Biomedical subjects

E Vicaut

Publications and source records attributed to E Vicaut.

At least 55 records · Page 3Linked to original sources

PubMed2001

Distribution of intracortical porosity in human midfemoral cortex by age and gender.

The purpose of this study was to describe the age-specific distribution of midfemoral intracortical porosity throughout the cortical width in males and females. Microradiography and an automated image analysis system were used to study midfemoral cortical bone specimens from 163 white people, including 77 males and 86 females, in a recent anthropological collection covering a broad age range. In each specimen, porosity (percentage of the cortical bone area occupied by pores), pore number, and pore size were measured throughout the entire cortex and in three cortical subregions of equal width labeled the periosteal, midcortical, and endosteal subregions. For each gender, relationships linking age to porosity, pore number, and mean pore size were assessed using regression analysis. In addition, age- and site-related changes in these three variables were tested for significance using two-way analysis of variance (ANOVA). Age explained 52% of the porosity variance in females and 13.5% in males. In each gender, there were significant age- and site-related differences in porosity, pore number, and pore size. In adults aged 60 years or younger, both pore size and pore number increased with increasing age, whereas in adults older than 60 years, pore size continued to increase but pore number decreased. In males, the age-related changes in pore size and pore number were proportionally similar in the three cortical subregions. In females, in contrast, the changes predominated in the endosteal subregion and resulted in significant cortical thinning.

Adolescent↗

PubMed2001

[Observations on the management of cardiac failure in ambulatory patients. Results of a survey of cardiologists].

An enquiry was undertaken amongst 71 cardiologists in 1999 evaluating 600 ambulatory patients with cardiac failure (64% men; mean age 73 years; NYHA Class I: 9%, Class II: 52%, Class III: 33%, Class IV: 6%). Cardiac failure is commoner in men (81%) before the age of 70. After the age of 80, the tendency is inversed (53% of women). Fifty-two per cent of patients had a history of hospital admission for cardiac failure: 26% in the year before the enquiry (on average 13.1 days' hospital stay). On inclusion, the diagnosis was made 4.2 +/- 4.6 years previously and the patients had been followed up for an average of 3.04 +/- 3.3 years. The diagnosis of cardiac failure was made by the cardiologist (57%), the general practitioner (37%), or another category of physician (6%). Eight per cent of patients were treated with a single drug before inclusion, 22% had a bi-therapy and 70% a polytherapy. The most frequently prescribed drugs were: diuretics (71%), angiotensin converting enzyme (ACE) inhibitors (54%) and digitalis (35%). The prescription of betablockers was only reported in 14% of the population. In the over-80's, only 45% of patients were prescribed ACE inhibitors. These results confirm that ambulatory patients with cardiac failure are mainly in NYHA Classes II and III, that the pathology concerns elderly patients and that it is the cause of recurrent hospital admission. The prescription of diuretics is the main therapy in all NYHA Classes. ACE inhibitors were only prescribed in 2/3 of patients and in less than half of patients over 80 years of age. The prescription of betablockers remains marginal. The reason for the underprescription of recommended drugs (International Recommendations) would justify further investigation.

Adrenergic beta-Antagonists↗

PubMed2000

Reduced reactive hyperemia in HIV-infected patients.

