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Biomedical subjects

E Vicaut

Publications and source records attributed to E Vicaut.

At least 127 records · Page 7Linked to original sources
PubMed1992

In vivo effects of Escherichia coli endotoxemia on diaphragmatic microcirculation in rats.

We investigated the effects of Escherichia coli endotoxin administration on diaphragmatic microcirculation in rats by in vivo videomicroscopy. Rats were allocated into three groups: 1) intravenous inoculation of 10 mg/kg of E. col endotoxin (group E, n = 25), 2) intravenous inoculation of sterile 0.9% NaCl (group C, n = 20), and 3) induction of a controlled hemorrhage by reducing the vascular volume via an arterial catheter (group H, n = 15). Mean blood pressure (BP) and arteriolar diameters were measured at 15-min intervals and capillary perfusion pattern at 30-min intervals for 1 h. BP decreased similarly in groups E and H, whereas it was maintained in group C. Arterioles were classified as second (A2, n = 46), third (A3, n = 22), and fourth (A4, n = 21) order, according to their relative localization in the network. Basal diameters were the same in the three groups: 38.16, 17.33, and 6.80 microns in group C; 38.17, 17.41, and 7.04 microns in group E; and 37.82, 19.19, and 6.99 microns in group H for A2, A3, and A4, respectively. During the observation period, a significant and similar vasoconstriction of A2 arterioles was observed in groups E and H but not in group C. By contrast, in the three groups, no significant changes in diameter were found for the A3 and A4 arterioles. Capillary perfusion was markedly impaired in group E: at 60 min the percentage of non-perfused capillaries was 40.92 +/- 6.65% in group E compared with 21.17 +/- 5.45% in group C (P less than 0.05) and 18.18 +/- 8.11% in group H (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Diaphragmatic microcirculation during halothane and isoflurane exposure in pentobarbital-anesthetized rats.

We investigated the effects of halothane and isoflurane on diaphragmatic microcirculation in pentobarbital-anesthetized rats by in vivo video microscopy. After a baseline period, rats were randomly allocated into three groups according to administration of 0.5, 0.75, and 1 minimal alveolar concentration (MAC) of either halothane (group Hal, n = 16), isoflurane (group Iso, n = 14), or no halogenated agent (group C, n = 20) in three succeeding steps of 15 min. Mean arterial blood pressure (MAP), arteriolar diameters, and functional capillary density were analyzed in the last 3 min of each step. MAP remained unchanged in group C but decreased in a dose-dependent manner in both halogenated receiving groups. MAP was significantly lower in rats breathing Hal compared with those breathing Iso. Arterioles were classified in second (A2, n = 39), third (A3, n = 24), and fourth (A4, n = 30) order according to their relative location in the network. No changes in A2 and A3 diameters were noted in either group. A4 diameters remained unchanged in groups C and Iso, whereas a significant reduction was found in group Hal at 0.75 and 1 MAC exposure (P < 0.05 compared with baseline and with groups C and Iso, respectively). During Iso exposure, functional capillary density was not significantly different when compared with baseline and group C, whereas in group Hal it decreased significantly at 0.5, 0.75, and 1 MAC, amounting to 61.1 +/- 9, 30.7 +/- 10.3, and 22.8 +/- 6.3%, respectively, of baseline (P < 0.01 vs. baseline and P < 0.05 vs. groups Iso and C for 0.75 and 1 MAC).(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗
PubMed1991

Elevated blood cyanide concentrations in victims of smoke inhalation.

