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Biomedical subjects

E Martin

Publications and source records attributed to E Martin.

At least 343 records · Page 19Linked to original sources
PubMed1995

Cholangiographic features in fibrosis and cirrhosis of the liver. Radiological-pathological correlation.

The cholangiographic features of intrahepatic bile ducts associated with cirrhosis or fibrosis are not well known. In order to achieve a radiological-pathological correlation, we studied nine livers with fibrosis or cirrhosis excised at autopsy. Cholangiograms were obtained within 24 hr after death from the nonfixed liver and multiple tissues samples were taken for histologic examination. Radiological data were interpreted by two independent investigators blinded to the clinical and histological findings. Cirrhosis (alcoholic in 4, posthepatitis in two) was observed in six livers, fibrosis (alcoholic in 2, posthepatitis in one) in three. No liver with fibrosis had cholangiographic abnormalities. In contrast, cholangiography of all livers with cirrhosis was abnormal. Abnormalities were a diminished arborization, a decrease of the distal opacification, an irregularity of caliber, and a tortuous course of the bile ducts. Histological study showed that the irregular and tortuous course were due to compression of the bile ducts by regenerative nodules. Furthermore, a thick fibrosis was organized around the bile ducts. In conclusion, fibrosis alone was not associated with cholangiographic abnormalities. In cirrhotic livers, intrahepatic bile ducts showed an irregular and tortuous course, a diminished arborization and a decrease of the distal opacification. These abnormalities were secondary to the presence of regenerative nodules and fibrosis organized around the bile ducts.

Autopsy↗
PubMed1995

Withholding and withdrawing life-sustaining therapy in a Canadian intensive care unit.

The purpose of this study was to document the rationale and procedures for withholding and withdrawing life-sustaining treatment in critically ill patients. A prospective observational study was conducted over 12 mo in a Canadian academic intensive care unit. Of the 110 intensive care unit patients who died during the study period, 71 (64.5%) died after treatment was withheld or withdrawn. Compared with the other 39 patients who died despite full therapy, these patients were found to have a longer hospital and ICU stay, more organ systems failed, and a higher rate of malignancy. Intensivists rated poor prognosis for survival and poor quality of life should the patient survive as being the two most important factors when making a decision to withhold or withdraw treatment, while patient age and physical health prior to hospital admission were the two least important factors. There was a consistent approach to withdrawing therapy in 68 of the 71 patients who had treatment either withheld or withdrawn. In these 68 patients, the first step was to write a do-not-resuscitate order, vasopressor drugs were then stopped and, lastly, the patient was weaned from mechanical ventilation and the trachea was extubated. The results of this study demonstrate that life-supporting treatment is commonly withdrawn in critically ill patients when continued therapy is thought to be unlikely to restore the patient to health.

Age Factors↗
PubMed1995

Intraoperative identification of parathyroid gland pathology: a new approach.

Technetium 99m-sestamibi, a radiopharmaceutical used for the diagnostic imaging of abnormal parathyroid tissue, and the Neoprobe 1000, a hand-held, gamma-detecting probe, were used concurrently, during surgical exploration, in three children with hyperparathyroidism. This novel combination assisted with the identification of an ectopic mediastinal parathyroid adenoma and with the localization of multiple hyperplastic parathyroid glands. 99mTc-sestamibi combined with the Neoprobe 1000 may prove to be a useful adjunctive technique for the intraoperative localization of abnormal parathyroid tissue in selected patients.

Adenoma↗
PubMed1995

Huntingtin is a cytoplasmic protein associated with vesicles in human and rat brain neurons.

The gene defective in Huntington's disease encodes a protein, huntingtin, with unknown function. Antisera generated against three separate regions of huntingtin identified a single high molecular weight protein of approximately 320 kDa on immunoblots of human neuroblastoma extracts. The same protein species was detected in human and rat cortex synaptosomes and in sucrose density gradients of vesicle-enriched fractions, where huntingtin immunoreactivity overlapped with the distribution of vesicle membrane proteins (SV2, transferrin receptor, and synaptophysin). Immunohistochemistry in human and rat brain revealed widespread cytoplasmic labeling of huntingtin within neurons, particularly cell bodies and dendrites, rather than the more selective pattern of axon terminal labeling characteristic of many vesicle-associated proteins. At the ultrastructural level, immunoreactivity in cortical neurons was detected in the matrix of the cytoplasm and around the membranes of the vesicles. The ubiquitous cytoplasmic distribution of huntingtin in neurons and its association with vesicles suggest that huntingtin may have a role in vesicle trafficking.

