Biomedical subjects

E Vicaut

Publications and source records attributed to E Vicaut.

At least 19 recordsLinked to original sources

PubMed1999

A comparison of standard cardiopulmonary resuscitation and active compression-decompression resuscitation for out-of-hospital cardiac arrest. French Active Compression-Decompression Cardiopulmonary Resuscitation Study Group.

BACKGROUND: We previously observed that short-term survival after out-of-hospital cardiac arrest was greater with active compression-decompression cardiopulmonary resuscitation (CPR) than with standard CPR. In the current study, we assessed the effects of the active compression-decompression method on one-year survival. METHODS: Patients who had cardiac arrest in the Paris metropolitan area or in Thionville, France, more than 80 percent of whom had asystole, were assigned to receive either standard CPR (377 patients) or active compression-decompression CPR (373 patients) according to whether their arrest occurred on an even or odd day of the month, respectively. The primary end point was survival at one year. The rate of survival to hospital discharge without neurologic impairment and the neurologic outcome were secondary end points. RESULTS: Both the rate of hospital discharge without neurologic impairment (6 percent vs. 2 percent, P=0.01) and the one-year survival rate (5 percent vs. 2 percent, P=0.03) were significantly higher among patients who received active compression-decompression CPR than among those who received standard CPR. All patients who survived to one year had cardiac arrests that were witnessed. Nine of 17 one-year survivors in the active compression-decompression group and 2 of 7 in the standard group, respectively, initially had asystole or pulseless electrical activity. In 12 of the 17 survivors who had received active compression-decompression CPR, neurologic status returned to base line, as compared with 3 of 7 survivors who had received standard CPR (P=0.34). CONCLUSIONS: Active compression-decompression CPR performed during advanced life support significantly improved long-term survival rates among patients who had cardiac arrest outside the hospital.

Cardiopulmonary Resuscitation↗

PubMed1999

G894T polymorphism in the endothelial nitric oxide synthase gene is associated with an enhanced vascular responsiveness to phenylephrine.

BACKGROUND: Differences in vascular reactivity to phenylephrine (PE) responsiveness have been largely evidenced in patients undergoing cardiac surgery with cardiopulmonary bypass (CPB). Because nitric oxide (NO) strongly affects modulation of the vascular tone in response to vasopressor agents, we hypothesized that the G894T polymorphism of the endothelial NO synthase gene (eNOS) could be related to changes in the pressor response to PE. METHODS AND RESULTS: The protocol was performed in 68 patients undergoing coronary artery bypass grafting (n=33) or valve surgery (n=35) in whom mean arterial pressure decreased below 65 mm Hg during normothermic CPB. Under constant and nonpulsatile pump flow conditions (2 to 2.4 L. min-1. m-2), a PE dose-response curve was generated by the cumulative injection of individual doses of PE (25 to 500 micrograms). The G894T polymorphism of the eNOS gene was determined, and 3 groups were defined according to genotype (TT, GT, and GG). Groups were similar with regard to perioperative characteristics. The PE dose-dependent response was significantly higher in the allele 894T carriers (TT and GT) than in the homozygote GG group (P=0.02), independently of possible confounding variables. CONCLUSIONS: These results evidenced an enhanced responsiveness to alpha-adrenergic stimulation in patients with the 894T allele in the eNOS gene.

Adrenergic alpha-Agonists↗

PubMed1999

Elevated cardiac troponin I predicts a high-risk angiographic anatomy of the culprit lesion in unstable angina.

