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 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Determination of regional ventricular wall stress would allow quantification of both regional contractile state and its interplay with global function. Current methods for quantifying regional stress include mathematical modelling and measurements with strain gauges. Both methods are difficult to validate. We hypothesized that transverse stiffness (i.e., the ratio of indentation stress to strain as the ventricular wall is indented in the direction perpendicular to the wall) would be proportional to the stresses in the plane of the wall and could be used to estimate the latter. To test this hypothesis, 6 arterially perfused canine ventricular septa were mounted in an apparatus that could exert biaxial load in the plane of the wall. A servo system maintained the central third of the septa isometric during active contractions while the septa were paced at 30-60 pulses/min. In the center of the isometric region, a probe of 7 mm diameter indented the septa while the transverse indentation stress and strain were measured. For values of peak systolic in-plane stress from 0.56 to 2.6 g/mm2, the transverse stiffness varied from 1.2 to 11.7 g/mm2 and was linearly related to the in-plane wall stress in each septum (p less than 0.001, ANOVA). After cardioplegia, the transverse stiffness also correlated with passively applied wall stress for each dog (p less than 0.001). The slopes of the individual relations between transverse stiffness and wall stress from active contractions were similar to those from passively applied stress (mean +/- SEM; 1.82 +/- 0.36 versus 1.45 +/- 0.31, NS).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Transverse stiffness: a method for estimation of myocardial wall stress. 366 76

A BASIC program is described which, upon the input of raw data from an experiment comparing several treatment groups to a control, will output group parameters (mean, SEM), test for outliers in each group (maximum normalized residual test), and examine the homogeneity of variance (Bartlett's test). Subsequently, one-way ANOVA and Dunnett's multiple comparison test are performed. The user also has the option of examining the data by nonparametric means using the Kruskal-Wallis test and a nonparametric multiple comparison test (Dunn's test). As a convenience, the program contains algorithms to generate critical table values for all the tests employed.
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PMID:Computer program for the parametric and nonparametric comparison of several groups to a control. 381 63

The ability of parenteral lipid emulsions to support microbial growth was compared using commercially available brands of lipid emulsion. Both 10 and 20% concentrations of soybean and safflower oil emulsions were used. Washed cultures of six gram-negative, three gram-positive, and one yeast, in concentrations of 1 x 10(4) to 2 x 10(4) colony-forming units/ml, were inoculated into lipid emulsion aliquots and stored at room temperature. There were than subcultured at 0, 6, 12, 24 and 48 hr. After 48 hr at 37 degrees C, growth was recorded as colony-forming units/ml. Normalized growth curves were expressed as mean +/- SEM. ANOVA demonstrated no difference in growth patterns due to the nature of the oil or its concentration. Gram-negative organisms multiplied faster when compared to gram-positive (p less than 0.05 at 12 hr, p less than 0.01 at 24 hr, and p less than 0.005 at 48 hr). Yeast grew as well as bacteria. The Center for Disease Control's recommendation of a 12-hr hang time for parenteral lipid emulsions should be observed until correlation of laboratory microbial growth patterns and clinical use are studied further.
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PMID:Microbial growth comparisons of five commercial parenteral lipid emulsions. 637 17

Peripheral concentrations of immunoreactive relaxin are undetectable in primates during the nonfertile menstrual cycle, but become measurable during the interval when chorionic gonadotropin (CG) rises in early pregnancy. The objectives of the current study were to determine if exogenous CG, administered in a dosage regimen which invoked patterns and concentrations resembling those of early pregnancy, would induce relaxin secretion in nonpregnant rhesus monkeys, and whether the induction was dependent on the age of the corpus luteum (CL) at the onset of treatment. Female rhesus monkeys received twice-daily i.m. injections of increasing doses of human CG (hCG) for 10 days beginning in the early (n = 4), mid (n = 6) or late (n = 4) luteal phase of the menstrual cycle [5.3 +/- 0.3, 8.3 +/- 0.5, and 12.0 +/- 0.4 days after the midcycle luteinizing hormone (LH) surge, respectively; means +/- SEM]. Whereas immunoreactive relaxin was nondetectable in the luteal phase of posttreatment cycles, detectable levels of relaxin were observed in 2 of 4, 5 of 6, and 3 of 4 monkeys during hCG treatment in the early, mid and late luteal phase, respectively. Although CG treatment rapidly enhance progesterone levels, the appearance of relaxin was deferred; relaxin was first detectable 9.0 +/- 1.0 and 4.7 +/- 1.9 days after the onset of CG treatment at early and late luteal phases. Patterns of relaxin concentrations differed among groups (P less than 0.05, ANOVA; split plot design) and relaxin levels were lowest (P less than 0.01) in monkeys treated during the early luteal phase.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Induction of relaxin secretion in rhesus monkeys by human chorionic gonadotropin: dependence on the age of the corpus luteum of the menstrual cycle. 651 24

