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Biomedical subjects

E Myhre

Publications and source records attributed to E Myhre.

At least 19 recordsLinked to original sources
PubMed2003

A new method for normalized interpretation of antimicrobial resistance from disk test results for comparative purposes.

OBJECTIVE: To evaluate a calibration method for disk diffusion antibiotic susceptibility tests, using zone diameter values generated in the individual laboratory as the internal calibrator for combinations of antibiotic and bacterial species. METHODS: The high-zone side of zone histogram distributions was first analyzed by moving averages to determine the peak position of the susceptible population. The accumulated percentages of isolates for the high zone diameter values were calculated and converted into probit values. The normal distribution of the ideal population of susceptible strains was then determined by using the least-squares method for probit values against zone diameters, and the ideal population was thereby defined, including mean and standard deviation. Zone diameter values were obtained from laboratories at the Karolinska Hospital (KS) and Växjö Hospital (VX), and from two laboratories (LabA, LabB) in Argentina. The method relies on well standardized disk tests, but is independent of differences in MIC limits and zone breakpoints, and does not require the use of reference strains. Resistance was tentatively set at below 3 SD from the calculated, ideal mean zone diameter of the susceptible population. RESULTS: The method, called normalized interpretation of antimicrobial resistance, was tested on results from the KS and VX clinical microbiology laboratories, using the disk diffusion method for antimicrobial susceptibility tests, and for two bacterial species, Staphylococcus aureus and Escherichia coli. In total, 114 217 test results were included for the clinical isolates, and 3582 test results for control strains. The methodology at KS and VX followed the standard of the Swedish Reference Group for Antibiotics (SRGA). Zone diameter histograms for control strains were first analyzed to validate the procedure, and a comparison of actual means with the calculated means showed a correlation coefficient of r = 0.998. Results for clinical isolates at the two laboratories showed an excellent agreement for 54 of 57 combinations of antibiotic and bacterial species between normalized interpretations and the interpretations given by the laboratories. There were difficulties with E. coli and mecillinam, and S. aureus and tetracycline and rifampicin. The method was also tested on results from two laboratories using the NCCLS standard, and preliminary results showed very good agreement with quality-controlled laboratory interpretations. CONCLUSIONS: The normalized resistance interpretation offers a new approach to comparative surveillance studies whereby the inhibition zone diameter results from disk tests in clinical laboratories can be used for calibration of the test.

Anti-Bacterial Agents↗
PubMed2000

Effects of NO inhalation on pulmonary leukocyte sequestration and blood volume in porcine endotoxaemia.

OBJECTIVE: Sequestration and migration of activated neutrophils plays a major role in the pulmonary injury typical of septic shock and the adult respiratory distress syndrome. Inhaled NO may counteract alveolar-capillary damage attributed to activated neutrophils. The present study describes a method to directly demonstrate the effects of NO inhalation on endotoxin-induced sequestration of 99mTc-labelled leukocytes [As(t)] in the lungs of pigs. DESIGN: Prospective controlled study. SETTING: Laboratory for experimental surgery at a university medical centre. SUBJECTS: Anaesthetised and ventilated pigs. INTERVENTIONS: To induce inflammatory shock 26 animals received a continuous endotoxin infusion. Thirteen animals inhaled NO from the start of the experiments, while 13 served as controls. In 13 animals from both groups, leukocytes were labelled in vitro and reinjected, while in the 13 others erythrocytes were labelled in vivo to provide corrections for changes in blood volume. MEASUREMENTS AND RESULTS: The pulmonary distribution of 99mTc-labelled leukocytes or erythrocytes was studied dynamically for 180 min. After correction for changes in pulmonary and heart blood volume (PBV, HBV), leukocyte sequestration curves were generated. Endotoxin induced pulmonary vasoconstriction, reduced PBV, impaired oxygenation, and caused a maximum increase in As(t) of 30% in the lungs. NO inhalation attenuated pulmonary vasoconstriction and the reduction in PBV. The maximum increase in As(t) was reduced to 15% of baseline. CONCLUSIONS: Inhaled NO exerts its main vascular effects in the pulmonary microvasculature, the primary site of physiological neutrophil margination and pathological adhesion of activated leukocytes. Early use of NO inhalation may offer protection against the development of more lasting pulmonary failure in septic shock by reducing leukocyte sequestration in the lungs.

Administration, Inhalation↗
PubMed1999

Intestinal and hepatic perfusion and metabolism in hypodynamic endotoxic shock. Effects of nitric oxide synthase inhibition.