BACKGROUND: This study assessed the relation between the angiographic appearance of the culprit lesion and cardiac troponin I (cTnI) or C-reactive protein (CRP) elevations within the first 24 hours in unstable angina. Intracoronary thrombus or a complex morphology, is frequently observed on angiography in patients with unstable angina and is associated with a higher rate of spontaneous or coronary angioplasty-related complications. Biochemical parameters related to myocardial injury (eg, cTnI) or to systemic inflammation (eg, CRP) are known prognostic markers for clinical outcome and may help in angiographic risk stratification to provide new adjunctive therapy. METHODS AND RESULTS: We studied 100 patients admitted for unstable angina with angiographically proven coronary artery disease (with normal creatine kinase [CK] and CK-MB mass). Serum concentrations of cTnI (N < 0.4 ng/mL) and CRP (N < 3 mg/L) were measured at admission and 12 and 24 hours later. Multivariate analysis showed that elevated cTnI (>/=0.4 ng/mL) within 24 hours (35 patients) was an independent predictor of an angiographic appearance of the culprit lesion carrying a high risk of major cardiac events in the outcome and whether angioplasty is attempted (coronary thrombus, occlusion, or type C lesions; odds ratio 4.1, 1. 6 to 10.5). cTnI levels at admission and CRP at 0, 12, and 24 hours were not predictive of high-risk angiographic anatomy. CONCLUSIONS: In patients with unstable angina and angiographically proven coronary artery disease, increased cTnI within 24 hours of admission but not increased CRP is associated with an angiographic appearance of the culprit lesion carrying a high risk of complication, especially in the event of angioplasty.

Angina, Unstable↗

PubMed1999

Apolipoprotein(a) size polymorphism in young adults with ischemic stroke.

High serum lipoprotein(a) (Lp(a)) concentration which is largely determined by genetic factors, mainly the apolipoprotein(a) (apo(a)) polymorphism, is associated with ischemic cerebrovascular disease. The aim of this study was to investigate whether apo(a) size was associated with acute ischemic stroke in young adults for which causal factors often remain undetermined. Lipid parameters, Lp(a) concentration and apo(a) isoform size distribution were determined in 90 young patients (37.4+/-8.7 years) with acute cerebral ischemia, and compared to those of control subjects with similar age and sex ratio. Apo(a) size was expressed as its apparent number of kringle 4 (Kr 4) repeats. Serum Lp(a) concentrations were significantly higher in patients than in controls (median values: 0.18 vs. 0.07 g/l, P=0.009) and were as expected inversely related to the number of kringle 4 repeats in both controls (r2=-0.61, P < 0.001) and patients (r2=-0.56, P < 0.001). However there was no difference in the apo(a) isoform size distributions between the two groups (median isoform size: 27 vs. 27 Kr 4, P=0.25). Lp(a) levels were increased as well in patients with size apo(a) isoform < or = 22 Kr 4 as in those with isoforms > 25 Kr 4. Multivariate analysis showed that apo(a) phenotype did not appear as a risk factor for cerebrovascular infarction. Thus, our results indicate that serum Lp(a) was significantly increased in young people with ischemic stroke but fail to reveal a role of small-sized apo(a) isoforms in the occurrence of this event. They suggest that other factors, genetic or environmental in nature, than the apo(a) size contribute to increase the serum Lp(a) concentrations in these young patients.

Acute Disease↗

PubMed1999

Estimation of intraoperative aortocoronary bypass saphenous vein graft circumference from its preoperative compliance.

The aim of this study was to determine if the intraoperative circumference of aortocoronary saphenous vein bypass grafts could be predicted from preoperative measurement with B-mode ultrasound sonography in 50 patients. The circumference of the saphenous vein was measured during stepwise increments of a thigh congestive cuff from 0 to 60 mmHg. The circumference of the corresponding segment of the coronary bypass vein graft was measured intraoperatively with callipers. The intraoperative circumference was higher (11.8+/-2.3 mm) than the preoperative circumference (10.2+/-2.4 mm, P=0.006) matched to its corresponding intraoperative mean arterial pressure (57+/-15 mmHg). The prediction of the intraoperative circumference by estimation from the preoperative pressure-circumference relationship fitted by a linear model (r = 0.412, P = 0.004) did not improve on the preoperative circumference matched by arterial pressure alone (r = 0.429, P = 0.003). The intraoperative circumference of the graft vein exceeded its preoperative circumference by 12%. Prediction of the intraoperative graft vein circumference is underestimated by a linear model of its preoperative compliance.

