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Biomedical subjects

P Foëx

Publications and source records attributed to P Foëx.

At least 91 records · Page 5Linked to original sources
PubMed1991

Verapamil and nitrous oxide exert only minor effects on the normal myocardium in the presence of fentanyl.

While the association of inhalational anaesthetics and verapamil has been shown to cause myocardial dysfunction, the interactions between fentanyl, verapamil and nitrous oxide on regional function in normal hearts have not been investigated. Seven mongrel dogs were instrumented to measure aortic and left-ventricular pressure, aortic blood flow and apical and basal regional left-ventricular function (sonomicrometry). Haemodynamic values were recorded during anaesthesia with 1% halothane, fentanyl 100 micrograms kg-1 (followed by 1.5 micrograms kg-1 min-1) and then after the addition of verapamil 250 micrograms kg-1 over 30 min (followed by 60 micrograms kg-1 min-1). At each stage 67% nitrous oxide was added and recordings obtained before and during its administration. The addition of verapamil during fentanyl anaesthesia caused a moderate depression of global haemodynamics. Only little dysfunction of the apical region (9.5 +/- 2.4% post-systolic shortening) was noted. The addition of nitrous oxide caused a small amount of additional depression without significant regional dysfunction.

Anesthesia, Inhalation↗
PubMed1990

[Beta blockers and anesthesia].

Beta-adrenoceptor antagonists (BB) demonstrate a competitive antagonism with endogenous catecholamines. Beta-1 receptor blockade mediates the depressive action on contractility, heart rate and atrio-ventricular conduction. Beta-2 receptor blockade mediates vascular, bronchial and uterine smooth muscle constriction. BB with beta-1 selective and intrinsec sympathomimetic activity do not increase systemic vascular resistance. BB are mostly used to treat ischaemic heart disease, hypertension and arrhythmias. Bradycardia, hypotension and bronchospasm are the main hazards in BB treated patients undergoing anaesthesia. However giving BB with premedication to patients taking usely this treatment allows better perioperative haemodynamic stability and avoids rebound effect. Experimentally, oxprenolol reverses regional dysfunction in ischaemic myocardium under halothane anaesthesia. During and after anaesthesia, intravenous (i.v.) BB must be used with caution to treat hypertension associated with tachycardia. In controlled hypotension, i.v. BB potentialise other agents. In phaechromocytoma surgery, alpha-blocking drugs are essential but additional BB can control tachycardia successfully. In coronary artery bypass surgery, giving BB prior to induction decreases cardiac enzymes serum levels. Esmolol, a new ultra-short-acting BB, would control perioperative tachycardia and hypertension without risk of prolonged cardiac depression.

Adrenergic beta-Antagonists↗
PubMed1989

Effect of verapamil on canine left ventricular function in the presence of fentanyl when apical blood flow is critically limited.

Instruments were inserted to seven dogs under halothane anaesthesia, to measure global and regional left ventricular function. Anaesthesia was continued with fentanyl (100 micrograms kg-1 bolus, then 1.5 micrograms kg-1 min-1). Critical constriction was applied to the left anterior descending coronary artery. Control recordings were made, followed by bolus administration of verapamil 0.08, 0.16 and 0.32 mg kg-1, with recordings 10 min after each bolus. At the highest dose, verapamil decreased systemic arterial pressure, left ventricular dP/dt, stroke volume and systemic vascular resistance, and increased heart rate significantly. Coronary perfusion pressure decreased and, in the presence of critical constriction, coronary flow per beat decreased significantly. In the region with constriction, systolic shortening of myocardium decreased and post-systolic shortening increased significantly with addition of verapamil. The addition of a high dose of verapamil to fentanyl anaesthesia caused reduction in systolic function and development of early diastolic dysfunction in myocardium with critically limited blood supply.

Anesthesia, Intravenous↗
PubMed1989

Regional differences in left ventricular wall motion in the anesthetized dog.

Data regarding left ventricular function suggest that the extent of shortening may differ between regions. This study was undertaken to determine the effects of negative inotropic drugs used during anesthesia on different areas of the left ventricle. Forty mongrel dogs were anesthetized and instrumented for measurement of global and regional function. Regional function in the short axis of the basal and apical territories of the left ventricle was assessed by subendocardial sonomicrometry. Three different interventions were performed: In the first group 67% N2O, replacing 67% N2, was added to opiate anesthesia; in the second group halothane was given by stepwise increases in inspired concentration to 2%; in the third group verapamil (60 micrograms.kg-1.h-1) was infused during isoflurane anesthesia. Apical and basal segmental shortening were compared. During baseline conditions and with agents in concentrations that caused minimal myocardial depression (67% N2O or 1.0% as opposed to 0.5% halothane) differences in systolic shortening between regions were statistically significant. Further myocardial depression affected the apex significantly more than the base: when substantial myocardial depression was induced by halothane (1.5 or 2%) or verapamil, differences in regional function were abolished. Thus, the apical region of the left ventricle is more dynamic and more sensitive to negative inotropic interventions than the basal region. This should be borne in mind when segmental myocardial function is evaluated.

