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Biomedical subjects

D Payen

Publications and source records attributed to D Payen.

At least 19 recordsLinked to original sources
PubMed1992

Activated macrophages depress the contractility of rabbit carotids via an L-arginine/nitric oxide-dependent effector mechanism. Connection with amplified cytokine release.

Inflammatory mediators released by macrophages (M phi) are believed to be involved in septic vasoplegia. To investigate the effect of M phi on vascular reactivity, excised rabbit carotids were exposed intraluminally either to peritoneal rabbit M phi, activated by 18 h of incubation with 1 microgram/ml lipopolysaccharide, or to the supernatants (SPN) derived from them. The contractile responses to phenylephrine (PE, 10(-6) M) were determined by measuring changes in diameter using an ultrasonic microdimensiometer 1, 2, and 3 h after the first control contraction. In control arteries (n = 12), PE-induced contractions were, respectively, 102.9 +/- 3.3%, 95.2 +/- 4.1%, and 89.7 +/- 3.8% of the first contraction, after 1, 2, and 3 h. Activated M phi significantly reduced PE-stimulated contractions after as little as 1 h of carotid exposure (percentage of controls at 1, 2, or 3 h: 74.1 +/- 5.6, 57.2 +/- 5.2, and 34.2 +/- 5.6, n = 10, P less than 0.001). The activated macrophage-derived SPN took longer to diminish carotid contractility than the M phi themselves, and became significant only after 2 h. The greater effect of M phi might be due to cooperation between M phi and vascular cells, as suggested by the amplified interleukin-1 release observed after M phi infusion. The presence of the endothelium partially protected carotid contractility from depression by activated M phi. Extraluminal addition of NG-monomethyl-L-arginine, an inhibitor of nitric oxide synthesis prevented this depression in arteries with or without endothelium. No products of the oxidative pathway of L-arginine were detected in rabbit activated M phi. These results suggest that activation of this pathway in smooth muscle cells seems to be involved in vascular hypocontractility.

Animals↗
PubMed1992

Doppler cardiac output and left ventricular performance after cardiac surgery. Pulsed Doppler ascending aorta and pulmonary blood flows and left ventricular function using implanted microprobes.

We have developed novel implantable Doppler microprobes to monitor beat-by-beat stroke volume and cardiac output (CO) after cardiac surgery. In 11 adults undergoing either coronary artery bypass grafting (n = 6) or valve replacement (n = 5), Doppler microprobes were implanted on the ascending aorta or the main pulmonary artery to measure aortic blood flow (ABF) or pulmonary artery blood flow (PBF). The diameters of both vessels were determined before surgery using two-dimensional echocardiography. Stroke volume was obtained from velocity tracings measured by a 4-MHz zero-crossing pulsed Doppler flowmeter. Simultaneous measurements of Doppler and thermodilution CO (TDCO) were compared. We found the following: ABF = 1.03 TDCO - 0.22 L/min (r = 0.89); while PBF = 0.69 TDCO - 1.24 L/min (r = 0.75). Furthermore, peak flow velocity and maximum acceleration of blood in the ascending aorta were measured after inotropic stimulation with dobutamine; both values increased significantly from control values (25.2 +/- 6.1 percent and 44.6 +/- 8.6 percent, respectively, at 7.5 micrograms/kg/min). We conclude that implanted aortic Doppler microprobes provide a sensitive and reliable method to measure aortic blood flow velocity after surgery and then allow monitoring of stroke volume and CO and analysis of left ventricular function after cardiac surgery.

Aorta↗
PubMed1992

Usefulness of perioperative pulsed Doppler flowmetry in predicting postoperative local ischemic complications after ileocolic esophagoplasty.