Aged↗

PubMed1999

Role of endothelial factors in the specific response of mouse tumour-feeding arterioles to stimulation of 5-HT1 receptors.

PURPOSE: To investigate the possible role of endothelial mediators on the increased vasoconstriction to 5-HT1 receptor stimulation by the host-modified arterioles feeding a Meth-A tumour implanted in the flank of female Balb/c mice. MATERIALS AND METHODS: Using intravital microscopy, the response to the topical administration of the general 5-HT1 agonist 5-carboxamidotryptamine maleate (5-CT; 10(-6) M to 10(-4) M) by the tumour-feeding arterioles with the responses of tumour-independent arterioles and those of control arterioles from mice without tumour after antagonization or inhibition of the synthesis of endothelial mediators was compared. RESULTS: The dramatically higher vasoconstriction to 5-CT observed in tumour-feeding arterioles than in tumour-independent or control arterioles still persisted when either nitric oxide synthase, cyclooxygenase, lipoxygenase, or phospholipase A2 were inhibited or when thromboxane A2 or endothelin were antagonized. CONCLUSIONS: It was concluded that the higher reactivity to 5-HT1 stimulation by tumour-feeding arterioles is not due to changes in endothelial mediator release but probably due to changes affecting arteriolar smooth muscle.

Animals↗

PubMed1999

Effects of epinephrine, norepinephrine, or the combination of norepinephrine and dobutamine on gastric mucosa in septic shock.

OBJECTIVES: To compare in the same patient with septic shock, respective effects of epinephrine, norepinephrine, and the combination of norepinephrine and dobutamine (5 microg/kg/min) on systemic hemodynamic parameters and gastric mucosal perfusion using gastric tonometry and laser-Doppler flowmetry techniques. DESIGN: Prospective, controlled, randomized, crossover study. SETTING: University hospital intensive care unit. PATIENTS: Twelve patients with septic shock. INTERVENTIONS: Each patient received in a random succession epinephrine, norepinephrine, and norepinephrine plus dobutamine. Dosages of epinephrine and norepinephrine were adjusted to achieve a mean arterial pressure between 70 and 80 mm Hg. A laser-Doppler probe and a tonometer were introduced into the gastric lumen. MEASUREMENTS AND MAIN RESULTS: The increase in gastric mucosal perfusion detected by laser-Doppler flowmetry was higher with epinephrine and the combination of norepinephrine and dobutamine than with norepinephrine alone (p < .05). In addition, the ratio of gastric mucosal perfusion (local oxygen delivery) to systemic oxygen delivery was increased after norepinephrine plus dobutamine as compared with norepinephrine alone and epinephrine (p< .05). Although values of intramucosal pH and gastroarterial PCO2 tended to be higher with norepinephrine plus dobutamine compared with those obtained with norepinephrine and epinephrine, differences were not statistically significant. CONCLUSIONS: For the same mean arterial pressure in patients with septic shock, our study showed that administration of epinephrine increased gastric mucosal perfusion more than norepinephrine administration alone. Addition of dobutamine (5 microg/kg/ min) to norepinephrine improved gastric mucosal perfusion. This result could be explained by a vasodilating effect of dobutamine on gastric mucosal microcirculation.

Adrenergic beta-Agonists↗

PubMed1999

Comparison of the acute hemodynamic effects of hypertonic or colloid infusions immediately after mitral valve repair.