Animals↗
PubMed1995

Continuous versus intermittent cardiac output measurement in cardiac surgical patients undergoing hypothermic cardiopulmonary bypass.

OBJECTIVE: Continuous thermodilution cardiac output (CCO) measurement was clinically evaluated in patients who underwent coronary revascularization using hypothermic low-flow, low-pressure cardiopulmonary bypass (CPB). DESIGN: Prospective study. SETTING: University hospital setting. PARTICIPANTS: 30 cardiac surgical patients. INTERVENTIONS: CCO was correlated to standard bolus thermodilution cardiac output (ICO) obtained at end-expiration. MEASUREMENTS AND MAIN RESULTS: Measurements were taken at selected time points (n = 18) before anesthesia induction, before CPB, and 5 minutes to 12 hours after CPB. A total of 540 data pairs were thus obtained. ICO ranged from 1.9 to 9.9 L/min, CCO from 1.5 to 9.9 L/min. Correlation between ICO and CCO was highly significant (r = 0.872; p < 0.01), accompanied by an excellent accuracy (bias -0.0213 L) and precision (0.59 L) before CPB and more than 45 minutes after CPB. However, during the first 45 minutes after CPB, there was no correlation (r = 0.273) between ICO and CCO, and ICO tended to be relatively high, whereas CCO measurements showed relatively low values. During the first 45 minutes after hypothermic CPB, but not during the ensuing time period, central blood temperature decreased, which may be interpreted as a lack of thermal equilibration between central and peripheral compartments. It is hypothesized that thermal instability in combination with increased respiratory variations in pulmonary artery blood temperature caused inhomogenous rewarming of different body sites and might be the main reason for the lack of correlation between ICO and CCO. CONCLUSIONS: Despite an excellent correlation, accuracy, and precision between CCO and ICO before CPB and more than 45 minutes after hypothermic CPB, a lack of correlation in the early phase after CPB has been found. Further investigation is needed to elucidate the underlying cause of these findings and to clarify whether ICO or CCO or both fail to represent the real cardiac output up to 45 minutes after weaning from hypothermic CPB.

Adult↗
PubMed1995

[Behavior of intraocular pressure in anesthesia with isoflurane in comparison with propofol/alfentanil].

AIM: To investigate the influence of isoflurane anaesthesia versus total intravenous anaesthesia with propofol/alfentanil on intraocular pressure (IOP). METHODS: 40 patients undergoing ophthalmic surgery were randomly allocated to two study groups. In group 1 (n = 20), anaesthesia was induced with thiopentone 4 mg/kg and alfentanil 15 micrograms/kg. Maintenance of anaesthesia was achieved with isoflurane 0.5-0.8 Vol.% and 70% nitrous oxide in oxygen. Patients in group 2 (n = 20) received propofol 1.5 mg/kg, which was followed by a continuous infusion of 6 mg/kg/h. In addition, alfentanil 15 micrograms/kg was administered, followed by a continuous infusion of 15 micrograms/kg/h. In both groups, endotracheal intubation was facilitated by succinylcholine 1 mg/kg, and further muscle relaxation was achieved with vecuronium 0.07 mg/kg. Measurements of IOP using an applanation tonometer were taken in each patient at 10 different time points. RESULTS: In both groups, there was a significant decrease in IOP after induction of anaesthesia. No significant differences in IOP occurred between groups, with patients in group 2 showing a trend towards lower IOP values. CONCLUSION: We conclude from our results that both anaesthetic techniques can be administered if increases in IOP have to be avoided.

Aged↗
PubMed1995

[Thrombomodulin as endothelial cell marker in heart surgery patients].

