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Biomedical subjects

E K Walsh

Publications and source records attributed to E K Walsh.

16 recordsLinked to original sources
PubMed2004

Control of myocardial oxygen consumption in transgenic mice overexpressing vascular eNOS.

Our objective was to investigate the potential role of selective endothelial nitric oxide (NO) synthase (eNOS) overexpression in coronary blood vessels in the control of myocardial oxygen consumption (MVO2). Transgenic (Tg) eNOS-overexpressing mice (eNOS Tg) (n=22) and wild-type (WT) mice (n=24) were studied. Western blot analysis indicated greater than sixfold increase of eNOS in cardiac tissue. Echocardiography in awake mice indicated no difference in cardiac function between WT and eNOS Tg; however, systolic pressure in eNOS Tg mice decreased significantly (126 +/- 2.3 to 109 +/- 2.3 mmHg; P <0.05), whereas heart rate (HR) was not different. Total peripheral resistance (TPR) was also decreased (9.8 +/- 0.8 to 7.6 +/- 0.4 4 mmHg.ml(-1).min; P <0.05) in eNOS Tg. Furthermore, female eNOS Tg mice showed even lower TPR (7.2 +/- 0.4 mmHg.ml(-1).min) compared with male eNOS mice (8.6 +/- 0.5, mmHg.ml.min(-1); P <0.05). Left ventricular slices were isolated from WT and eNOS Tg mice. With the use of a Clark-type oxygen electrode in an airtight bath, MVO2 was determined as the percent decrease during increasing doses (10(-10) to 10(-4) mol/l) of bradykinin (BK), carbachol (CCh), forskolin (10(-12) to 10(-6) mol/l), or S-nitroso-N-acetyl penicillamine (SNAP; 10(-7) to 10(-4) mol/l). Baseline MVO2 was not different between WT (181 +/- 13 nmol.g(-1).min(-1)) and eNOS Tg (188 +/- 14 nmol.g(-1).min(-1)). BK decreased MVO2 (10(-4) mol/l) in WT by 17% +/- 1.1 and 33% +/- 2.7 in eNOS Tg (P < 0.05). CCh also decreased MVO2, 10(-4) mol/l, in WT by 20% +/- 1.7 and 31% +/- 2.0 in eNOS Tg (P <0.05). Forskolin (10(-6) mol/l) or SNAP (10(-4) mol/l) also decreased MVO2 in WT by 24% +/- 2.8 and 36% +/- 1.8 versus eNOS 31% +/- 1.8 and 37% +/- 3.5, respectively. N-nitro-L-arginine methyl ester (10(-3) mol/l) inhibited the MVO2 reduction to BK, CCh, and forskolin by a similar degree (P <0.05), but not to SNAP. Thus selective overexpression of eNOS in cardiac blood vessels in mice enhances the control of MVO2 by eNOS-derived NO.

Animals↗
PubMed1994

The Jarisch-Herxheimer reaction in leptospirosis.

Three patients with leptospirosis whose condition worsened after initiation of antibiotic therapy are reported. Their clinical deterioration appeared to be due to the development of the Jarisch-Herxheimer reaction rather than to progression of their underlying infection. Relevant aspects of the management of patients with leptospirosis are discussed.

Adolescent↗
PubMed1991

Contribution of brain distortion and displacement to CSF dynamics in experimental brain compression.

The present study was designed to determine the contribution of brain distortion and displacement to changes in cerebrospinal fluid (CSF) dynamics [pressure-volume index (PVI), compliance (C), and outflow resistance (Ro)] during progressive brain compression and the effect of compression on brain mechanical properties. In 10 dogs measurements were made of CSF dynamics, brain elastic behavior, cerebral perfusion pressure, local cerebral blood flow, and suprainfratentorial intracranial pressure (ICP) during the incremental expansion of a supratentorial extradural balloon. PVI appeared more as a measure of the compressibility of the cerebral vascular compartment than of intracranial bulk compliance. Reciprocal changes in CSF dynamics behaved as expected when the balloon expanded predominantly supratentorially causing a moderate increase in ICP. A significant increase in ICP, however, caused a rise in PVI and a decrease in compliance. Under these conditions PVI alone could not differentiate between a falling cerebral perfusion pressure and an increasing suprainfratentorial ICP gradient. In contrast, the compliance decreased with balloon expansion while the outflow resistance showed an inverse correlation with compliance and a linear correlation with baseline ICP; Go, an elastic response parameter, consistently decreased, implying that C, Ro, and Go can be used as a trend of intracranial compensatory reserve during intracranial mass expansion.

