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Biomedical subjects

D Payen

Publications and source records attributed to D Payen.

At least 109 records · Page 6Linked to original sources
PubMed1989

[Criteria for brain death: cessation of cerebral circulation demonstrated by Doppler ultrasonography of the carotid arteries].

If human death is defined by brain death, its diagnosis needs medicolegal criteria based on clinical examination and EEG. However, this evaluation could be difficult because technical or physiological limitations might impair the interpretation, especially after barbiturates and/or hypothermia. Since brain death is characterized by an intracranial circulatory arrest, methods assessing this phenomenon are warranted. Among these methods, conventional or isotopic cerebral angiography appears the most promising, but it cannot be easily performed everywhere. Because superficial blood flow in arteries is now accurately measured by the pulsed Döppler technique, this prompted us to test the specificity and sensitivity of common carotid blood flow data for brain death diagnosis. Two series of age-matched patients (36 yrs in mean) were studied. Series 1 (n = 28) was used to define the discriminant parameters between 14 severe coma patients and 14 brain-dead patients diagnosed by the classical criteria. Then these parameters were prospectively tested in a blind manner on a second series of 28 patients suffering from severe coma. The parameters allowing us to classify patients as brain dead or not with a 100% specificity and sensitivity were: end diastolic blood flow (QED in ml/min), end diastolic blood flow velocity (VED), and cerebral metabolic index (CMI = QED x AV D 02). The most powerful discriminant parameter was QED, allowing a strictly non-invasive diagnosis of brain death.

Adult↗
PubMed1989

[Calcium inhibitors: effects on cerebral blood flow and intracranial pressure].

Calcium entry blockers (CEB) have been a major advance in pharmacologic research in the last decade, especially in cardiovascular diseases. In neurology and intensive care, prescription of CEB seems to be more selective. CEB are potent cerebrovascular vasodilating drugs especially after KCL induced vasoconstriction. This property appears less evident when vasoconstriction is achieved by agonist substances. CEB act selectively on cerebral vessels, an effect which prevents the occurrence of systemic arterial hypotension. However they greatly modify the cerebrovascular response to arterial CO2. Concerning the cerebrovascular response to arterial CO2. Concerning their potential benefits in brain ischemia, it is now well admitted that CEB are useful in subarachnoid hemorrhage. Several controlled and uncontrolled human studies have demonstrated the CEB potency in vasospasm prevention and in cerebral ischemic consequences. Nonetheless when the vasospasm is installed, the benefit of the CEB appears less evident. In focal cerebral ischemia, data are few and unclear suggesting a cautious prescription of CEB. Finally CEB seem to increase intracranial pressure in humans, although this effect depends on the underlying neurologic pathology.

Animals↗
PubMed1989

[Feasibility of calcium inhibitors in the treatment of brain disease following cardiac arrest].

One of the crucial factors affecting mortality and morbidity after circulatory arrest the ischemic neuronal damage following complete cessation of cerebral blood-flow. To date, no accepted pharmacologic neuroprotective therapy has emerged. Cerebral ischemia causes a rapid shift of Ca++ from the extracellular spaces into cells and it is assumed that this excessive entry of Ca++ is the final pathway of cell death. In addition, Ca++ is involved in the diffuse vasospasm which occurs after global cerebral ischemia. Therefore, calcium entry blockers such as dihydropyridines derivatives have sparked considerable interest especially because of their preferential cerebrovasodilating effects. In vivo studies have demonstrated protection from brain ischemia with calcium entry blockers. However no direct protective effect of these drugs has been shown on neurons. More recent results have underscored the importance of excitatory amino acid neurotransmitters and receptors (particularly N-Methyl-D-Aspartate receptors) in causing intracellular calcium overload and neuronal death after ischemia. Blockade of these receptors or their associated channels may be an interesting way to protect the brain against ischemic damage.

Calcium Channel Blockers↗
PubMed1988

Forearm vascular tone and reactivity during lumbar epidural anesthesia.

Forearm vascular tone and sympathetic reactivity were investigated in ten unpremedicated patients during two levels of epidural sensory blockade, neither of which levels was high enough to block cardiac sympathetic pathways. An 8-MHz pulsed Doppler blood flowmeter was used to determine brachial artery diameter and flow characteristics. Measurements were made before and during sympathetic stimulation induced by a contralateral isometric handgrip. The lower level of sensory blockade (T11) in the absence of sympathetic stimulation was associated with decreases in right atrial pressure, brachial artery diameter (3.9 +/- 0.2 vs 4.2 +/- 0.2 mm, P less than 0.05) and brachial blood flow (42 +/- 5 vs 66 +/- 7 ml.min-1, p less than 0.001), whereas forearm vascular resistance increased significantly (2.2 +/- 0.3 vs 1.5 +/- 0.2 mm Hg.ml-1.min-1, P less than 0.01). Neither heart rate nor mean arterial pressure changed. At the higher level of blockade (T7), right atrial pressure and systemic arterial pressure decreased further without change in heart rate. Brachial artery diameter (3.8 +/- 0.2 mm) remained unchanged while brachial blood flow additionally decreased (30 +/- 3 ml.min, P less than 0.05), and forearm vascular resistances further increased (3.0 +/- 0.2 mm Hg.ml-1.min-1, P less than 0.01). Changes in heart rate and in mean arterial pressure associated with isometric exercise were similar before and during epidural anesthesia at both levels of epidural blockade.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Pulsed Doppler ascending aortic, carotid, brachial, and femoral artery blood flows during caudal anesthesia in infants.

