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

This study evaluates the potential for endothelial seeding of a collagen-impregnated Dacron graft with or without surface modifiers (fibronectin, heparin) to attach and retain these cells during flow. Human umbilical endothelial cells were harvested, cultured, labeled with Indium111-oxine and seeded onto 30 mm X 4 mm diameter grafts. Six graft surfaces were studied: 1) a collagen-impregnated Dacron graft, HemashieldR (C); 2) C + fibronectin (C + F); 3) C + heparin (C + H); 4) C + F + H; 5) HytrelR + F (Hyt + F); and 6) Hyt + F + H. Radioactive loss determined the percentage attachment and then percentage retention of labeled inoculum after a one-hour in vitro perfusion. Scanning electron and light microscopy demonstrated the endothelium on the graft surface following perfusion. Fibronectin-coated grafts had a significantly higher percentage attachment than those without fibronectin (ANOVA, P less than 0.05). However, the percentage retention following perfusion was similar for all Dacron grafts and statistically inferior to the HytrelR grafts studied (ANOVA, P less than 0.05). SEM evaluation of the C + F + H graft surface was qualitatively the most impressive Dacron surface for seeding, yet was inferior to the HytrelR graft. We conclude that fibronectin benefits the initial attachment of endothelium to collagen-coated Dacron rivaling the HytrelR surface. Fibronectin does not improve percentage retention of the HemashieldR surface during perfusion, therefore, some of its initial benefit is lost.
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PMID:An experimental collagen-impregnated Dacron graft: potential for endothelial seeding. 252 47

Plasma glucose and insulin responses and basal and insulin-stimulated glucose uptake were determined in 24 non-obese, healthy, physically active individuals, divided into two groups on the basis of age. The mean (+/- SEM) age of the younger group was 33 +/- 3 years, in contrast to an age of 64 +/- 2 years for the older group. Plasma glucose concentrations were significantly higher (two-way ANOVA, P less than .001) for three hours after a 75 g oral glucose challenge in the older group, as was the plasma insulin response (two-way ANOVA, P less than .001). Furthermore, there was a significant correlation between age and total plasma glucose (r = 0.63, P less than .001) and insulin (r = 0.44, P less than .01) during the glucose tolerance test. However, the magnitude of the decrease in glucose tolerance with age was relatively modest. For example, total plasma glucose response was only 11% higher in the older group, and the plasma glucose concentration 120 minutes after the oral glucose load only increased approximately 2 mg/dL per decade. Glucose uptake during euglycemic clamp studies was also reduced in the older group, and this was true if the clamps were performed at plasma insulin concentration of approximately 10 microU/mL (P less than .05) or 60 microU/mL (P less than .10). However the differences were relatively modest in magnitude, ie, 10-25%. The fact that the increase in glucose uptake when plasma insulin was raised six-fold was similar in both groups suggests that insulin sensitivity does not decline with age.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of age on glucose tolerance and glucose uptake in healthy individuals. 235 37

Subclinical structural abnormalities may accompany some congenital cardiovascular abnormalities. Echocardiographic observations led us to hypothesize that the positions of the left ventricular papillary muscles are abnormal in hearts with aortic valvar stenosis. To test this hypothesis, we examined 6 normal heart specimens and hearts with congenital cardiovascular malformations, including 5 with pulmonary atresia and an intact ventricular septum, 6 with tetralogy of Fallot and 5 with aortic valvar stenosis. We marked the papillary muscles and the mitral commissures, X-rayed the hearts, and measured the angular positions of the papillary muscles using the midpoint of a chord drawn between the mitral commissures as a reference point. The direction from the midpoint to the lateral commissure was designated as 0 degrees. The data (mean +/- SEM) were analyzed using a computer program (ANOVA). In normal hearts, the anterolateral and posteromedial papillary muscles were positioned, respectively, at 43 +/- 19 degrees and 126 +/- 26 degrees. The positions of the papillary muscles were similar to normal in the hearts with pulmonary atresia (62 +/- 38 degrees and 128 +/- 27 degrees) and tetralogy of Fallot (40 +/- 13 degrees and 130 +/- 37 degrees). In aortic stenosis, the locations of the papillary muscles (-76 +/- 42 degrees and 71 +/- 25 degrees) were significantly different from normal (P less than 0.05). The arc between the papillary muscles was 83 +/- 16 degrees in normals and 147 +/- 45 degrees in aortic stenosis (P less than 0.05). The length of the arc was similar to normal in other heart specimens. Thus, the papillary muscles were abnormally positioned in aortic stenosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Abnormalities in position of left ventricular papillary muscles in congenital aortic stenosis. 276 12