OBJECTIVE: Thrombomodulin is a high-affinity receptor for thrombin on the endothelial cell surface. The aim of our study was to investigate whether plasma thrombomodulin represents a marker of endothelial injury following cardiopulmonary bypass. METHODS: Plasma levels of thrombomodulin were quantitated in 70 plasma samples obtained from 14 adult cardiac patients undergoing hypothermic pulsatile low-flow low-pressure cardiopulmonary bypass. Blood samples were taken before cardiopulmonary bypass (T1), and 15 minutes (T2), 1 hour, 6 hours, and 20 hours after termination of bypass. Plasma thrombomodulin was quantitated with a sandwich enzyme-linked immunosorbent assay (ELISA). Statistical analysis was performed by the Friedman and Wilcoxon tests. RESULTS: Plasma thrombomodulin was significantly elevated 20 hours after discontinuation of cardiopulmonary bypass, when compared with T1 and T2. CONCLUSION: We conclude from our results that a moderate elevation of plasma thrombomodulin is seen in adult patients following hypothermic, low-flow low-pressure cardiopulmonary bypass, which may reflect endothelial injury. Circulating thrombomodulin levels are thus possibly useful for assessment of endothelial damage occurring in patients undergoing cardiopulmonary bypass.

Adult↗
PubMed1995

[Anesthesiologic management in cardiomyoplasty].

Dynamic cardiomyoplasty is a therapeutic possibility in irreversible cardiac insufficiency. With this operation, the latissimus dorsi muscle is mobilised and drawn into the thorax where it is placed around the heart. Lateral and supine positioning as well as thoracotomy and direct manipulation of the heart are associated with particular risks during surgery. Eight patients with the diagnosis of cardiomyopathy underwent cardiomyoplasty. The patients were classified as NYHA III-IV. Continuous dobutamine infusions were routinely started after induction of anaesthesia. All patients were intubated with single-lumen tubes. After sternotomy, lidocaine was administered. Monitoring included Swan-Ganz catheterisation and invasive blood pressure measurement. With early use of inotropic and vasodilatator agents the cardiac index and peripheral vascular resistance were adequately maintained. Double-lumen intubation seems to be unnecessary during cardiomyoplasty and only increases patient risk. Prophylactic lidocaine infusions are effective in preventing ventricular tachycardia and fibrillation. We conclude that adequate intraoperative management can improve the haemodynamic status of these patients so that cardiomyoplasty may be performed without significant morbidity.

Adult↗
PubMed1995

Testing the porphyrinogenicity of propofol in a primed rat model.

We evaluated the porphyrinogenicity of propofol in a rat model. After a pilot study had been conducted to determine an optimal dose, 48 fasting male Sprague-Dawley rats were allocated randomly to six groups. The animals in groups 1-3 received saline i.p. In groups 4-6, the animals were given allylisopropylacetamide (AIA). Twelve hours later, animals in groups 1 and 4 received saline, groups 2 and 5 were given propofol 150 mg kg-1 i.p., followed by 75 mg kg-1 3 h later, and groups 3 and 6 received phenobarbitone 50 mg kg-1 i.p. and 25 mg kg-1 i.p. The animals were anaesthetized and killed 3 h after the second drug bolus and we measured the concentration of cytochrome P450, total porphyrin content and the activity of delta-aminolaevulinic acid synthase (ALAS) in the liver. Urinary delta-aminolaevulinic acid (ALA) and porphobilinogen (PBG) concentrations were measured. Analysis of variance and the t test with Bonferroni's correction were used to compare data. The hepatic cytochrome P450 concentration in the non-primed groups varied from 28.1 to 31.1 nmol g-1; administration of AIA decreased this to 20.1-20.9 nmol g-1. Total hepatic porphyrins were between 0.78 and 1.22 nmol g-1 in the non-primed groups and between 2.71 and 3.54 nmol g-1 in the AIA-primed groups. Hepatic ALAS activity was 29.2 and 35.5 nmol h-1 g-1 in groups 1 and 2. In the primed saline group, ALAS activity was measured at 134.5 nmol h-1 g-1.(ABSTRACT TRUNCATED AT 250 WORDS)

5-Aminolevulinate Synthetase↗
PubMed1995

Propofol-induced alterations in the microcirculation of hamster striated muscle.