OBJECTIVE: To determine the acute hemodynamic effect of hypertonic saline and/or colloid solutions as volume resuscitation in postoperative mitral valve repair patients. DESIGN: Prospective, randomized trial. SETTING: Postoperative cardiac intensive care unit of Broussais Hospital. PATIENTS: Twenty-six patients who underwent mitral valve repair were prospectively studied. Two patients were excluded during the study. INTERVENTIONS: During the immediate postoperative period, when wedge pressure decreases to <8 mm Hg, patients were randomly assigned to receive 250 mL of either hypertonic saline 7.2%-hydroxyethyl starch 6% (molecular weight, 200,000; hydroxyethylation ratio, 0.5) solution (HS-HES group), hypertonic saline 7.2% solution (HS group), or hydroxyethyl starch 6% solution (HES group). The infusion was completed within 15 mins. No additional volume was infused throughout the study. MEASUREMENTS AND MAIN RESULTS: Standard hemodynamic measurements and echocardiographic data demonstrated that HS-HES and HS induced a higher increase in left ventricular end-diastolic area than HES. In the HS-HES and HS groups, systemic vascular resistances decreased significantly and end-systolic area tended to decrease. In the HES group, systemic vascular resistances did not change and end-systolic area tended to increase. Accordingly, ejection fraction increased significantly by 21% and 18% with HS-HES (from 50.5 +/- 5.5 to 61.2 +/- 4.8) and HS (from 49.7 +/- 3.6 to 58.8 +/- 3.3), respectively, and did not change with HES. A major increase in cardiac index was observed after hypertonic solutions infusion, from 2.9 +/- 0.3 to 4.1 +/- 0.4 L/min/m2 in the HS-HES group and from 2.7 +/- 0.3 to 3.8 +/- 0.4 L/min/m2 in the HS group. Then, cardiac index progressively returned to baseline values within the 3 hrs after the infusion. No significant difference was observed between HS-HES and HS. In these groups, plasma sodium increased significantly after the infusion and remained higher than baseline values throughout the study. Adverse events were observed only with hypertonic solution administration: hypotensive episodes, sudden increases in pulmonary capillary wedge pressure, and ventricular arrhythmias. These side effects are likely attributable to a too-high dose and/or rate of infusion. All patients included in the study were discharged from the hospital before the 10th postoperative day. CONCLUSION: We conclude that in patients who have undergone mitral valve repair, postoperative infusion of hypertonic saline solutions increases left ventricular preload and left ventricular ejection fraction. The use of these hypertonic solutions may be of interest in patients with valvular cardiomyopathy. A titrated dose and a low rate of infusion may substantially improve the safety.

Cardiac Surgical Procedures↗

PubMed1999

Acute modulation of albumin microvascular leakage by advanced glycation end products in microcirculation of diabetic rats in vivo.

Advanced glycation end products (AGEs) are nonenzymatic glycosylated adducts of proteins that accumulate in vascular tissue during diabetes and aging. The aim of this work was to study the role of AGEs and of the oxidative mechanisms in diabetes-induced changes in vascular permeability. Intravital videomicroscopy was used to study albumin microvascular leakage in cremaster muscle. The extravasation of a fluorescent macromolecular tracer (fluorescein isothiocyanate-albumin) was measured for 1 h and, after computer-aided image analysis, was expressed as variations of normalized gray levels (arbitrary units). Extravasation of the macromolecular tracer was much higher in diabetic rats than in control rats (slope of extravasation versus time increased by >100%, P < 10(-4)). This increase was significantly inhibited when we blocked AGEs binding to their endothelial receptor by intravenous bolus of soluble recombinant receptor to AGEs (rR-RAGE) (slope of extravasation versus time decreased by 19, 30, and 40%, for 0.5, 2.5, and 5.15 mg/kg rR-RAGE, respectively) or by a 6 mg/kg intravenous bolus of antibody against RAGE (slope decreased by 53%). Systemic injection of probucol (an antioxidant) also significantly inhibited the increase in the extravasation of the macromolecular tracer occurring in experimental diabetes (slope decreased by 51%, P < 10(-4)). These results strongly suggest that in experimental diabetes the interaction of circulating AGEs and endothelial RAGE mediates albumin micro-vascular leakage, possibly via AGE-RAGE-dependent enhanced oxidant stress.