BACKGROUND: Inhibition of nitric oxide synthase (NOS) has been claimed to be beneficial in septic shock. We investigated the overall and regional effects of a NOS-inhibitor on perfusion and metabolism during severe endotoxic shock. METHODS: Nineteen anaesthetised pigs were catheterised and ultrasonic flow-probes were placed around the portal vein, the hepatic artery, and the superior mesenteric artery. Thirteen animals were given a 3-h infusion of endotoxin; in 6 of these an infusion of NG-nitro-L-arginine-methyl-ester (L-NAME) was started an hour after the start of endotoxin while 7 animals served as controls and received endotoxin only. Six animals were sham operated with no further intervention. RESULTS: Endotoxin produced a hypodynamic shock with pulmonary hypertension. L-NAME did not increase arterial blood pressure, but deepened the fall in cardiac output and enhanced the increase in systemic and pulmonary vascular resistance. The infusion of endotoxin caused a decrease in flows in all regions. The addition of L-NAME induced a further decrease in the mesenteric artery flow only. L-NAME had no additional effect on hepatic artery flow ratio, while a transient decrease was seen in mesenteric flow ratio. Portal flow ratio decreased in the control group only. Global as well as regional oxygen extraction increased in both groups, more so in the L-NAME group. Lactate levels increased with no differences between the groups. CONCLUSION: In hypodynamic endotoxic shock, L-NAME infusion enhanced pulmonary vasoconstriction and increased left ventricular afterload. The resulting hypoperfusion caused an increase in mortality. The effects of L-NAME on global and mesenteric blood flow and metabolism were similar, while L-NAME had no additional effects on hepatic hypoperfusion or oxygen extraction. Thus, nitric oxide does not seem to be a major factor in the preservation of hepatic perfusion during unresuscitated endotoxic shock.

Animals↗
PubMed1998

The effects of nitric oxide inhalation on respiratory mechanics and gas exchange during endotoxaemia in the pig.

BACKGROUND: In the adult respiratory distress syndrome, nitric oxide (NO) inhalation improves oxygenation through reducing ventilation-perfusion mismatching, but detailed information on the pulmonary effects of NO inhalation in septic shock is scarce. The present study investigated the effects of inhaled NO on alveolar dead space (Vdalv) and venous admixture as well as on respiratory system compliance (Crs) and respiratory system resistance (Rrs) in a porcine model of septic shock. Protective effects of NO are discussed. METHODS: Thirteen anaesthetised and ventilated pigs were given an infusion of endotoxin for an observation time of 220 min to induce acute lung injury (ALI). In the NO-early group (n=6), an inhalation of 60 ppm NO was started simultaneously with the endotoxin infusion and continued for 190 min. In 7 control/NO-late animals, 60 ppm NO was administered for 30 min following 190 min of endotoxin infusion. Haemodynamics, single-breath CO2-, pressure-, and flow signals were recorded. RESULTS: Endotoxin induced haemoconcentration, pulmonary vasoconstriction, and a decrease in Crs, while venous admixture, Vdalv, and Rrs increased. In the NO-early group, the pulmonary vasoconstriction was attenuated, no increase in pulmonary venous admixture or in Vdalv was seen before cessation of NO, and the improvements in oxygenation outlasted the NO inhalation. In the control/NO-late group, the NO inhalation reversed the changes in dead space and venous admixture. NO had no effect on the changes in respiratory mechanics. CONCLUSION: In porcine ALI, 60 ppm NO diminishes pulmonary vasoconstriction and improves gas exchange by reducing pulmonary venous admixture and alveolar dead space, but does not prevent a fall in Crs. NO inhalation may help prevent long-lasting pulmonary failure.

Administration, Inhalation↗
PubMed1997

Differential effects of nitric oxide synthase modulation on porcine systemic and pulmonary circulation in vivo.

OBJECTIVE: To study and compare the effects of inhibiting endothelial nitric oxide synthase on systemic and pulmonary circulation in an in vivo model. DESIGN: Prospective, randomized, controlled study. SETTING: Laboratory for experimental surgery at a university medical center. SUBJECTS: Seventeen anesthetized, mechanically ventilated pigs. INTERVENTIONS: To produce a stable and continuous stimulation of endothelial nitric oxide synthase, an infusion of acetylcholine was given to one group of animals (n = 5) in a dose that decreased mean arterial pressure by 15%. After 45 mins, N(G)-monomethyl-L-arginine (L-NMMA) was given in a dose of 3 mg/kg for 5 mins in order to inhibit the enzyme. A second dose of 10 mg/kg was given 30 mins later. L-arginine was then given in a dose of 100 mg/kg to reverse the inhibition. One group of animals (n = 6) received a single dose of indomethacin (2.5 mg/kg) 15 mins after the start of acetylcholine infusion. L-NMMA and L-arginine were then given. In a control group (n = 5), the effects of L-NMMA and L-arginine were studied without acetylcholine. Circulatory parameters were monitored and resistance indices were calculated via arterial, central venous, and pulmonary artery catheters. MEASUREMENTS AND MAIN RESULTS: In control animals, 3 and 10 mg/kg of L-NMMA induced an increase in mean arterial pressure of 14% and 25%, respectively, with similar increases in systemic vascular resistance. Mean pulmonary arterial pressure increased by 22% and 48%, respectively. Acetylcholine lowered mean arterial pressure by 15% and did not affect the relative changes induced by L-NMMA. Acetylcholine had no effect on pulmonary resting tone but enhanced the pulmonary hypertension and increase in resistance induced by L-NMMA. This enhancement was abolished by indomethacin, which produced systemic hypertension while no effect on pulmonary pressure was seen. CONCLUSIONS: A basal release of nitric oxide contributes to the maintenance of normal vascular tone in the anesthetized pig. Stimulation of endothelial nitric oxide synthase by acetylcholine did not result in any further pulmonary vasodilation as was seen in the systemic circulation. Inhibition of nitric oxide synthase had a greater effect on pulmonary pressure than on systemic pressure. However, this difference was abolished by the administration of indomethacin. Increased nitric oxide release or acetylcholine itself seems to stimulate the production of a vasoconstricting prostanoid in the pulmonary circulation.