To investigate the effects of propofol on small vessels, we have measured changes in diameter and blood flow in microcirculatory venules and arterioles. Studies were carried out in the dorsal skinfold chamber of hamsters by intravital fluorescence microscopy. A bolus injection of propofol 25 mg kg-1 dilated small and collecting venules by a mean value of 18% and arterioles by 13%. Blood flow in venules increased by up to 69%. Intralipid dilated arterioles and post-capillary venules by 26% and 30%, respectively. After 4 h of continuous infusion (0.2-0.8 mg kg-1), only blood flow in post-capillary venules increased (66% propofol and 92% Intralipid). Post-capillary and collecting venules dilated in both groups. Therefore, propofol and Intralipid induced venodilatation and enhanced blood flow after bolus administration. After 4 h, despite dilatation in both groups, only post-capillary venules showed enhanced blood flow. These observations suggest redistribution of blood flow after prolonged administration of propofol.

Anesthetics, Intravenous↗
PubMed1995

Evaluation of the Epsilometer test (E test) for testing the susceptibility of coagulase-negative staphylococci to teicoplanin.

The antimicrobial susceptibilities of 118 clinical isolates of coagulase-negative staphylococci to teicoplanin were determined by disc diffusion and the Epsilometer test (E test) and the results were compared with the MICs determined by the agar dilution method of the National Committee for Clinical Laboratory Standards (NCCLS). There was a poor correlation of r = 0.5 between the zone diameters of inhibition and agar dilution MICs and 10 and four of the 11 isolates for which the MICs were > or = 32 mg/L were misclassified as susceptible by the disc test after applying the interpretative criteria of the NCCLS and the Comité de l'Antibiogramme de la Société Française de Microbiologie (CASFM), respectively. The E test tended to result in MICs that were lower than those determined by agar dilution and only 66% of MIC were within +/- 1 log2 dilution of each other. Only one of 11 resistant strains was detected by the E test and, although there was no false resistance, six resistant strains were misclassified as susceptible after applying the criteria of the NCCLS as were four such isolates when the criteria of the CASFM were employed, probably as a result of using too light an inoculum. Disc diffusion is not a reliable means of determining the susceptibility of coagulase-negative staphylococci but might be replaced by the E-test provided that discrepant results can be resolved by using a denser inoculum.

Anti-Bacterial Agents↗
PubMed1995

Ketamine has stereospecific effects in the isolated perfused guinea pig heart.

BACKGROUND: S(+)-Ketamine is judged to produce more potent anesthesia than either the racemate or the R(-) ketamine isomer because of differential activation of specific cerebral receptors. Other than central nervous system effects, the most important side effects of ketamine occur in the cardiovascular system. We examined the direct cardiac effects of the isomers and the racemate of ketamine in the isolated perfused guinea pig heart. METHODS: Twenty-three guinea pig hearts were perfused by the Langendorff technique with modified 37 degrees C Krebs-Ringer's solution (97% oxygen and 3% carbon dioxide) at a constant perfusion pressure. Eight animals were pretreated with reserpine to deplete hearts of catecholamines. These pretreated hearts were also perfused with Krebs-Ringer's solution containing propranolol, phenoxybenzamine, and atropine to block any remaining effects of catecholamines and of acetylcholine. Five additional hearts were perfused with naloxone to block cardiac opioid receptors. Ten hearts were not treated. All 23 hearts were then exposed to four increasing equimolar concentrations of each isomer and the racemate of ketamine for 10 min. Heart rate, atrioventricular conduction time (AVCT), left ventricular pressure, coronary flow, and inflow and outflow oxygen tensions were measured. Percentage oxygen extraction, oxygen delivery, and oxygen consumption were calculated. RESULTS: Both isomers and the racemate caused a concentration-dependent depression of systolic left ventricular pressure and an increase in AVCT. In the untreated hearts, S(+)-ketamine decreased heart rate and left ventricular pressure and, at higher concentrations, oxygen consumption and percentage oxygen extraction significantly less than R(-)-ketamine independent of blocked or unblocked opioid receptors. Racemic ketamine depressed cardiac function to a degree intermediate to that produced by the isomers. Coronary flow and AVCT were equally affected by the isomers and by the racemic mixture. In the catecholamine-depleted hearts both isomers and the racemate caused equipotent depression of all variables. In these hearts cardiac depression was greater, and AVCT, coronary flow, and oxygen delivery were significantly greater than in untreated and opioid receptor-blocked hearts. CONCLUSIONS: Lesser cardiac depression by the S(+) isomer is attributable to an increased availability of catecholamines, because previous depletion of catecholamine stores and autonomic blockade completely inhibited these differences. The inability of cardiac tissue to reuptake released catecholamines into neuronal or extraneuronal sites during exposure to ketamine is stereoselective and caused predominantly by the S(+) isomer. Cardiac opioid receptors are apparently not involved in this phenomenon.