In the stage 24 chick embryo, a paced increase in heart rate reduces stroke volume, presumably by rate-dependent decrease in passive filling. We hypothesized that rate-dependent stroke volume reduction could be abolished by volume loading. Dorsal aortic blood velocity was measured with a 20 mHz pulsed-Doppler meter from a 0.75-mm piezoelectric crystal (eight embryos), and atri-oventricular velocity was simultaneously measured from the ventricular apex (six embryos). Sinus venosus pacing (stimuli of 1 ms duration and less than 4 mA) was performed at intrinsic rate (P:I) and at 150% of intrinsic rate (P:150%I). Volume loading was performed during P:150%I by intravenous injection of 7.5 microL of chick Ringer's solution. Using atrioventricular velocity profile, stroke volume was divided into the proportion due to passive (E-phase) and active (A-phase) filling. Stroke volume was compared during P:I, P:150%I, immediately (P:150%I') and 30 s after (P:150%I") volume loading. Data (mean +/- SEM) were compared by ANOVA. During pacing, stroke volume (mm2/cycle) decreased but increased after volume loading (I, 0.43 +/- 0.03; P:I, 0.37 +/- 0.03; P:150%I, 0.19 +/- 0.03; P:150%I', 0.24 +/- 0.05; P:150%I", 0.28 +/- 0.04 (p less than 0.005). During P:150%I, E-phase filing disappeared and was not restored by volume loading, whereas, A-phase filling diminished but was restored by volume loading. In stage 24 chick embryos, rate-dependent stroke volume decrease is reversed by volume loading that restores stroke volume due to an increase in active filling but not passive filling. Thus, even at rapid heart rate, the embryonic ventricle responds to volume loading, indicating that the Frank-Starling relationship functions during tachycardia in the embryonic heart.
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PMID:Effect of heart rate increase on dorsal aortic flow before and after volume loading in the stage 24 chick embryo. 281 94

In a double blind, crossover study 6 h infusions of adrenaline (15 ng/kg/min; 1 ng = 5.458 pmol), noradrenaline (30 ng/kg/min; 1 ng = 5.911 pmol), and a 5% dextrose solution (5.4 ml/h), were given to ten healthy volunteers in random order 2 weeks apart. By means of intra-arterial ambulatory monitoring the haemodynamic effects were followed for 18 h after the infusions were stopped. Adrenaline, but not noradrenaline, caused a delayed and protracted pressor effect. Over the total postinfusion period systolic and diastolic arterial pressure were 6 (SEM 2)% and 7 (2)%, respectively, higher than after dextrose infusion (ANOVA, p less than 0.001). Thus, "stress" levels of adrenaline (230 pg/ml) for 6 h cause a delayed and protracted pressor effect. These findings are strong support for the adrenaline-hypertension hypothesis in man.
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PMID:Support for adrenaline-hypertension hypothesis: 18 hour pressor effect after 6 hours adrenaline infusion. 256 20

The hypotensive and hormonal effects of the angiotensin converting enzyme (ACE) inhibitor enalapril (10 mg twice daily) were compared with those of hydrochlorothiazide (25 mg twice daily), with the two drugs in combination and with placebo in 21 patients with essential hypertension. For each patient there were four randomised double-blind treatment phases, each of four weeks' duration, which comprised a 2 X 2 factorial experiment. All blood pressure parameters were reduced in the three active treatment phases compared to placebo (p less than 0.001). Supine mean blood pressures were 119 mmHg (placebo), 113 mmHg (hydrochlorothiazide), 108 mmHg (enalapril), and 98 mmHg (hydrochlorothiazide plus enalapril) (SEM 3 mmHg, ANOVA). Enalapril and hydrochlorothiazide were equally effective and well tolerated and their hypotensive effects were additive. Enalapril increased plasma renin activity (PRA), reduced plasma angiotensin II (AII) and aldosterone concentrations, and reduced ACE activity, whereas hydrochlorothiazide increased PRA, plasma AII, and aldosterone concentrations without altering ACE activity. With combination treatment the effects of enalapril on PRA and plasma AII concentrations were potentiated whereas those on plasma aldosterone concentration and ACE activity were additive. Atrial natriuretic factor plasma concentration in the placebo phase was 92 pg/ml and increased to 145 pg/ml in the hydrochlorothiazide phase (p less than 0.001, SEM 13 pg/ml), but there was no significant change in either the enalapril or combination phases.
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PMID:Effects of enalapril and hydrochlorothiazide on blood pressure, renin-angiotensin system, and atrial natriuretic factor in essential hypertension: a double blind factorial cross-over study. 302 94

Growth hormone (GH) responses to growth hormone-releasing factor (GRF) were evaluated in 55 children with growth failure. The study groups consisted of group 1, severe GH deficiency; group 2, partial GH deficiency; group 3, patients with prior cranial radiation for nonpituitary brain tumors; and group 4, children with idiopathic growth failure. Children in group 1 were unresponsive to GRF (mean GH peak +/- SEM, 1.6 +/- 0.5 ng/ml). Higher GH responses to GRF were observed in both groups 2 (17.2 +/- 4.1 ng/ml) and 3 (10.4 +/- 2.8 ng/ml). The highest GH responses to GRF were observed in group 4 (35.9 +/- 4.3 ng/ml). ANOVA revealed a significant difference between groups (F = 12.9; df = 3; p less than 0.01), and further analysis by the Scheffe and Student-Newman-Keuls tests revealed that group 4 was significantly higher than groups 1, 2, or 3 (p less than 0.05). These data suggest that GRF unresponsiveness is a reliable predictor of severe GH deficiency. In patients with partial GH deficiency or idiopathic growth failure, the GRF gives semiquantitative information about somatotrope responsivity to exogenous stimulation.
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PMID:Diagnostic value of the growth hormone-releasing factor stimulation test. 313 44