Regional ischemia may induce cervical anastomosis leakage or stenosis or graft necrosis after esophageal reconstruction by retrosternal interposition of an ileocolic graft. These complications may be related to systemic or local hemodynamic alterations. This study was designed to evaluate the relationship between immediate postoperative arterial blood supply to the graft, arterial patency monitored by angiography, and clinical outcome. Eight patients (mean age 30 +/- 4 years; standard deviation) were studied. Miniaturized Doppler implantable microprobes were sutured to the single artery supplying the graft and connected to an 8 MHz pulsed Doppler flowmeter. Systemic hemodynamic parameters and mesenteric hemodynamic data were collected 3 hours after the end of the surgical procedure. These data were compared with the angiogram of the right superior colic artery supplying the graft, systematically performed on the fifteenth postoperative day, and with the clinical course of follow-up for 3 months. Five patients (group 1) had excellent clinical and angiographic results. Mean mesenteric blood flow in these patients was 51 +/- 49 ml.min-1 (+/- standard deviation, ranging from 9 to 122). Three patients (group 2) had a poor clinical outcome. One had early complete graft necrosis and the two others had leakage of the cervical anastomosis with poor distal arterial vascularization of the graft on the angiogram. Mean mesenteric blood flow was nul in the first patient and, respectively, 24 and 28 ml.min-1 in the two others. Cardiac output and mean arterial pressure were in the same range for all patients. Phasic velocity shape analysis revealed that the three group 2 patients had an end-systolic or end-diastolic reverse flow pattern that was not observed in the five group 1 patients, which suggested a submaximal increase in downstream vascular resistance. This reverse flow pattern seems to be a good predictor of ischemia-related complications. We conclude that perioperative pulsed Doppler blood flow monitoring in an ileocolic graft may be useful for the diagnosis and prevention of ischemic complications.

Adult↗
PubMed1991

[Atrial natriuretic factor in men].

The atrial natriuretic peptide (ANP) is rapidly secreted in case of acute changes in atrial volume and heart rate. Its effects are mainly natriuretic and vasodilator. This hormone is of interest to the anaesthetist because induction of anaesthesia, epidural anaesthesia and administration of morphine all result in changes in ANP plasma concentration.

Anesthesia↗
PubMed1991

Isoflurane, and not halothane, increases mesenteric blood flow supplying esophageal ileocoloplasty.

Regional ischemia may induce anastomotic leakage or stenosis after esophageal reconstruction using retrosternal interposition of an ileocolic graft. These complications may be related to systemic or local hemodynamic alterations. This study was designed to evaluate the influence of inhalational anesthetic agents on the intestinal circulation supplying these ileocolic grafts. Seven patients (age 30 +/- 5 yr, mean +/- standard deviation [SD]) were studied in the immediate postlaparotomy period. Miniaturized Doppler implantable microprobes were sutured to the single artery supplying the graft and connected to an 8-MHz pulsed Doppler flowmeter. Continuous fentanyl infusion (300 micrograms.h-1) was maintained throughout the study. Measurements were performed at the end of four 30-min periods, which were, successively: first control; isoflurane or halothane anesthesia; second control; and isoflurane or halothane anesthesia. Isoflurane and halothane were administered in cross sequence with end-tidal concentration of 0.8% and 0.5%, respectively, to induce equipotent anesthesia. Both anesthetics induced similar decreases in mean systemic arterial pressure (MAP), cardiac output (CO), and systemic vascular resistance. During isoflurane, mean mesenteric blood flow (MBFm) supplying the graft was increased (+38%; P less than 0.05), and the mesenteric vascular resistance index (MVRI; -44%; P less than 0.05) was decreased, leading to an increase in the MBFm/CO ratio (P less than 0.05). Halothane changed neither the MBFm nor the MBFm/CO ratio, despite a mild decrease in MVRI (-14%; P less than 0.05). Diastolic blood flow velocity increased significantly (2.3 +/- 0.9 vs. 0.8 +/- 0.3 cm.s-1, P less than 0.05) only with isoflurane, suggesting a local vasodilation not observed with halothane.(ABSTRACT TRUNCATED AT 250 WORDS)

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

Monitoring the effect of CPAP on left ventricular function using continuous mixed-blood saturation.

