and four control dogs were given only isotonic glycerol. All were then switched to open-circuit air breathing for 4 h of Xe elimination. During this time Xe radioactivity-time curves were recorded from two intact hind leg muscles, and the Xe mean residence times during elimination were estimated using an analysis by moments and compared by group. Tissue blood flows were measured using microspheres once during Xe uptake and twice during Xe elimination, and cardiac outputs were measured by thermodilution at 30-min intervals. In the PFC group the measured circulating PFC fraction increased the calculated Xe solubility by an average factor of 1.77 and so was expected to increase the Xe elimination rate by 77%. The observed Xe mean residence times on elimination for the PFC group averaged 33.5 min [95% confidence interval (CI) 19.5-47.6] compared with the glycerol control average of 70.1 min (95% CI 56.1-84.2), representing an increase in the rate of Xe elimination by a factor of 2.09 or 109%.(ABSTRACT TRUNCATED AT 250 WORDS)

Multiple cold air exposures change oral triiodothyronine kinetics in normal men.

The influence of cold exposure on triiodothyronine (T3) kinetics was studied in 16 men before, during (biweekly), and after 80 (10/wk) cold (4 degrees C) air exposures. We used serum values before and up to 24 h after a pharmacological oral (o) dose of T3 [76.8 nmol (50 micrograms)] to calculate noncompartmental kinetic parameters. To assess the role of thyroxine (T4) and thyrotropin (TSH), we administered a replacement dose of T3 [46.0 nmol/day (30 micrograms)] to eight men (+T3 group) and placebo to eight others (-T3 group) for the 2-mo study. There was no group effect of T3 treatment (+T3) on oral total volume of distribution (TVdo), metabolic clearance rate (MCRo), or disposal rate (DRo). TVdo was not changed over the study. Cold increased MCRo by 5.4 +/- 2.0 l.day-1.m-2. DRo increased with cold by 10.2 +/- 4.4 nmol.day-1.m-2. Although serum TSH, total T4, and free T4 decreased by approximately 50% in the +T3 group, the changes in MCRo and DRo with cold were not different from those in -T3. We describe that human T3 kinetics are changed with brief repeated exposures to cold air and that these increases in MCRo and DRo do not appear to be dependent on TSH or T4.

Predicting the time of occurrence of decompression sickness.

Probabilistic models and maximum likelihood estimation have been used to predict the occurrence of decompression sickness (DCS). We indicate a means of extending the maximum likelihood parameter estimation procedure to make use of knowledge of the time at which DCS occurs. Two models were compared in fitting a data set of nearly 1,000 exposures, in which greater than 50 cases of DCS have known times of symptom onset. The additional information provided by the time at which DCS occurred gave us better estimates of model parameters. It was also possible to discriminate between good models, which predict both the occurrence of DCS and the time at which symptoms occur, and poorer models, which may predict only the overall occurrence. The refined models may be useful in new applications for customizing decompression strategies during complex dives involving various times at several different depths. Conditional probabilities of DCS for such dives may be reckoned as the dive is taking place and the decompression strategy adjusted to circumstance. Some of the mechanistic implications and the assumptions needed for safe application of decompression strategies on the basis of conditional probabilities are discussed.

How countercurrent blood flow and uneven perfusion affect the motion of inert gas.

Monte Carlo simulations of the passage of inert gas through muscle tissue reveal that countercurrent gas exchange is more important than heterogeneity of flow in determination of the shape of inert gas washout curves. Semilog plots of inert gas washout are usually curved rather than straight. Two explanations often offered are that countercurrent flow may distort the shape and that uneven perfusion of the tissue gives rise to nonuniform washout. The curvature of the semilog plot may be summarized by the relative dispersion (RD), which is the ratio of the standard deviation of transit times to the mean transit time. For straight semilog plots, RD is 1. Semilog plots of data showing xenon washout from dog tissues are curved and have and RD of approximately 2. We have simulated the transit of gas particles through a vascular bed composed of repeating units of 100 mg of tissue perfused by three small vessels 80 microns in diameter and several levels of branching that direct flow through 190,000 capillaries. Geometric distribution of flow is important. Similar degrees of flow heterogeneity affect the curvature of the washout curve more if regions of heterogeneous flow are widely spaced than if they are close together. Diffusion blunts the effects of heterogeneous flow by mixing particles in high-flow regions with particles in low-flow regions. Because of this mixing, alternating regions of high flow and low flow spaced at intervals of less than 0.5 cm are unlikely explanations for the curved semilog plots.(ABSTRACT TRUNCATED AT 250 WORDS)