BACKGROUND: Given that several pathology-based studies reported some degree of coronary and arterial vasculopathy in HIV-infected patients, we investigated whether abnormal vascular reactivity may also be found in these patients. METHODS: Vascular reactivity was assessed noninvasively using finger-skin blood-flow monitoring by laser-Doppler flow measurement in 10 HIV-infected-patients (mean CD4 T-cell count, 350+/-84 cells/mm3) with cardiac symptoms (previous myocardial infarction or left-ventricular dysfunction) and/or HIV-related protease inhibitor-induced hyperlipemia (group 1, symptomatic), 19 HIV-infected patients free of cardiac disease, hyperlipemia, and previous opportunistic infections (mean CD4 T-cell count, 333+/-175 cells/mm3; group 2, asymptomatic), and 19 healthy control subjects (group 3). Laser-Doppler flow was measured at baseline, during postocclusive hyperemic response following transient interruption of brachial blood flow (reactive hyperemia), during transcutaneous delivery of acetylcholine (Ach) using iontophoresis (endothelium-dependent dilation) and after sublingual nitroglycerin administration (endothelium-independent dilation). RESULTS: During reactive hyperemia, the absolute increase in flow was found to be lower in asymptomatic HIV-infected patients than in controls (median values [25th-75th percentile]: asymptomatic: 300 [200-400]; versus controls: 600 [400-750] arbitrary units [AU]; p< or =.0001). This abnormality was more pronounced in symptomatic patients (100 [100-200]; p< or =.0001). There was also a reduced peak/baseline flow ratio (symptomatic: 1.14 [1.1-1.2]; asymptomatic: 1.40 [1.25-1.5]; versus controls: 1.83 [1.6-2.2]; p<.0001 for both comparisons) and a reduced hyperemic response, as assessed by the curve of area under the flow versus time from deflation to the end of the hyperemic response (symptomatic: 1850 [1100-2225]; asymptomatic: 6000 [2850-7950]; versus controls: 23,735 [16,000-31, 800] AU x sec; p<.0001 for both comparisons). Although there was no statistically significant difference in acetylcholine (Ach)-induced increases in flow between asymptomatic HIV patients and controls (peak/baseline flow ratio: 6 [4.4-10] versus 5.3 [4-8]; p =.47), a trend to lower values was seen in symptomatic patients (4.4 [1.2-5]; p =.06). Administration of 0.4 mg sublingual nitroglycerin resulted in increases in flow without statistically significant difference between patients and controls: peak/baseline flow ratio for symptomatic: 2.4 [1.9-2.7]; asymptomatic: 2.1 [1.75-2.34] versus controls: 1.97 [1.8-2.4]; p =.2 and.83, respectively). CONCLUSIONS: Postischemic reactive hyperemia is reduced in HIV-infected patients. In addition, there was is trend for a reduced response to Ach only in those with cardiac disease and/or hyperlipemia.

Acetylcholine↗

PubMed2000

Effects of various anticoagulant treatments on von Willebrand factor release in unstable angina.

OBJECTIVES: We tested the hypothesis that different anticoagulant treatments may produce different platelet effects and von Willebrand factor (vWf) release in unstable angina. BACKGROUND: The early increase of vWf has been reported to be a risk factor for adverse outcome in unstable angina. Anticoagulant drugs play a key role in stabilization of unstable angina, but they may not have the same efficacy and the same effects on acute vWf release. METHODS: We studied 154 patients enrolled in several clinical trials testing four different anticoagulant treatments in unstable angina or non-Q-wave myocardial infarction. Patients were treated during at least 48 h by either intravenous unfractionated heparin, one of two different low molecular weight heparins (enoxaparin or dalteparin) or the direct thrombin inhibitor PEG-hirudin. All patients received aspirin but no Ib/IIIa inhibitors. RESULTS: The release of vWf over the first 48 h (delta vWf) did not relate to the baseline clinical characteristics. At 30 days of follow-up, delta vWf was sevenfold higher in patients with an end point (death, myocardial infarction, revascularization) than in patients free of events (+53 +/-7% vs. +7 +/-14%, p = 0.004). The same trend was present for each component of the composite end point with the highest levels for one-month mortality (+87 +/- 32% vs. +26 +/- 8%, p = 0.09). The vWf values did not increase over 48 h in patients receiving either enoxaparin or PEG-hirudin (+10 +/- 9% and -5 +/- 20%, respectively). A serious rise ofvWf was measured in unfractionated heparin-treated patients (+87 +/- 11%), which differed significantly from the enoxaparin group (p = 0.0006) and PEG-hirudin group (p < 0.0001). In dalteparin-treated patients, delta vWf was elevated (+48 +/- 8%) and did not differ from the unfractionated heparin group (NS). CONCLUSIONS: We confirm that, in unstable angina patients, a rise of vWf over the first 48 h is associated with an impaired outcome at 30 days. Moreover, the four different anticoagulant treatments tested here do not provide the same protection with regards to vWf release, which may have important prognostic implications and explain different results observed in recent clinical trials.

Aged↗

PubMed2000

Impact of serotonin on tumour growth.