The hypothetic benefit of CPAP on cardiac performance and on a reduction in VO2 was tested in a patient before heart transplantation after acute myocardial infarction using continuous SvO2 monitoring. The CPAP added to inotropic support (enoximone plus dobutamine) and intraaortic balloon pumping dramatically increased SvO2 in relation to both an increase in cardiac output and a decrease in VO2 secondary to respiratory work reduction, validating the initial hypotheses.

Cardiotonic Agents↗
PubMed1991

[Nitrate derivatives and anesthesia-resuscitation: physiopathologic bases and therapeutic indications].

This review briefly describes the cellular mechanisms of nitrates and the tolerance. Nitrates activate NO production thus GMPc in the smooth muscle cell explaining their vasodilating properties even in absence of an intact endothelium. The biologic pathway of AMPc is stimulated by prostaglandin activated by nitrates. Tolerance to these agents could result from depletion of sulfhydryl radical but also from reflex cardiovascular adaptation. After a brief recall of pharmacokinetic, pharmacodynamic properties are detailed. Therapeutic use in cardiac surgery, non-cardiac surgery, controlled hypotension, aortic surgery, heart failure, unstable angina, myocardial infarction and systolic hypertension in the elderly are discussed.

Anesthesia↗
PubMed1990

[Atrial natriuretic factor].

Although ANF research started 30 years ago, the atrial natriuretic factor (ANF) was only discovered recently (1981). The presence of such a factor has been suspected for many years because of histological and physiological arguments. In 1956, Kish found "dense granules" in the atrial walls of guinea pigs. Gauer and Henry could explain some of their experimental results on diuresis and natriuresis only by suggesting the presence of a third hormonal factor, but neither by the renin-angiotensin system, nor the anti-diuretic hormone. Hall et al. were the first to recognize a link between the granules and water and sodium metabolism. But it was De Bold who published the crucial experiment in 1981: injecting right atrial extracts to anaesthetized rats rapidly induced intense and transitory diuresis and natriuresis. ANF was born, and, at the same time, the concept of the heart as an endocrine gland. Indeed, ANF corresponds to the strict definition of a hormone. It has the following properties: natriuresis and diuresis via an increase in glomerular filtration fraction without any major changes in renal plasma flow; direct vasodilation of the large arteries with only few effects on small arterioles and veins. The stimuli for ANF secretion are mechanical and pharmacological, especially drugs currently used by anaesthetists. Atrial distension is the main mechanical stimulus. An increase in atrial transmural pressure is always followed by a release in ANF, but this effect is not constant for increases in intra-luminal pressure. It is the former pressure gradient alone that reflects the volume of the right atrium, the mechanical stimulus for ANF secretion. Tachycardia, or, more precisely, an increase in the atrial contraction rate, also leads to an important release of ANF. Cardiac nerves are not necessary for this, as demonstrated by studies in heart transplant patients. Only few pharmacological agents have been shown to really stimulate ANF secretion. In rats, morphine has a direct secretory effect, whereas ketamine hydrochloride, diethylether and chloral hydrate do so by increasing the release of catecholamines. The effects of alpha, beta adrenergic agonists and calcium agonists remain controversial. ANF, which has diuretic and vasodilator effects, plays a part, together with the renin-angiotensin system and the anti-diuretic hormone, in blood volume control in mammals. However, it has a special role to play, because it is a rapid release hormone: rapid vascular filling leads to an increase in ANF in less than 1 minute, with a parallel increase in diuresis.

Anesthetics↗
PubMed1990

[Cachectin or TNF (tumor necrosis factor): clinical implications].