Acetylcholine↗
PubMed1993

On the interaction between protein L and immunoglobulins of various mammalian species.

Protein L, a cell wall molecule of certain strains of the anaerobic bacterial species Peptostreptococcus magnus, shows high affinity for human immunoglobulin (Ig) light chains. In the present study protein L was tested against a panel of human myeloma proteins of the IgG, IgM, IgA and IgE classes, and strong binding was seen with antibodies carrying kappa light chains. A high degree of specificity for Ig was demonstrated in binding experiments with human plasma proteins. Apart from human Ig, strong protein L-binding activity was also detected in the serum of 12 out of 23 tested additional mammalian species, including other primates and rodents. Subsequent analysis with purified Ig samples demonstrated the binding of protein L to Ig of important laboratory animal species such as the mouse, the rat and the rabbit. The affinity constants for the interactions between protein L and polyclonal IgG of these species were 2.6 x 10(9), 3.9 x 10(8) and 7.4 x 10(7), respectively. In non-human species, the binding of protein L was also found to be mediated through Ig light chains, and the results demonstrate the potential value of protein L as an immunochemical tool.

Animals↗
PubMed1991

[Prolonged action nitrates in stable angina pectoris].

A randomized double blind comparison of transdermal nitroglycerin and isosorbide dinitrate tablets was conducted in 100 men with stable angina pectoris. Subjective and objective effects were virtually identical for both regimens (number of angina attacks/nitroglycerin consumption and exercise ECG test variables). The pattern of side effects was also similar for both drugs. A considerable dissociation was observed between subjective effects and effects measured by ergometer test in the individual patient. Lack of both subjective and objective effects--i.e. nitrate tolerance--was observed in approximately one fourth of the patients, and was not prevented by a twelve-hour dosing interval on isosorbide dinitrate nor a six hour transdermal nitroglycerin-free interval. Our data lends credence to the notion that the effects of long-acting nitrates in daily life and the effects measured during stress testing may involve different mechanisms.

Administration, Cutaneous↗
PubMed1989

Effects of verapamil on left ventricular relaxation and filling dynamics in coronary artery disease: a study by pulsed Doppler echocardiography.

The effect of verapamil on left ventricular diastolic function in coronary artery disease was assessed by Doppler echocardiography of transmitral flow velocities in 20 patients. At baseline, isovolumic relaxation time was prolonged compared with that in 18 age-matched normal subjects (95 +/- 13 msec versus 74 +/- 12 msec, p less than 0.001), but decreased to 80 +/- 14 msec (p less than 0.001) after treatment. The ratio between early and atrial-induced transmitral velocities (E/A-ratio) at baseline was lower in patients than in normal subjects (1.1 +/- 0.2 versus 1.4 +/- 0.3, p = 0.01), as was the filling fraction of the first third of diastole (43% +/- 5% versus 50% +/- 4%, p less than 0.001). Verapamil treatment increased the E/A-ratio to 1.3 +/- 0.4 (p less than 0.001) and filling fraction to 45% +/- 4% (p = 0.055) because of increased early filling. No change in systolic performance or heart rate was observed. Thus, coronary artery disease was associated with retarded relaxation and impairment of early filling. However, verapamil treatment enhanced relaxation and induced a filling shift toward early diastole, which indicated improved diastolic performance. The changes probably reflected reduced myocardial ischemia.

Adult↗
PubMed1988

Plasma atrial natriuretic peptide in cardiac transplant recipients. A prospective study.