The purpose of this study was to characterize and evaluate the acute effects of walking performed of fairly light (50% VO2max) and moderate (70% VO2max) intensities on serum lipids and lipoproteins in a group of premenopausal (n = 11) and a group of postmenopausal (n = 10) women. Premenopausal women were (x +/- SEM) 34.5 +/- 1.1 years of age, had 22.8 +/- 1.7% body fat and a 2.47 +/- 0.08 l.min-1 VO2max. Postmenopausal women were 54.8 +/- 2.5 years of age, had 37.9 +/- 0.9% body fat and a 2.06 +/- 0.15 l.min-1 VO2max. All subjects walked on a motor-driven treadmill at each respective intensity of exercise for a total duration sufficient to expend 350 kcal of energy. Dependent variables included total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C) and its subfractions HDL2-C and HDL3-C, low-density lipoprotein cholesterol (LDL-C), and triglycerides (TG). Blood samples were obtained at baseline (pre-exercise), immediately post-exercise (IPE), and at 24 hours and 48 hours post-exercise. A repeated measures design was employed controlling for diet, menstrual cycle periodicity, natural menopause, and plasma volume shifts. A 2 x 4 ANOVA was used to test for differences among means for each group separately. Significant (p < 0.05) time exercise intensity interactions were found for TC and LDL-C for the premenopausal women. This non-parallel change across exercise intensity condition created significant differences at IPE for both TC and LDL-C. Furthermore, an IPE increase in TG (p < 0.05) was observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acute effects of walking on serum lipids and lipoproteins in women. 747 93

Serine proteinases participate in many inflammatory events in the airway. We therefore screened perfusates of isolated rat tracheas for tryptic, elastolytic, and chymotryptic serine proteinases. Only chymotryptic activity, indicated by hydrolysis of the synthetic substrate N-succinylalanylalanylprolylphenylalanyl p-nitroaniline (AAPF), was consistently detected in these perfusates. Basal levels of chymotryptic activity were not increased significantly by electrical field stimulation (EFS) (mean change +/- SEM: -0.05 +/- 0.05 m o.d. units, n = 4) or by 10(-7) M substance P (SP) (+0.04 +/- 0.02 m o.d. units, n = 14). However, the mean change after the stimuli were jointly administered (0.17 +/- 0.06 m o.d. units, n = 12) was significantly greater than control or after EFS (P = 0.01, one-way ANOVA). The SP + EFS-induced chymotryptic activity was inhibited by PMSF, soybean trypsin inhibitor, and chymostatin and was associated with an increase in histamine concentration and immunoreactivity to rat mast cell proteases (RMCP), indicating that the activity is due to mast cell degranulation. However, the activity was not significantly decreased by pretreating rats with systemic compound 48/80. SP + EFS-induced chymotryptic activity peaked rapidly and was associated with modest histamine release and an immediate peak in immunoreactivity to RMCP II, a marker of mucosal mast cells. Immunoreactivity to RMCP I, a marker of connective tissue mast cells, also increased after SP + EFS, but this immunoreactivity was either delayed or more sustained and did not coincide with the peak of chymotryptic activity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chymotryptic activity in perfusates of isolated rat trachea: correlation with mucosal and connective tissue mast cell secretion. 752 16

Ninety-two-kilodalton type IV collagenase (MMP-9) is present in aortic aneurysms and may be important to the pathogenesis of this disease. Alteration in expression of MMP-9 or its inhibitor, the tissue inhibitor of metalloproteinase type 1 (TIMP-1), could increase degradation of extracellular matrix and lead to aneurysm formation. The purpose of this study was (1) to measure tissue levels of MMP-9 and TIMP-1 mRNA in aneurysmal (AAA), atherosclerotic occlusive (AOD), and normal (NL) human infrarenal aorta; (2) to test for their expression by cultured AAA and NL vascular smooth muscle cells (VSMCs); and (3) to locate in situ the cells responsible for mRNA production within AAA, AOD, and NL aortic wall. Total RNA extracted from AAA (n = 8), AOD (n = 8), and NL (n = 7) tissue was subjected to Northern analysis. Signals for MMP-9 and TIMP-1 were normalized to alpha-tubulin. Mean values +/- SEM were compared by ANOVA. NL and AAA VSMCs were cultured, passaged, and grown to confluence before RNA extraction and Northern analysis. In situ hybridization with digoxigenin-labeled RNA probes localized cells responsible for MMP-9 and TIMP-1 mRNA expression within sections of AAA (n = 5), AOD (n = 2), and NL (n = 2) aorta. MMP-9 mRNA levels were significantly greater in AAA (0.855 +/- 0.180) than NL (0.046 +/- 0.23) (P < .02), but differences between AOD (0.406 +/- 0.196) and AAA or AOD and NL were not significant.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:In situ localization and quantification of mRNA for 92-kD type IV collagenase and its inhibitor in aneurysmal, occlusive, and normal aorta. 762 7