BACKGROUND: The nature of the toxic gases that cause death from smoke inhalation is not known. In addition to carbon monoxide, hydrogen cyanide may be responsible, but its role is uncertain, because blood cyanide concentrations are often measured only long after exposure. METHODS: We measured cyanide concentrations in blood samples obtained at the scene of residential fires from 109 fire victims before they received any treatment. We compared the results with those in 114 persons with drug intoxication (40 subjects), carbon monoxide intoxication (29 subjects), or trauma (45 subjects). The metabolic effect of smoke inhalation was assessed by measuring plasma lactate at the time of admission to the hospital in 39 patients who did not have severe burns. RESULTS: The mean (+/-SD) blood cyanide concentrations in the 66 surviving fire victims (21.6 +/- 36.4 mumol per liter, P less than 0.001) and the 43 victims who died (116.4 +/- 89.6 mumol per liter, P less than 0.001) were significantly higher than those in the 114 control subjects (5.0 +/- 5.5 mumol per liter). Among the 43 victims who died, the blood cyanide concentrations were above 40 mumol per liter in 32 (74 percent), and above 100 mumol per liter in 20 of these (46 percent). There was a significant correlation between blood cyanide and carbon monoxide concentrations in the fire victims (P less than 0.001). Plasma lactate concentrations at the time of hospital admission correlated more closely with blood cyanide concentrations than with blood carbon monoxide concentrations. Plasma lactate concentrations above 10 mmol per liter were a sensitive indicator of cyanide intoxication, as defined by the presence of a blood cyanide concentration above 40 mumol per liter. CONCLUSIONS: Residential fires may cause cyanide poisoning. At the time of a patient's hospital admission, an elevated plasma lactate concentration is a useful indicator of cyanide toxicity in fire victims who do not have severe burns.

Adolescent↗
PubMed1991

Peripheral vascular effects of thiopental and propofol in humans with artificial hearts.

The peripheral vascular effects of thiopental 5 mg/kg and propofol 2.5 mg/kg were compared in five patients whose lungs were being ventilated and in whom a Jarvik-7 artificial heart had been implanted. The patients were monitored, using catheters that had been surgically inserted into the radial artery, the right and left atria, and the pulmonary artery. The Jarvik-7 settings were modified to render the artificial heart "preload independent" and to maintain cardiac output constant. Each patient received both drugs, with the interval between each drug ranging from 16 to 28 h. Hemodynamic parameters and catecholamine and atrial natriuretic peptide plasma concentrations were measured before drug administration and 5, 10, 15, 30, and 45 min later. Both drugs significantly decreased arterial pressure, systemic vascular resistance index, pulmonary arterial pressure (PAP), and right and left atrial pressures (RAP and LAP, respectively). However, propofol 2.5 mg/kg induced a significantly greater and more prolonged decrease in arterial pressure, systemic vascular resistance index, and RAP than that after administration of thiopental 5 mg/kg (P less than 0.05). Five minutes after drug injection, mean arterial pressure decreased by 21% after thiopental and by 39% after propofol (P less than 0.01); systemic vascular resistance index decreased by 21% after thiopental and by 44% after propofol (P less than 0.05); RAP decreased by 20% after thiopental and by 50% after propofol (P less than 0.05); mean PAP decreased by 18% after thiopental and by 32% after propofol (P less than 0.09); and LAP decreased by 40% after thiopental and by 46% after propofol (P less than 0.2). With both drugs, atrial natriuretic peptide, norepinephrine, and epinephrine plasma concentrations remained stable throughout the study period. Because cardiac output was maintained constant throughout the study, these results suggest that propofol 2.5 mg/kg is a more potent vasodilator of venous and arterial beds than is thiopental 5 mg/kg.

Adult↗
PubMed1991

Acute effects of tumor necrosis factor on the microcirculation in rat cremaster muscle.