Albumins↗

PubMed1999

Microcirculation and arterial hypertension.

A large part of the pressure gradient takes place in the microvascular network (which corresponds to vessels less than 150 microns in diameter). Most of the changes in the peripheral resistance associated with hypertension affect the microvascular network. From the brief review presented here, it appears that the functional characteristics of arterioles are significantly modified in hypertension. Sensitivity to numerous vasoconstrictive substances is increased. Local ACE activity is considerably higher, and endothelium-dependent dilation is lower, in genetically hypertensive animals than in control models. The myogenic response, which represents the vasoconstriction of arterioles in response to a stepped increase in pressure, is also amplified by mechanisms dependent on both prostanoids and endothelin. Changes also affect the structure of the microvascular network. Morphological alterations in the arteriolar wall are not observed for all types of hypertension. Conversely, arteriolar and capillary rarefaction appears to be the most commonly observed change affecting the structure of the microvascular network. The first stage of rarefaction is functional and affects the number of vessels perfused but not the total number of vessels of the microvascular network. At this stage, potent dilators can induce a recruitment of microvessels, which may cancel the difference between the number of perfused vessels in hypertensive and normotensive animals. The second stage is the anatomical rarefaction corresponding to a decrease in arterioles and/or the total number or density of capillaries. Microvascular rarefaction has also been described in patients even in the early stages of hypertension. This led us to consider the microvascular network not only as one of the putative factors responsible for increased pressure but also as a key target of hypertension. Consequently, antihypertensive drugs should also be assessed and differentiated in terms of their efficacy in preventing or reversing the microcirculatory damage associated with hypertension.

Animals↗

PubMed1999

Microcirculation and arterial hypertension.

Animals↗

PubMed1998

Comparison of the prognostic value of C-reactive protein and troponin I in patients with unstable angina pectoris.

This study assessed the prognostic value of cardiac troponin I (cTnI) and C-reactive protein (CRP) in unstable angina, and specifically in patients with angiographically proven coronary artery disease. These biochemical parameters, which are related to myocardial injury or to systemic inflammation, may help in short-term risk stratification of unstable angina. We prospectively studied 195 patients with unstable angina, 100 of whom had angiographically proven coronary artery disease (with normal creatine kinase [CK] and CK-MB mass). Serum concentrations of cTnI (N < 0.4 ng/ml) and CRP (N < 3 mg/L) were measured at admission, 12, and 24 hours later. The rate of in-hospital major adverse cardiac events (death, myocardial infarction, or emergency revascularization) was higher in patients with increased cTnI within the first 24 hours, regardless of the results of coronary angiography (23% vs 7%; p < 0.001). Conversely, events occurred at similar rates in patients with or without increased CRP. In patients with angiographic evidence of coronary artery disease, multivariate analysis showed that increased cTnI within 24 hours of admission (35 patients) was an independent predictor of major adverse cardiac events (odds ratio 6.7, range 1.7 to 27.3), but not cTnI levels at admission and CRP at 0, 12, and 24 hours. Thus, both in unselected patients with unstable angina and in patients with angiographically proven coronary artery disease, increased cTnI within 24 hours of admission, but not CRP, is a predictor of in-hospital clinical outcome. We also found a temporal link between cTnI increase and late elevation of CRP, suggesting that systemic inflammation may partially be a consequence of myocardial injury.

Angina, Unstable↗

PubMed1998

Early increase of von Willebrand factor predicts adverse outcome in unstable coronary artery disease: beneficial effects of enoxaparin. French Investigators of the ESSENCE Trial.