Animals↗
PubMed1990

Brain tissue elasticity and CSF elastance.

In the analysis of the pressure-volume relationship of the intracranial system, the concept of brain elastance, sometimes called tissue elastance or CSF elastance, is often used. It is generally designated as Ecsf and is calculated as the slope of the pressure-volume curve of the system. Variations in Ecsf are related to, for example, changes in the buffering capacity of the system which, however, could be influenced by the cerebral vascular volume, compressibility of the meningeal membranes, and compressibility of the subpial brain tissue. Our interest is in isolating the effect of controlled changes in the intracranial system with changes in the subpial tissue only. Here we discuss the measurement of brain tissue elasticity and describe two experimental conditions in which simultaneous measurements showed distinct differences between the behaviour of the system CSF elastance and brain tissue elastic behaviour.

Animals↗
PubMed1989

Attenuation of decompressive hypoperfusion and cerebral edema by superoxide dismutase.

This study tested the hypothesis that ischemia-reperfusion injury initiated by the superoxide anion radical is a major component of postdecompression hypoperfusion and cerebral edema, and could be attenuated by superoxide dismutase (SOD). A supratentorial extradural balloon was placed in 20 fasting, lightly anesthetized, mechanically ventilated dogs and inflated in 0.5-ml increments (0.07 ml/sec) at 15-minute intervals. The end-point of balloon expansion was the onset of an isoelectric electroencephalogram, near-arrest of hemispheric cerebral blood flow (CBF) (measured by H2 clearance), and the appearance of a suprainfratentorial intracranial pressure gradient, which was held for 15 minutes. The in vivo development of brain edema was detected by measuring brain elastic response (BER) extradurally, and was correlated with postmortem measurement of brain water content (gravimetry); blood-brain barrier integrity was tested by Evans blue dye given after the insult. After decompression, the dogs were randomly assigned to one of four treatment groups: Group I received hyperventilation (PaCO2 28 +/- 1 mm Hg, mean +/- standard deviation); Group II received furosemide (2.4 mg/kg) and pentobarbital (10 mg/kg) every 8 hours; Group III received 20% mannitol in a 1.4-gm/kg bolus plus furosemide, 0.5 mg/kg; and Group IV received SOD, 15,000 U/kg every 15 minutes for 3 hours. At 4 hours of decompression Group IV had significantly greater recovery in local CBF and BER than Groups I, II, and III (p less than 0.05). The 24-hour survival rate was 20% for Group I, 60% for Group II, 80% for Group III, and 100% for Group IV. The survival rate appeared to correlate with a variable degree of postmortem intraparenchymal hemorrhages, blood-brain barrier disruption, and moderate to severe brain edema for Groups I, II, and III. In contrast, Group IV had the least brain edema (p less than 0.05) and Evans blue dye extravasation (p less than 0.05) and the fewest intraparenchymal hemorrhages. These data support the hypothesis that, under the experimental conditions described here, the superoxide anion plays a major role in the pathophysiology of postdecompression ischemic edema.

Animals↗
PubMed1988

Brain tissue elastic behavior and experimental brain compression.

This study was designed to test the hypothesis that the progressive expansion of an extradural mass causes detectable changes in brain mechanical response properties, in particular the nonlinear elastic behavior, before any significant changes in intracranial cerebrospinal fluid pressure can be detected. In 10 chronically prepared and anesthetized dogs, incremental inflation (0.07 ml/s) of an extradural balloon caused 1) a progressive fall in the brain nonlinear elastic parameter (G0, mmHg/mm2), 2) nonsignificant changes in brain tissue elasticity (G0, mmHg/mm), 3) a disproportionate progressive rise in subpial tension, and 4) a progressive fall in local cerebral blood flow (H2 clearance), despite a modest decrease in cerebral perfusion pressure (extracranial). In previous brain compression experiments (Brain Res. 305: 141-143, 1984) we have shown that the compression site becomes compacted and stiffer (increased G0) and its nonlinear elastic parameter (G0) increases markedly. These earlier findings, coupled with the present observation of a loss in tissue nonlinearity distally to the compression site, are most likely the major mechanisms by which, with a rapidly expanding intracranial mass, tissue pressure gradients and brain displacement, including transtentorial herniation, develop.