Responses to the nondepolarizing muscle relaxant, metocurine, were studied in eight hemiplegic and eight unmatched patients with normal motor strength during the general anesthetic given for various neurosurgical operations. Metocurine, 0.3 mg/kg, was administered intravenously, and indirectly evoked thumb twitch tensions were measured on both sides in the hemiplegic patients, and on one side in the normal patients. Arterial blood samples were obtained as twitch tension was recovering, and serum metocurine concentrations were determined using a specific radioimmunoassay. Percentage of paralysis was plotted as a function of log [metocurine] and the data were compared by analysis of covariance. For the normal motor strength patients, r = 0.84; for the unaffected arm of the hemiplegic patients, r = 0.69; and for the affected arm of the hemiplegic patients, r = 0.86, all significant at P less than 0.001. The mean plasma metocurine concentrations at 20, 25, 50, 75, and 80% paralysis were significantly different for all groups (P less than 0.001). The regression lines, in turn, did not overlap and were significantly different, each from the other (P less than 0.005). We were, however, unable to detect any significant deviation from parallelism among the three regression lines. We also measured time to 50% return of single twitch height for each data group as follows (mean +/- SEM: for NMS patients, 242 +/- 73 min; for the unaffected arm of hemiplegic patients, 116 +/- 60 min; and for the affected arm of hemiplegic patients, 59 +/- 36 min. By ANOVA and the Bonferroni test, each value was different from the other at P less than or equal to 0.01.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Decreased sensitivity to metocurine in patients with upper motoneuron disease. 316 Feb 62

Six children (boys and girls, 8 to 13 years old) with allergic asthma (AA) had their total pulmonary resistance (R1) measured at four fixed times (0730, 1130, 1630 and 2230 hr), before and again 10 min after a 2 mg orciprenaline (beta-agonist) aerosol inhalation. R1 was measured by means of the esophageal balloon technique. Subjects were socially synchronized in May with a diurnal activity from 0700 to 2100 and a nocturnal rest. Patients had had no asthma attacks and had received no medication for 8-15 days. Time series were analyzed according to conventional (t-tested mean time point differences) ANOVA, and cosinor methods. The 24 hr adjusted means (cm H2O.l/s +/- SEM) were 5.7 +- 0.4 in seven previously documented healthy children. 7.4 +/- 1.2 in AA before orciprenaline, and 4.9 +/- 0.2 in healthy children, 5.2 +/- 0.8 in AA after beta-agonist inhalation. Circadian rhythms were detected in both groups before but not after treatment. The treatment had its maximal effect on R1 around 0730 (when bronchial patency is close to its trough) and had no effect around 1630 (peak time of airway patency) in both groups (P less than 0.01; ANOVA). Thus, inhaled orciprenaline was mainly effective around 0730 and to a lesser extent around 2230 whereas there was no detectable effect during the day (1230 and 1630).
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PMID:Circadian rhythm in total pulmonary resistance of asthmatic children. Effects of a beta-agonist agent. 321 58

Previous animal studies support the presence of an upper airway reflex mechanism that when blocked by topical anesthesia of the upper airway results in upper airway occlusion. We sought a similar reflex mechanism in humans. Nine normal male volunteers 20 to 28 yr of age underwent 3 successive overnight sleep studies: a control study (C); a study in which selective topical oropharyngeal anesthesia (OPA) was achieved prior to sleep using a 10% lidocaine spray and 0.25% bupivocaine solution; a study in which selective nasal anesthesia (NA) was achieved prior to sleep using a mixture of 2% lidocaine and 0.25% bupivocaine solutions instilled into the nose while the nasal airway was positioned as the most dependent part of the upper airway. Total sleep times were similar during the 3 study nights as were the amounts of slow-wave and rapid-eye-movement (REM) sleep. Obstructive apneas and hypopneas (OAH) differed significantly between the 3 study nights [13(3.8), mean (SEM), during OPA as compared to 3(1.8) during C and 7(2.5) during NA; p less than 0.01 by ANOVA] and were most frequent during REM sleep. Total apneas and hypopneas also differed significantly between the 3 study nights [19(3.9) during OPA as compared to 8(2.1) during C and 14(3.9) during NA; p less than 0.01 by ANOVA]. Movement arousals terminating periods of abnormal respiration also differed significantly [21(6.1) during OPA as compared to 12(3.6) during C and 14(4.6) during NA; p less than 0.05 by ANOVA]. No subject, however, developed clinically significant sleep apnea or significant oxygen desaturation during sleep.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Upper airway obstruction during sleep in normal subjects after selective topical oropharyngeal anesthesia. 359 5


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