Animals↗
PubMed1995

Ketamine attenuates endotoxin-induced leukocyte adherence in rat mesenteric venules.

OBJECTIVES: To determine the influence of ketamine on endotoxin-induced leukocyte adherence and venular microhemodynamics. DESIGN: Randomized, controlled trial. SETTING: Experimental laboratory. SUBJECTS: Thirty male Wistar rats. INTERVENTIONS: The rats were pretreated with ketamine (10 mg/kg iv) or 0.9% saline, and both groups were given endotoxin (Escherichia coli lipopolysaccharide; 5 mg/kg iv). The control group received two doses of 0.9% saline. MEASUREMENTS AND MAIN RESULTS: The rates of leukocyte adherence and changes in microhemodynamics were monitored in rat mesenteric venules, using in vivo video microscopy. The number of adherent leukocytes was determined on-line in 10-min intervals from 60 mins before until 2 hrs after endotoxin administration. Venular diameters, red blood cell velocity, volumetric blood flow, and the venular wall shear rate were monitored before and at 10, 30, and 60 mins after endotoxin exposure. A 6.3-fold increase in the number of adherent leukocytes was observed 10 mins after administration of endotoxin when compared with control animals (5.87 +/- 0.69 vs. 0.93 +/- 0.21 adherent cells/100 microns; p < .001). This increase remained unchanged for 120 mins. In ketamine-pretreated rats, a 2.6-fold increase in leukocyte adherence occurred during the first 20 mins after endotoxin exposure (2.40 +/- 0.46 vs. 0.93 +/- 0.21 adherent cells/100 microns; p < .01). However, no difference in the number of adherent leukocytes between ketamine-pretreated and control animals was found after this 20-min period. In animals of the control group, no increase in leukocyte adherence occurred during the entire observation time. Diameters of mesenteric venules did not change after endotoxin exposure in any of the groups. Red blood cell velocity and venular blood flow in the endotoxin-treated groups decreased 10 mins after the injection of endotoxin when compared with controls, but these values did not show any difference when they were compared between ketamine and saline-pretreated animals. Similarly, venular wall shear rate in the endotoxin-treated groups decreased 10 and 30 mins after injection of endotoxin. However, no significant difference occurred between ketamine and saline-pretreated animals. CONCLUSIONS: Pretreatment with ketamine attenuates endotoxin-induced leukocyte adherence by a shear rate-independent mechanism, suggesting reduced expression of adhesion molecules. These results indicate that ketamine exerts an anti-inflammatory effect, which might be beneficial in septic patients.

Animals↗
PubMed1995

Lignocaine metabolite formation: an indicator for liver dysfunction and predictor of survival in surgical intensive care patients.

Formation of the lignocaine metabolite monoethyl-glycine-xylidide (MEGX) by hepatic cytochrome P450 enzymes is a new method for evaluating liver function. The purpose of this study was to compare MEGX formation with other liver function parameters in surgical intensive care unit patients. The study include 29 critically ill patients who had been admitted to the unit for more than 3 days with a median APACHE III score-predicted mortality > 30%. On day 4, lignocaine was given intravenously at a dose of 1 mg.kg-1 over 2 min and MEGX formation was measured 15 min later. Eighty-nine percent of the patients had MEGX values below 90 micrograms.l-1 indicating impaired liver function. Eleven patients died, 18 patients survived. The group of patients with fatal outcome had significantly lower MEGX values (median: 23 micrograms.l-1) than the group of survivors (median: 53 micrograms.l-1, p < 0.01). Bilirubin values were elevated in the non-survivor group (median: 2.8 mg.dl-1) compared to the survivors (median: 0.9 mg.dl-1, p < 0.05). There was no significant difference between two groups in the other liver function tests. We conclude from our results that the MEGX test can be considered an indicator for hepatic dysfunction and predictor of survival in critically ill patients.

Aged↗