The acute effects of TNF on the microcirculation were studied by in vivo microscopy in rat cremaster muscle. The changes in arteriolar diameter after topical administration of recombinant TNF (rTNF; 10(-4)-10(4) ng/ml) were studied in second-, third-, and fourth-order arterioles (A2-A4) whose mean diameters under control conditions were 64.3, 30.7, and 14.8 microns respectively. rTNF induced a concentration-dependent vasodilation whose amplitude was largest for the smallest arterioles. At the highest concentration tested, arteriolar diameter increased by 21, 29, and 41% of control diameter for the A2, A3, and A4 arterioles, respectively. Indomethacin or mefenamic acid, two structurally different prostaglandin synthesis inhibitors, markedly inhibited the degree of vasodilation induced by rTNF in the three arteriolar orders. As regards the effect of rTNF on vasoconstriction in response to norepinephrine, vasoconstriction was greatest for the smallest arterioles, and did not change 10 min after rTNF administration for any of the three arteriolar orders. We conclude that (a) rTNF has a direct vasodilatory effect which is greatest in the smallest arterioles, (b) this vasodilation is at least partly mediated by prostaglandins, and (c) administration of rTNF in itself does not acutely alter the response of the arterioles to vasopressive drugs.

Animals↗
PubMed1991

Microvascular effects of cocaine; interaction with nitrendipine and enalaprilat.

Cocaine abuse can cause cardiovascular damage leading to hypertension, myocardial ischaemia and infarction. This might be partly due to the effects of cocaine on the microcirculation about which little is known, although its effects on the macrovessels are well documented. Accordingly, we used in vivo videomicroscopy to study the vasoconstrictive effect of cocaine on arterioles of different diameter. They were classified into three orders (A2, A3, A4) according to their position in the microvascular network and their diameter. Since calcium antagonists have been reported to exert a protective effect against the cardiovascular disorders induced by cocaine, we tested the hypothesis that this protective action occurs in the microcirculation. We found that intra-arterial administration of the calcium antagonist Nitrendipine greatly inhibited the vasoconstriction induced by cocaine in all three arteriole orders. The degree of inhibition ranged from 44 to 56%. Combined administration of benzodiazepine and an angiotensin converting enzyme inhibitor has also been reported to protect rats against cocaine-induced hypertension and to increase survival rates after a toxic dose of cocaine. Since the mechanisms of this protection are not yet clear, we also studied the effect of the angiotensin converting enzyme inhibitor Enalaprilat on cocaine-induced vasoconstriction. Intra-arterial administration of Enalaprilat inhibited this vasoconstriction slightly but significantly in arteriole orders 2 and 3 by 27 and 24% respectively, but not in order 4. We concluded that Nitrendipine is a powerful inhibitor of cocaine-induced vasoconstriction in the microcirculation. The small but significant inhibition found with Enalaprilat for the larger arterioles suggests that the local angiotensin II level may affect the response to cocaine. However, since the Enalaprilat-induced inhibition was very limited, we conclude that mechanisms other than those occurring in the peripheral microcirculation account for the protection afforded by Enalaprilat against the harmful effects of cocaine.

Animals↗
PubMed1990

A preparation for in vivo study of the diaphragmatic microcirculation in the rat.

A new preparation is described for the study of the microcirculation of the rat diaphragm by in vivo microscopy. After midline laparotomy, the abdominal site of the diaphragm muscle was exposed. The rat was mechanically ventilated and placed in the Trendelenburg position, thus allowing a microscope placed on a three-dimensional articulated system to be set up perpendicular to the diaphragm. The diaphragm was then transilluminated by inserting fiberoptic microprobes into the thorax cavity by thoracotomy in the fifth intercostal space. This preparation allowed us to describe the morphological characteristics of the arteriolar network in vivo. As regards the venular network, two parts were distinguished: one part collects the blood of the external half of the diaphragm, runs roughly parallel to the arterioles, and converges toward the internal mammary and intercostal veins; the other part collects the blood of the central half of the diaphragm and converges on the central venous arcade along its central tendon. Anastomotic channels between these two parts were observed, as well as spontaneous inversion of the direction of the blood flow, indicating the presence of unsteady pressure gradients in some branches of the venular network. Capillary density was also studied by measuring intercapillary distance, whose mean value was 21.43 +/- 0.67 microns. No differences in intercapillary distance were found between the external and central parts of the diaphragm. In conclusion, we describe a preparation which allowed us to study the diaphragmatic microcirculation for at least 2 hr under good hemodynamic conditions. The study of this specific microcirculation is important because the diaphragm's metabolism and functions are specific and because it is essential to life that its perfusion should be adapted to its specific metabolic requirements.