BACKGROUND: The pathogenesis of unstable angina and non-Q-wave myocardial infarction is still poorly understood, and early evaluation of prognosis remains difficult. We therefore studied the predictive value of 5 biological indicators of inflammation, thrombogenesis, vasoconstriction, and myocardial necrosis, and we examined the effects of enoxaparin and unfractionated heparin on these markers after 48 hours of treatment. METHODS AND RESULTS: Sixty-eight patients with unstable angina or non-Q-wave myocardial infarction randomized in the international ESSENCE trial participated in this French substudy. C-reactive protein, fibrinogen, von Willebrand factor antigen, endothelin-1 and troponin I were measured on admission and 48 hours later. The composite end point of death, myocardial infarction, recurrent angina, or revascularization was significantly lower at 14 and 30 days of follow-up in patients allocated to enoxaparin compared with unfractionated heparin. All acute-phase reactant proteins were elevated on admission and increased further at 48 hours. Multivariate analysis demonstrated that the rise of von Willebrand factor over 48 hours was a significant and independent predictor of the composite end point at both 14 days and 30 days. Moreover the early increase of von Willebrand factor was more frequent and more severe with unfractionated heparin than with enoxaparin (mean change was +8.7+/-8.8% with enoxaparin versus +93.9+/-11.7% with unfractionated heparin, P<0.0001). The other clinical and biological variables did not predict outcome. CONCLUSIONS: In patients with unstable angina or non-Q-wave myocardial infarction, the acute-phase proteins increase over the first 2 days despite medical treatment. The early rise of von Willebrand factor is an independent predictor of adverse clinical outcome at 14 days and at 30 days. Enoxaparin provides protection as evidenced by the reduced release of von Willebrand factor, which represents a favorable prognostic finding.

Aged↗

PubMed1998

CD28 expression in T cell aging and human longevity.

Functional decrements of the immune system have a major contribution to aging and age-related diseases. Here, we further characterize the decline in proportion of CD28-positive T cells previously identified in centenarians. Cohorts of 97 centenarians, 40 subjects aged 70-90 (ELD group), and 40 young adults (under age 40) were phenotyped for T cell surface expression of CD28, CD4, and CD8 antigens. The significant decline in T cells expressing CD28 (p < 10(-4) for comparisons between adults and either ELD or centenarians) affects preferentially the CD8+ subset of T cells. This decline accounts largely for the age-related diminution of T cell responsiveness to mitogenic signals. CD28 expression is modulated in T cell cultures in a growth-related fashion and this modulation is dampened in cultures from centenarians. We propose that the decrease in CD28 expression reflects a compensatory adaptation of the immune system during aging in the face of chronic stimulation.

Adult↗

PubMed1998

Theophylline dilates rat diaphragm arterioles via the prostaglandins pathway.

1. We investigated by intravital microscopy in rats, the in vivo direct effects of theophylline on the diameters of second and third order diaphragm arterioles. 2. Theophylline (1-100 microM) dilated second and third order diaphragm arterioles significantly, and with an amplitude which was not statistically different from the one obtained with adenosine (1-100 microM). Enprofylline (1-100 microM), a theophylline analogue with poor adenosine-receptor antagonism but with similar or higher phosphodiesterases inhibition properties than theophylline, also dilated diaphragm arterioles, causing however, a significantly smaller dilatation than theophylline. 3. Neither the A1 adenosine receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (CPX, 50 nM), nor the A2 adenosine receptor antagonist 3,7-dimethyl-1-proparglyxanthine (DMPX, 10 microM) reduced significantly theophylline-induced arteriolar dilatation. 4. Theophylline (100 nM) abolished adenosine-induced arteriolar dilatation. 5. The dilatation induced by theophylline was unchanged by the nitric oxide (NO) synthase inhibitor N(omega)-nitro-L-arginine (NNA, 300 microM). 6. Theophylline-induced arteriolar dilatation was abolished by the prostaglandin synthesis inhibitors mefenamic acid or indomethacin (20 microM). 7. These findings show that theophylline induced a significant dilatation of diaphragm arterioles via the release of prostaglandins.

Adenosine↗

PubMed1998

Assessment of the acute arterial effects of converting enzyme inhibition in essential hypertension: a double-blind, comparative and crossover study.