Cardiac transplantation in 10 patients with congestive heart failure resulted in reduction of high plasma concentrations of atrial natriuretic peptide (ANP), preoperatively five-fold above normal, to a level two-fold above normal, which was maintained throughout a 12-week follow-up period. Cardiac function was normalized in all patients. Transient increases in plasma ANP, in four cardiac recipients 3-10-fold their basal levels, could neither be related to rejection episodes nor to cardiac dysfunction, but rather to signs of fluid and sodium retention. High plasma ANP levels in cardiac transplant recipients suggest that the capacity to secrete ANP is preserved in the transplanted heart.

Adolescent↗
PubMed1987

Reproducibility of cardiac stroke volume estimated by Doppler echocardiography.

Doppler echocardiography was used to measure cardiac stroke volume in 10 patients with coronary artery disease who were treated with cardioactive drugs. Stroke volume estimates were determined at the aortic orifice by multiplying area by systolic velocity integral measured both from the suprasternal and the apical approach. Recordings were done independently by 2 experienced observers on the same day and repeated once after 1 to 21 days. Analysis of variance showed that no systematic differences were introduced by the 2 observers and Doppler approaches or by measuring on different days. The coefficient of variation between any pair of measurements in each patient was 9%. This variability is probably a result of the method or spontaneous fluctuations of the stroke volume and not of the varying recording conditions. The ultrasonic method detects day-to-day changes of cardiac stroke volume larger than 20% with a probability greater than 0.95.

Adult↗
PubMed1987

Quantification of mitral regurgitation by Doppler echocardiography.

The present study was undertaken to evaluate a new non-invasive approach to the quantification of mitral regurgitation. Doppler echocardiography and left ventriculography were performed in 20 patients without valvular heart disease (group A), and in 30 patients with pure mitral regurgitation (group B). Volumetric flows through the aortic and mitral valve orifices were determined by Doppler technique. The aortic flow (AF) was calculated as the product of the aortic orifice area by the systolic velocity integral. The mitral flow (MF) was computed as the product of the corrected mitral orifice area by the diastolic velocity integral. The mitral regurgitant fraction (RF) was calculated as: RF = 1 - AF/MF. In group A, there was a close agreement between aortic and mitral flows (r = 0.94, P less than 0.001), and there was no significant difference between the two measurements. In group B, the mitral flow was significantly higher than the aortic flow. The regurgitant fraction assessed by Doppler echocardiography correlated well with the grades of severity of regurgitation obtained at left ventriculography. We conclude that combined measurement of both aortic and mitral flows by Doppler echocardiography provides a new and promising approach to the noninvasive quantification of mitral regurgitation.

Adult↗
PubMed1986

Measurement of aortic regurgitation by Doppler echocardiography.

In an attempt to develop a new approach to the non-invasive measurement of aortic regurgitation, transmitral volumetric flow (MF) and left ventricular total stroke volume (SV) were measured by Doppler and cross sectional echocardiography in 23 patients without aortic valve disease (group A) and in 26 patients with aortic regurgitation (group B). The transmitral volumetric flow was obtained by multiplying the corrected mitral orifice area by the diastolic velocity integral, and the left ventricular total stroke volume was derived by subtracting the left ventricular end systolic volume from the end diastolic volume. The aortic regurgitant fraction (RF) was calculated as: RF = 1 - MF/SV. In group A there was a close agreement between the transmitral volumetric flow and the left ventricular total stroke volume, and the difference between the two measurements did not differ significantly from zero. In group B the left ventricular total stroke volume was significantly larger than the transmitral volumetric flow, and there was good agreement between the regurgitant fractions determined by Doppler echocardiography and radionuclide ventriculography. Discrepancies between the two techniques were found in patients with combined aortic and mitral regurgitation or a low angiographic left ventricular ejection fraction (less than 35%). The effective cardiac output measured by Doppler echocardiography accorded well with that measured by the Fick method. Doppler echocardiography provides a new and promising approach to the non-invasive measurement of aortic regurgitation.

Adolescent↗
PubMed1986

Analysis of methodology for quantifying mitral regurgitation by Doppler echocardiography.

It is generally agreed that Doppler echocardiography is highly sensitive and specific for the detection of mitral regurgitation. There is more confusion about its ability to quantitate the degree of mitral regurgitation. Studies of the intensity of the Doppler signals, as well as cross sectional Doppler studies apparently can provide a straightforward, but rough estimate of the degree of regurgitation in term of atrial extent of the disturbed flow. The methods are also sensitive to methodological errors as beam direction, movement of the heart, signal/noise relationship and the size of the left atrium. Another approach to the non-invasive measurement of mitral regurgitation includes the use of Doppler echocardiography for the determination of both aortic and mitral volumetric flow. In a study of patients with mitral regurgitation, we found a close correlation between the regurgitant fraction determined by Doppler echocardiography, and the regurgitant severity determined by left ventriculography. This technique can only be used in pure mitral regurgitation, while associated atrial fibrillation, mitral stenosis, and combined aortic and mitral regurgitation make correct measurements difficult.

Cardiac Output↗