Animals↗
PubMed1990

Peripheral vascular effects of halothane and isoflurane in humans with an artificial heart.

The peripheral vascular effects of isoflurane and halothane were compared in five critically ill patients in whom a Jarvik-7 artificial heart had been implanted. The lungs of all patients were mechanically ventilated in the postoperative period and the patients were monitored with an arterial catheter and with catheters that had been surgically inserted into the right and left atria and into the pulmonary artery. Norepinephrine and epinephrine plasma concentrations were measured using a radioenzymatic assay. The Jarvik-7 settings were modified to render the artificial heart "preload independent" and to maintain cardiac output constant. Each patient was anesthetized twice using halothane and isoflurane at two different MAC levels, 1 and 1.5 (Datex vapour analyzer), with the interval between each anesthetic ranging from 12 to 26 h. Both anesthetics significantly decreased mean arterial pressure (from 100 +/- 11 mmHg to 66 +/- 13 mmHg for halothane and from 102 +/- 17 mmHg to 48 +/- 11 mmHg for isoflurane; mean +/- SD) and systemic vascular resistance index (from 27 +/- 11 Wood units/m2 to 18 +/- 6 Wood units/m2 for halothane and from 30 +/- 6 Wood units/m2 to 13 +/- 3 Wood units/m2 for isoflurane; mean +/- SD), but with isoflurane to a significantly greater extent than with halothane (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Independent role of arterial O2 tension in local control of coronary blood flow.

The aim of this study of a blood-perfused isolated rabbit heart preparation was to differentiate the effects on coronary resistance of large changes in arterial O2 tension (arterial PO2 = 45-400 Torr) from the effects of variations in arterial O2 content or myocardial O2 delivery. Standard stored human blood was resuspended in Krebs-Henseleit buffer and was oxygenated to obtain normal PO2, high PO2, and low PO2. Hemoglobin concentrations were adjusted to obtain the same arterial O2 content (CaO2) for the three PO2s. In a first set of experiments, in which coronary blood flow (CBF) was free and adapted to a constant perfusion pressure, switching from control [138 +/- 17 (SE) Torr] to high PO2 blood (380 +/- 27 Torr) induced a significant decrease in CBF and myocardial O2 consumption (MVO2). Switching from control (125 +/- 3 Torr) to low PO2 blood (49 +/- 5 Torr) induced a significant increase in CBF and MVO2. In a second set of experiments, the switch from control (159 +/- 5 Torr) to high PO2 (389 +/- 32 Torr) was performed in a preparation in which CBF and consequently O2 delivery were constant. Under these conditions, the increase in perfusion pressure demonstrated that PO2 affected coronary resistance, even though the O2 delivery was constant. No significant change in myocardial performance was observed in any of these experimental procedures. These results show that arterial PO2 may affect coronary blood flow regulation independently of any mediation by the autonomic nervous system and of any associated changes in O2 content or O2 delivery.

Animals↗
PubMed1990

Transmural hematocrit gradient in left ventricular myocardia of rats.

The transmural distribution of tissue hematocrit was determined in rat left ventricular myocardium. Intramyocardial distribution volumes of 99Tc-labeled red blood cells and 131I-labeled albumin were measured in hearts arrested in a relaxed state by KCl or in a contracted state by BaCl2. Hearts were frozen in situ immediately after arrest by bathing in a mixture of liquid nitrogen and isopentane. After excision of the heart, a parallelepipedic portion was cut in a transverse section of the left ventricular free wall and subjected to en face serial sectioning through the thickness of the wall from the epicardium to the endocardium. 99Tc and 131I activity allowed determination of red blood cell and plasma volume and consequently of tissue hematocrit in each section. In both the relaxed and the contracted states of the hearts, a significant decreasing gradient of tissue hematocrit was found from the outer to the inner layers of myocardium. Tissue hematocrit in the subendocardial layers was approximately 70% of its value in the subepicardial layers.