Hemodynamic effects of caudal bupivacaine anesthesia were studied in eight infants 6.5 +/- 0.5 months old (mean +/- SD), weighing 7.4 +/- 4.4 kg anesthetized with halothane 0.2% end-tidal and 60% nitrous oxide. Heart rate and systolic, diastolic, and mean arterial pressure remained unchanged. Cardiac index and stroke index assessed by pulsed Doppler and total vascular resistances were not altered by the caudal block. However, after caudal anesthesia, the authors observed a significant decrease (P less than 0.05) in brachial blood flow assessed by pulsed Doppler (from 49.0 +/- 28.3 to 31.7 +/- 24.6 ml-1.min) and a significant increase (P less than 0.05) in brachial vascular resistance (from 2.9 +/- 1.7 to 5.5 +/- 1.0 mmHg.min.ml-1). Blood flow and vascular resistance in both the femoral and carotid arteries did not change. This study suggests that, in supine position, caudal anesthesia in infants induces a blood pooling in the denervated lower extremities and a reflex vasoconstriction in innervated areas which maintains cardiac output. We conclude that volume loading is not necessary in normovolemic infants after caudal anesthesia with cutaneous analgesia below T5.

Anesthesia, Caudal↗
PubMed1987

Low molecular weight heparin fractions as an alternative therapy in heparin-induced thrombocytopenia.

Eight patients with a delayed-onset heparin-induced thrombocytopenia, with thrombotic complications requiring immediate anticoagulation in 7 of them, were given low molecular weight heparin (LMWH) fractions as alternative therapy. This treatment led to normalization of platelet count within 3-5 days in 6 patients with clinical recovery in 5. In 2 patients, thrombocytopenia persisted despite LMWH therapy. In vitro platelet aggregation tests performed in all patients gave evidence of a relationship between the presence (or absence) of a LMWH-dependent platelet-aggregating factor in the patients' plasma and the persistence (or correction) of the thrombocytopenia with LMWH therapy. Although positive in vitro tests may not necessarily be associated with thrombocytopenia, in vitro testing may prove to be a useful guide before giving LMWH fractions as an alternative therapy in patients with heparin-induced thrombocytopenia requiring immediate anticoagulation.

Adult↗
PubMed1986

Comparison of perioperative and postoperative phasic blood flow in aortocoronary venous bypass grafts by means of pulsed Doppler echocardiography with implantable microprobes.

Although graft dimension and hemodynamic variables have been suggested as important determinants of the functional results of aortocoronary bypass grafting, there is no easy-to-use bedside method of monitoring phasic blood flow in coronary bypass grafts. We developed a miniaturized implantable silicone pulsed Doppler flow probe linked to a classic 8 MHz pulsed Doppler system. This apparatus has an adjustable range-gated time system that permits accurate measurement of diameter (D, in mm), cross-sectional blood flow velocity (Vm, in cm/sec), and coronary bypass graft flow (CBGF, in ml/min) as pi D2/4 X Vm X 60. Ten patients (55 +/- 7.2 years SD) with preoperative left ventricular ejection fractions over 45% received the implantable flow probes during the aortocoronary venous bypass procedure. Closure of the chest altered systolic and diastolic components of flow velocity and CBGF decreased from 131 +/- 65.8 to 94 +/- 55 ml/min (-28%; p less than .01). Comparison between early postoperative values (intensive care unit) and values 6 days later showed significant increases in diameter from 4.2 +/- 0.9 to 5.3 +/- 0.9 mm (p less than .01) and in CBGF from 130 +/- 112 to 204 +/- 86 ml/min (p less than .01). We conclude that the implantable pulsed Doppler microprobe is a sensitive bedside method for monitoring aortocoronary bypass graft diameter and blood flow in the postoperative period.

Blood Flow Velocity↗
PubMed1985

[Plasma renin activity and prostaglandin E2 in hypotension induced by nicergoline].

The hypotensive actions of nicergoline, a new alpha 1-adrenoreceptor blocking agent, were studied in six dogs during stable anaesthesia under mechanical ventilation. Systemic haemodynamic parameters were measured before the infusion of nicergoline (500 micrograms X kg-1 in 5 min), and regularly after it during 2 h. Plasma renin activity (PRA), right atrial (V PGE2) and arterial (A PGE2) prostaglandin E2 concentrations measured by radio-immunoassay were collected before, and 10 and 20 min after nicergoline infusion. The mean aortic pressure fell to its lowest figure (-30%) at the 5th min, this being maintained for 45 min. Heart rate and cardiac output remained unchanged. Pulmonary wedge pressure (p less than 0.01) and central venous pressure (p less than 0.05) decreased. All parameters reached their control values in 120 min. PRA was unchanged. V PGE2 (p less than 0.01) and pulmonary extraction in PGE2 (V PGE2 - A PGE2/V PGE2) (p less than 0,05) increased whilst A PGE2 was unmodified. The fall in mean aortic pressure was linked (p less than 0.001) to the increase in V PGE2. Nicergoline infusion induced hypotension by reducing vascular tone of resistance and capacitance beds. Hypotension was related to the vasoplegia and to an inhibition of the rapid pressor control mechanisms. The reasons for the lack of renin release were unknown. V PGE2 release was stimulated by the hypotension. The increase in pulmonary extraction in PGE2 was involved in the maintenance of A PGE2 concentration. Nicergoline gave mild hypotension without reflex sympathetic activation. Its alpha-adrenoreceptor blocking properties were similar to those of prazosin.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, General↗