Animals↗
PubMed1984

Brain elastic behavior in experimental brain compression: influence of steroid therapy.

In chronically prepared dogs we studied the influence of large doses of steroids on experimentally increased brain stiffness. The latter was quantified by measuring brain elastic response, in terms of the (instantaneous) initial tangent, Go (mm Hg/mm). After epidurally induced brain compression (45 min), Go increased and remained elevated in spite of steroid therapy. The data suggest that steroids are ineffective in congestive hyperemia consequent to ischemic compression.

Animals↗
PubMed1984

Calculation of brain elastic parameters in vivo.

In an earlier study [Am. J. Physiol. 232 (Regulatory Integrative Comp. Physiol. 1): R27-R30, 1977], we defined the concept of brain elastic response in vivo as measured by a pressure-depth ratio (G0) derived from a graphic analysis of the elastic response tests. These tests have shown that brain elastic response in vivo is sensitive to changes in the intracranial system and that the response is nonlinear. In this study we identify a second parameter, G0, a second-order pressure-depth ratio that characterizes the nonlinear behavior and, along with G0, can be evaluated from a mathematical relation that models the experimental results obtained from the elastic response test. The equation is a logarithmic function relating the pressure and the subpial insertion depth. From this we obtain G0 and G0 as the slope and curvature of the response function at the subpial position. In animal experiments we correlated the changes in these parameters with those of cerebral hemodynamics during hemorrhagic and drug-induced hypotension. The calculated values of G0 and G0 are reproducible and reflect changes in cerebral blood flow and/or volume.

Animals↗
PubMed1981

Occlusal forces during chewing and swallowing as measured by sound transmission.

Forces during the phase of occlusal contact during chewing and swallowing are surprisingly high (36.2% and 41%), about 40% of the subject's maximum biting force. Previous studies using transducers in fixed partial dentures measured only a portion of the total force and have given the impression that chewing forces are much less than the data reported in this study. The importance of occlusal stability in the intercuspal position is of utmost clinical significance. Steep anterior guidance does not appear to expose the teeth to extreme lateral forces. The gliding contacts of the teeth while entering and leaving the intercuspal position have been shown to be of short duration and low magnitude when compared with the forces generated in the intercuspal position. During chewing, the peak occlusal force occurred well after the peak EMG activity. EMG activity by itself does not directly correlate with the force generated during chewing. The sound transmission method for measuring interjaw force during chewing, which was developed as part of this project, proved to be practical for research purposes. No intraoral devices are required, and the time relationship to force is accurate to within 15 ms.

Adolescent↗
PubMed1977

On measurement of brain elastic response in vivo.

The elastic response behavior of brain tissue in vivo has been shown to be sensitive to the physiological environment of the brain and thus represents a useful parameter for identifying effects of controlled changes on the system. Here we describe a method for measuring brain elastic response using an epidural pressure-depth transducer and a minimum number of insertions. The method also serves to identify the nonlinear response of brain tissue.

Animals↗
PubMed1976

Elastic behavior of brain tissue in vivo.

A measurement system and a test sequence have been developed to determine the in vivo elastic response of brain tissue in terms of a pressure-depth ratio. This parameter appears sensitive to changes in the tissue environment that may occur due to the influence of, e.g., anesthetic agents, hyperventilation, etc., and thus may be useful in evaluating such influences. The measurements are made with the dura-arachnoid membranes intact, thus maintaining the influence of the cerebrospinal fluid compartment on the response behavior of the brain tissue that comprises the subpial region. As an integral part of the test, the procedure also serves to determine the depth or position of the subpial region and thus assures that the subsequent pressure-depth measurements invole brain tissue response. Finally, some discussion is given to relating the measured pressure-depth ratio to the classical elastic modulus. Values of the pressure-depth ratio and the corresponding elastic modulus for seven dogs are given.

Animals↗