Animals↗
PubMed1989

Clinical and ultrasound results after aortic valve replacement: intermediate-term follow-up with the St. Jude Medical prosthesis.

Mortality, morbidity, quality of life, and left ventricular (LV) function were evaluated in 49 patients after aortic valve replacement with the St. Jude prosthesis. Total follow-up was 2577 patient-months; survivors were followed-up for 4 to 7 years by clinical examination and echocardiography. The actuarial survival rate at 6 years was 79.6%, and there were no valve-related deaths. The linearized rates for thromboembolism and hemorrhage were 0.93% and 3.26% per patient-year, respectively. In 34% of the survivors the quality of life was poor. In the first three postoperative months, patients with aortic stenosis (n = 12) had a significant decrease in the muscle cross-sectional area (p less than 0.01) and patients with aortic regurgitation (n = 11) had decreases in both LV end-diastolic diameter (p less than 0.05) and cross-sectional area (p less than 0.001). All of these results were maintained at 5 years without modification of LV systolic function. Despite the good overall results, six patients deteriorated and had major LV dilatation. Multivariate logistic regression analysis identified two independent preoperative variables associated with a poor outcome defined as death of LV dysfunction (p less than 0.05): age and end-diastolic diameter. Thus meticulous follow-up showed a high incidence of hemorrhage and a poor quality of life in many of the survivors. It was concluded that in high-risk patients (age and end-diastolic diameter) surgery should probably be considered earlier.

Aortic Valve↗
PubMed1989

Arteriolar vasoconstriction and tachyphylaxis with intraarterial angiotensin II.

Several aspects of the differences between the responses of the second- to fifth-order arterioles (A2 to A5) to intraarterial administration of angiotensin II (AII) were studied by intravital microscopy on an original preparation of rat cremaster muscle. Dose-response curves displayed a leftward shift when the arteriolar order increased. Doses inducing 50% vasoconstriction were 15.1, 0.51, and 0.08 micrograms for A3, A4, and A5, respectively. For A2, very small vasoconstriction was found even at the highest dose of angiotensin II. The dynamics of the response were also dependent on the arteriolar order. The duration of the peak of vasoconstriction increased from A3 to A5, and the interval between the contact of vascular wall with drug and the response was smaller in A4 and A5 than in A3. To understand the effect of diameter as a determinant of heterogeneity in the degree of arteriolar vasoconstriction, norepinephrine was administered under the same conditions as angiotensin II, and responses were measured on arterioles with the same morphological characteristics as those examined after angiotensin II. When comparing the regression curves for the percentage of vasoconstriction vs diameter, we found that this relationship was drug dependent. The significantly steeper slope for angiotensin II than for norepinephrine excluded the possibility that heterogeneity of the degree of vasoconstriction is solely due to differences between the morphological characteristics of the arterioles. Since tachyphylaxis to AII is considered to be a reflection of the drug-receptor interaction, we also studied the magnitude of this phenomenon from proximal to distal parts of the arteriolar network. We showed that the degree of partial tachyphylaxis after 1 microgram AII was dependent on the arteriolar order and a decreasing tachyphylaxis gradient was evidenced from A3 to A5 arterioles.

Angiotensin II↗
PubMed1989

[Capillary permeability. Fundamental problems and modeling].

This brief paper reviewed some of the most currently used mathematical models in the field of transcapillary exchange. Mathematical formalism was reduced to its simplest expression and a special emphasis was given to the principles and simplifying hypotheses of each kind of model. We described the simplified formulation of capillary-tissue exchange used for the multiple indicator methods and its generalization using the equations derived from thermodynamics. "Black box" models taking into account the complexity of microcirculatory hemodynamics were also presented. We stressed the importance of interactions between adjacent portions of tissue and the potential influence of tissue-lymphatic exchange in the transcapillary exchange phenomenon.

Capillary Permeability↗