In subjects with essential hypertension, angiotensin-converting enzyme (ACE) inhibition increases arterial diameter, compliance and distensibility of peripheral muscular arteries in association with blood pressure reduction. Whether pulse pressure amplification is modified by ACE inhibition and whether changes in compliance and distensibility are due to a drug effect on the arterial wall, to the blood pressure reduction or to a combination of both factors, is largely ignored. In a randomised, double-blind crossover trial, we used the ACE inhibitor quinapril as a marker to evaluate the changes in: pulse pressure amplification (applanation tonometry), carotid compliance and distensibility (echo-tracking technique), and aortic distensibility (measured from pulse wave velocity). Quinapril decreased in the same extent carotid and brachial pulse pressure, thus causing a resetting of pulse pressure amplification toward normal values. Carotid compliance and distensibility as well as aortic distensibility increased significantly. Based on three-way analysis of variance, it was shown that, whereas the changes in carotid stiffness were exclusively due to blood pressure reduction and not to a drug-induced relaxation of the arterial wall, the changes in aortic distensibility were due to the combination of both factors. Thus, using an atraumatic non-invasive procedure, it was possible to show that: (i) ACE inhibition is able to maintain pulse pressure amplification, an important factor contributing to reduce the afterload of the heart; and (ii) ACE inhibition alters the hypertensive arterial wall in a very heterogeneous manner, with a maximal drug effect on muscular large arteries like the abdominal aorta, and not on elastic arteries like the carotid artery and the thoracic aorta.

Adult↗

PubMed1998

Characterization of the specific response to serotonin of mouse tumour-feeding arterioles.

PURPOSE: To investigate the role of tumour versus non-tumour factors in the specific response to serotonin (5-HT) of tumour-feeding arterioles (TFA). MATERIALS AND METHODS: Using mouse models of intra-vital microscopy, the response to topical administration of 5-HT was studied in arterioles feeding tumours: fibrosarcoma (Meth A), murine mammary adenocarcinoma (EMT6) and human colo-rectal carcinoma (HRT18) intra-cutaneously implanted. RESULTS: For all types of tumour, 5-HT induced a far more pronounced constriction of TFA than of control arterioles. The presence of a tumour implanted in the connective tissue between the skin and the cremaster muscle also affected the reactivity of muscle arterioles. Conversely, the response to serotonin by neovessels grown after implantation of an exogenous element under the skin did not differ from that of control arterioles. CONCLUSIONS: Changes in reactivity to serotonin were not dependent on the type of tumour implanted in the skin and were not present for a non-tumour implant. The presence of the tumour can alter the reactivity of vessels from tissue in contact with the tumour even if these vessels did not feed the tumour. This phenomenon is local and was not found in the vessels at a distance from the tumour.

Animals↗

PubMed1998

Effects of etomidate, propofol and thiopental anaesthesia on arteriolar tone in the rat diaphragm.

We have assessed, by intravital microscopy in rats, the effects of different anaesthetics on diaphragmatic arteriolar diameter. Rats were anaesthetized with etomidate, propofol or thiopental (groups E, P and T, respectively) and the diameters of the arterioles were measured sequentially at baseline and after topical application of either mefenamic acid (MA, 20 mumol litre-1) or N omega-nitro-L-arginine (NNA, 300 mumol litre-1), inhibitors of prostaglandins and nitric oxide, respectively. In group E, baseline arteriolar diameters were significantly higher than those in the two other groups (P < 0.01). MA and NNA induced significant constriction in the three groups (P < 0.001). However, whereas constriction induced by NNA was similar in the three groups, constriction induced by MA was significantly higher in group E compared with groups P and T (P < 0.05). We conclude that diaphragmatic arteriolar diameters in rats were greater during etomidate than during thiopental or propofol anaesthesia. This phenomenon may be mediated by prostaglandins.

Anesthetics, Intravenous↗