Several opposite effects of serotonin (5HT) on tumour growth have been reported. On one hand, 5HT is known as a growth factor for several types of nontumoural cells, and it has been proposed to take part in the autocrine loops of growth factors contributing to cell proliferation in aggressive tumours such as small cell lung carcinoma. Depending on the tumour type either 5HT2 or 5HT1 receptor antagonist have been found to inhibit the 5HT-induced increase in tumour growth. In contrast, several authors have also reported that 5HT and 5HT2 agonist can inhibit tumour growth. Most often this effect has been considered to be related with the specific vasoconstrictive effect of 5HT or 5HT2 agonists on the vessels irrigating the tumour, which has been evidenced by intravital microscopy. Intravital microscopy studies have also shown that vessels perfusing the tumour exhibit a specific vasconstrictive response to 5HT1 agonists. In addition, 5HT has been shown to be involved in the effects of several anticancer treatments associated with the reduction of tumour flow. Finally, the specific vasoconstrictive effect of 5HT or 5HT receptor subtype agonists might also be useful in inducing hypoxia in tumours, which could be exploited in a strategy using hypoxia-selective cytotoxins or hypoxia-selective gene therapy.

Animals↗

PubMed2000

[Role of oxidative stress in permeability changes observed in the microcirculation of diabetic rats in vivo].

AIM: Since an increase in the generation of free radicals has been shown in diabetes, we were interested on its involvement in changes in microvascular permeability during diabetes. METHODS: Intravital microscopy was used to study changes in microvascular permeability during diabetes. The extravasation of a fluorescent macromolecular tracer (FITC-Albumin) was measured for one hour and, after computer-aided image analysis, was expressed as variations of normalized grey levels (arbitrary units). RESULTS: The extravasation of the tracer was increased in diabetic rats. An intravenous bolus of probucol (an other anti-oxidant) inhibits this increase (fig. 1). The increase of the extravasation of the macromolecular tracer can also be inhibited when both superoxide dismutase, (which dismutates superoxide to hydrogen peroxide) and catalase (which reacts with hydrogen peroxide to form water and molecular oxygen) are administered simultaneously (fig 2). When administered separately, these enzymes failed to inhibit the increase of the extravasation of the macromolecular tracer. Five-week treatment of diabetic rats by pentoxifyllin, a drug which inhibits leukocyte activation did not have any effect on the increase of albumin extravasation (fig. 3a). In addition, no difference was found in adherent leukocytes or in the leukocyte rolling flux between diabetic and normoglycemic rats (fig. 3b). CONCLUSION: Reactive oxygen species are responsible for an increase in microvascular permeability likely by leukocyte-independent mechanisms.

Animals↗

PubMed2000

[Advanced glycation end products are involved in microvascular permeability changes observed in microcirculation of diabetic rats in vivo].

AIM: Since chronic hyperglycemia leads to Advanced Glycation End Products (AGE) formation, we were interested in its involvement in changes in microvascular permeability during diabetes. METHODS: Intravital microscopy was used to study changes in microvascular permeability during diabetes. The extravasation of a fluorescent macromolecular tracer (FITC-Albumin) was measured for one hour and, after computer-aided image analysis, was expressed as variations of normalized grey levels (arbitrary units). RESULTS: The extravasation of the tracer was increased in diabetic rats. An intravenous bolus of s-RAGE (extracellular domain of the AGE receptor) inhibits dose-dependently this increase (fig. 1). The increase of the extravasation of the macromolecular tracer can be inhibited when s-RAGE are administered 1 and 3 hours before the experiment, but not when administered 1/4 hour and 12 hours before experiment (fig. 2). Administration of antibodies against AGE receptors also inhibits the increase of permeability observed in diabetic rats (fig. 3). CONCLUSION: AGE interaction with their receptor is responsible for an increase in microvascular permeability.

Animals↗

PubMed2000

Evaluation of fluorescein-labeled autologous leukocytes for examination of retinal circulation in humans.