Chickens (n = 18), ranging in age from 30 to 50 weeks and in body weight from 1.1 to 2.1 kg, were anesthetized with isoflurane. Ventilation was controlled, and temperature was maintained at 40.1 +/- 1.0 C. The minimal anesthetic concentration (MAC) of isoflurane was determined by use of a bracketing technique based on purposeful movement in response to a toe clamp. After determining isoflurane MAC in triplicate, birds were given a mu-opioid agonist (morphine, n = 9) or a kappa-opioid agonist (U50488H, n = 9). Determination of MAC was repeated after each IV administration of agonist in progressive doses of 0.1, 1.0, and 3.0 mg/kg of body weight. Heart rate and mean arterial blood pressure (MAP) were recorded immediately before and after each injection. Control MAC (mean +/- SEM) was 1.24 +/- 0.05% and 1.05 +/- 0.03% for the mu- and kappa-opioid agonist groups, respectively. Morphine and U50488H caused a dose-dependent decrease in isoflurane MAC in all birds. Reduction of MAC from control (mean +/- SEM) was 15.1 +/- 2.7, 39.7 +/- 3.1, and 52.4 +/- 4.0% after the 3 successive doses of morphine and was 13.3 +/- 3.0, 27.6 +/- 3.3, and 40.8 +/- 3.8% after U50488H was given. Each opioid injection resulted in significant (P < or = 0.05, repeated measures ANOVA) lowering of MAC. Heart rate and MAP did not change significantly (P < or = 0.05, paired Student's t-test) after any dose of opioid. In conclusion, morphine or U50488H decreased isoflurane MAC in dose-dependent manner without significant effect on heart rate and MAP.
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PMID:Influence of a mu- and kappa-opioid agonist on isoflurane minimal anesthetic concentration in chickens. 765 92

The effectiveness and tolerability of captopril and verapamil SR were compared in a double-blind, crossover study in 23 elderly hypertensives [15 males and 8 females, aged (mean +/- SEM) 68 +/- 1 years]. After 2 weeks of placebo run-in, patients were randomized to a starting dose of captopril, 12.5 mg b.i.d. or verapamil SR, 120 mg q.d. plus matched placebo of the opposite drug. Medication was titrated up over 6 weeks to a maximum dose of 75 mg of captopril or 360 mg of verapamil SR to achieve a sitting diastolic blood pressure of < 90 mm Hg. After 2 weeks of placebo washout, captopril and verapamil were crossed over. In the 20 patients who completed the study, the dose at the end of the respective treatment periods averaged 63 +/- 4 mg of captopril and 270 +/- 21 mg of verapamil SR. Blood pressure at the end of the run-in and washout placebo periods were comparable: 164 +/- 4/97 +/- 1 and 163 +/- 4/98 +/- 2 mm Hg, respectively. However, the blood pressure was significantly lower after verapamil, i.e., 147 +/- 4/86 +/- 2 mm Hg, than after captopril, i.e., 155 +/- 4/90 +/- 1 mm Hg (p < 0.05, ANOVA). There was no significant change in heart rate and laboratory parameters and no orthostatic hypotension. Captopril-treated patients reported a positive change in well being compared with placebo, although there was no overall difference between the drugs in any of the ten quality of life measurements. Three patients discontinued treatment, two because of constipation (verapamil) and one due to lack of efficacy (captopril).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of verapamil and captopril in elderly hypertensive subjects: results of a randomized, double-blind, crossover study. 767 84

Adhesion molecules play a critical role in the interaction of circulating neutrophils with vascular endothelium during inflammation. Increased quantities of soluble, circulating intercellular adhesion molecule-1 (cICAM-1) are present in various inflammatory conditions. The purpose of this investigation was to measure cICAM-1 levels in septic adults, as well as to examine the relationship between this potential marker of endothelial-cell activation and the consequences of sepsis (i.e., multiple organ failure and death). Using a sandwich-type enzyme-linked immunosorbent assay (ELISA), we measured cICAM-1 in blood samples obtained within 12 h of admission to an intensive care unit (ICU) for sepsis and other conditions. We found cICAM-1 levels to be increased in 25 septic patients (1,259 +/- 159 ng/ml, mean +/- SEM) as compared with 12 healthy volunteers (355 +/- 41 ng/ml, p < 0.0001) and four ICU patients without systemic inflammatory response syndrome (SIRS) (585 +/- 76 ng/ml, p < 0.001). Twenty-five patients with SIRS but no evidence of causative infection also had elevated levels of cICAM-1 (937 +/- 144 ng/ml, p = 0.12 versus sepsis). Serial measurements over the first week of sepsis demonstrated persistent elevation in most patients. Day 1 cICAM-1 levels were higher (p = 0.017, ANOVA) in 16 patients with septic shock than in seven with severe sepsis and two with sepsis but without hypotension or hypoperfusion. There was a positive correlation (r = 0.50, p = 0.009) between Day-1 cICAM-1 measurements and severity of shock as determined by the presence of hypotension and vasopressor use.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Circulating ICAM-1 is increased in septic shock. 773 95


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