Septic shock remains an acute condition with a bad prognosis and a high mortality rate. This could be related to our incomplete understanding of the pathophysiological mechanisms involved, especially in the immunological field. Recently, several studies have stressed the key role of cytokines. Amongst these, the tumour necrosis factor (TNF) seems to be the most important. This peptide is a hormone secreted by monocytes and macrophages under the effect of various stimuli such as lipopolysaccharides or endotoxin. Giving TNF mimicks the clinical and biological patterns of septic shock. Moreover, high concentrations of TNF have been found in patients suffering from septic shock. Pretreatment with monoclonal antibodies against TNF prevents the occurrence of septic shock after endotoxin administration. TNF acts directly via ubiquitous specific receptors; this probably explains its diffuse activity. The therapeutic implications of these recent advances are not clear. It is not known, for the moment, whether TNF secretion is beneficial or deleterious for the patient.

Antibodies, Monoclonal↗
PubMed1990

Determinants of systolic and diastolic flow in coronary bypass grafts with inotropic stimulation.

Using implanted pulsed Doppler microprobes sutured on saphenous bypass grafts in ten patients we studied, 6 h after cardiac surgery, the effects of 5 and 10 micrograms.kg-1.min-1 of dobutamine on mean (Qm), systolic (Qs), and diastolic (Qd) coronary bypass graft flows, as well as on coronary systolic (integral of Qs) and diastolic (integral of Qd) blood volumes entering the myocardium per cardiac beat. Qm increased during the inotropic stimulation from 61.8 +/- 19.2 to 81.1 +/- 21.8 ml.min-1 (P less than 0.001) and resulted from an unchanged Qs and from a large increase in Qd (P less than 0.01). Qd increased more than did diastolic arterial pressure and was related to rate pressure product taken as an index of myocardial oxygen consumption (r = 0.76, P less than 0.001). Despite the dobutamine-induced increase in heart rate (P less than 0.01), integral of Qs, and integral of Qd, the systolic and diastolic inflow volumes per cardiac beat were unchanged. We conclude that increased myocardial blood supply through the saphenous vein bypass graft during inotropic stimulation by dobutamine resulted from different systolic and diastolic events. The oxygenated blood volume entering the coronary vascular bed per beat was unchanged despite tachycardia.

Coronary Artery Bypass↗
PubMed1990

[Postoperative enoximone in coronary surgery. Systemic and coronary hemodynamics and regional systolic function].

The effects of Enoximone (50 mg in 20 minutes) on systemic, pulmonary and coronary haemodynamics and on regional systolic function were examined after surgical myocardial revascularisation in 5 patients without overt cardiac failure. The flow in mammary artery grafts and the study of regional systolic function were assessed by Doppler probes implanted during the operation. Enoximone increased Qc and Qco without changing blood pressure or cardiac output, due to arterial vasodilatation and inotropic stimulation. Pulmonary vasodilatation resulted in hypoxemia which must be prevented. The increase in VO2 was unrelated to oxygen transport suggesting a specific drug related effect.

Cardiotonic Agents↗
PubMed1990

[Vascular smooth muscle fibers and the autonomic nervous system].

Vascular Smooth Muscle cell (V.S.M.C) plays a major role in the regulation of vasomotion. Sympathetic system play a key role in vascular smooth muscle function. Epinephrine (humoral pathway) and norepinephrine (nervous pathway) can both stimulate V.S.C.M. via delta and beta adrenergic receptors. The function of parasympathetic system is more controversial. Acetylcholine induces the release of a relaxing factor by the endothelial cell (E.D.R.F.) but it has a direct contracting effect on V.S.C.M. Neural vasodilation is also concerned by noradrenergic mechanisms.

Autonomic Nervous System↗
PubMed1990

Head injury: clonidine decreases plasma catecholamines.

Seven patients who had suffered head injury 3 to 5 days before the study was undertaken received clonidine (2.5 micrograms/kg iv over 10 min). This resulted in a reduction of plasma norepinephrine (p less than .05) and in normalization of plasma epinephrine (p less than .05). Neither common carotid blood flow nor diastolic blood flow as index of global cerebral perfusion as measured by pulsed Doppler changed. The reduction of sympathetic overactivity, probably due to the specific action of clonidine on alpha 2-adrenoceptors within the rostral ventrolateral medulla, may be of interest in the management of head injury because of the maintenance of cephalic hemodynamics.

Acute Disease↗