PURPOSE: Increased leukocyte-endothelium interaction have been suggested as a phenomenon contributing to capillary occlusion and/or rupture of the blood-retina barrier during human retinal vascular diseases. This study was performed to evaluate if fluorescein-labeled autologous leukocytes (FLALs) can be used for examination of leukocyte transit in the human retina. METHODS: The preparation consisted of human dextran-separated leukocytes mixed with fluorescein. After reinjection in normal subjects and in one diabetic patient, a confocal scanning laser ophthalmoscope was used to visualize them in the retinal circulation. The changes between FLALs and control leukocytes in the expression of leukocytes adhesion molecules CD11b and CD62L were evaluated by flow cytometry. RESULTS: The circulating FLALs were clearly visible in retinal vessels. The mean (+/- SD) capillaries velocity was 1.43 (+/- 1.3) mm/s in the macula and 1.82 (+/- 1.4) mm/s in the peripapillary area. No leukostasis was detected in the normal subjects, while it was detected in te diabetic patient. Flow cytometry revealed an increase in CD11b and a decrease in CD62L expression of leukocytes after labeling, suggesting that compared to normal leukocytes FLALs are more susceptible to interact with vascular endothelium. CONCLUSIONS: The use of FLAL is presently the only technique applicable in humans for study of leukocyte transit in the retina. Their preparation is technically simple and unexpensive. Precise measurement of the velocity of leukocytes in small vessels can be obtained. Despite evidence of a certain degree of leukocyte activation after the labeling procedure, no leukostasis was detected in vivo in normal subjects. Potential applications for this technique may include the detection of leukostasis in the human retina during severe forms of diabetes and retinal phlebitis.

Adult↗

PubMed2000

[Endothelium and hypertension].

Many changes in endothelial function have been described in hypertension. Endothelium-dependant dilatation due to the stimulation of specific receptors or related to changes in flow, are reduced both in experimental models and in clinical observations of hypertensive patients. Many mechanisms of this endothelial dysfunction have been proposed. Reduction of the activity of the enzyme synthesising nitric oxide has been found in some animal modes of hypertension (salt-related) and in hypertensive subjects whereas in other experimental models, this enzyme's activity is increased. Other mechanisms, therefore, play a role, such as increased synthesis of constricting prostanoids and increased synthesis of oxygen radicals. The inhibition of cyclooxygenase or intra-arterial administration of Vitamin C in hypertensive patients may restore endothelium-dependant vasodilatation. In view of the many endothelium-dependant mechanisms described in the pathogenesis of hypertension, the authors underline the fact that in most studies each mechanism has been studied individually. However, understanding the interactions of the different endothelial dependant mechanisms is the key to reconciling the many physiopathological disturbances observed in hypertension, differentiating direct from indirect changes induced by the complex network of interactions one with another. This will also result in a more accurate appreciation of the similarities and differences of effects of antihypertensive drug therapy targeted on endothelial function.

Animals↗

PubMed2000

Hemorheology in asymptomatic HIV-infected patients.

Although cardiac and vascular complications have been recognized among patients infected with the Human Immunodeficiency Virus-1 (HIV-1), their vascular biology and rheology have not been studied. Rheology of red blood cells (RBC) was assessed with an erythroaggregometer in 22 HIV-1 infected asymptomatic patients (pts) and 17 healthy HIV negative controls (C). All participants were normotensive, nondiabetics, had normal lipid levels and had an hematocrit ranging from 37 to 44% and hemoglobin levels > or = 12 g/100 ml. Patients had a shorter RBC aggregation characteristic time than controls (1.49 +/- 0.17 vs. 2.04 +/- 0.41 s, p = 0.001) and an increased disaggregation shear rate (166 +/- 34.9 vs. 122 +/- 25.4 s(-1), p = 0.001). This hyperaggregation tendancy was associated with increased gamma-globulin (18.3 +/- 3.3 vs. 13.7 +/- 1.9 g/l, p = 0.01) and fibrinogen (3.52 +/- 0.57 vs 3.03 +/- 0.48 g/l, p = 0.003) levels and with an increased erythrocyte sedimentation rate (ESR) (25 +/- 14.3 vs. 12.3 +/- 7.5 mm, p = 0.02). Even in patients with ESRs ranging within normal values (< or = 20 mm), the aggregation characteristic time was found lower in patients than in controls (p = 0.004). There was no correlation between these rheological changes and the CD4+ T-cell count. The 17 patients receiving an antiviral therapy had lower CD4+ T-cell counts than their 5 untreated counterparts (244.7 +/- 167 vs. 410 +/- 106/mm3, p = 0.025), and a higher disaggregation shear rate (177.4 +/- 38.2 vs. 127 +/- 25.4, p = 0.01). Thus, an impairment of rheological characteristics is observed in asymptomatic HIV-I infected patients in association with changes in plasma proteins.

Adult↗

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↗