Anesthesia, General↗
PubMed1989

Effects of halothane on left ventricular relaxation and early diastolic coronary blood flow in the dog.

The effects of graded concentrations of halothane on left ventricular relaxation and phasic coronary blood flow (CBF) were studied in six open-chest, anesthetized dogs. Global and regional left ventricular function were measured. Besides the expected dose-dependent depression of contractility, regional shortening, and cardiac output, halothane caused significant increases in the time constant of relaxation (Trelax), and decreased and delayed the nadir of peak negative left ventricular dP/dt. Dose-dependent reductions of CBF were noted. Percentage CBF during isovolumic relaxation was significantly reduced and showed a strong inverse correlation with Trelax. Halothane appears to interfere with the inactivation process of the heart; this in turn may impede the early rise in CBF during isovolumic relaxation.

Animals↗
PubMed1988

Endocardial viability ratio and ischaemic dysfunction of the left ventricle during halothane anaesthesia.

In normal hearts, the critical value of the endocardial viability ratio (EVR) is thought to be less than 0.5. As myocardial regional dysfunction is a sensitive index of subendocardial ischaemia, the relationship between EVR and regional function has been studied in an experimental model of coronary artery constriction. In 13 dogs anaesthetized with halothane (0.5-2.0% inspired concentration), diastolic and systolic pressure time indices were obtained by planimetry, and their ratio (EVR) correlated with regional function. Halothane alone caused a significant reduction in EVR from 1.38 +/- 0.08 to 1.15 +/- 0.04 (mean +/- SEM). In the presence of coronary artery constriction a similar decrease in EVR was observed and was accompanied by post-systolic shortening (PSS), an indicator of regional dysfunction. At high concentrations of halothane, there was an inverse correlation between reduction in EVR and increase in PSS. Mean EVR of approximately 0.9 (mean = 0.92 +/- 0.02) was associated with significant worsening of regional function.

Anesthesia, Inhalation↗
PubMed1988

Effects of lignocaine and bupivacaine on regional myocardial function and coronary blood flow in anaesthetized dogs.

Empirical i.v. doses of lignocaine or bupivacaine of equal local anaesthetic potency were administered to halothane-anaesthetized dogs. Both local anaesthetics caused the expected depression of global haemodynamic function. Regional myocardial systolic shortening was depressed similarly by both agents. Regional myocardial dysfunction, seen as post-systolic shortening, occurred to a similar extent with both lignocaine and bupivacaine. Coronary blood flow and coronary perfusion pressure were significantly correlated during the administration of lignocaine; bupivacaine had erratic effects on coronary blood flow and no correlation between coronary blood flow and coronary perfusion pressure was seen. These results suggest that regional myocardial dysfunction occurs with both local anaesthetics and does not account for the apparent increased cardiotoxicity of bupivacaine. Bupivacaine did, however, cause wider individual variations compared with lignocaine with respect to coronary blood flow.

Anesthesia, General↗
PubMed1988

Isoflurane and large coronary artery haemodynamics. A study in dogs.

In the dog, stepped increases in isoflurane concentration (up to 1.5 MAC) caused peripheral and coronary vasodilatation. In the presence of significant decreases in arterial pressure (-35%), contractility (-46%), cardiac output (-17%) and coronary perfusion pressure (-40%), coronary blood flow remained unchanged, while the effective coronary vascular resistance was halved. The coronary reserve, estimated by the hyperaemic response to short periods (10 s) of coronary occlusion was reduced by the stepped increases in isoflurane concentration. Linear relationships were observed between peak hyperaemic flow, volume repayment, repayment: deficit ratio and coronary perfusion pressure. The vasodilation induced by isoflurane was of such magnitude that, at 1.5 MAC, the repayment: deficit ratio was close to unity, indicating that the vasodilatory reserve was almost exhausted.

Anesthesia, Inhalation↗
PubMed1988

Risk of myocardial ischaemia during anaesthesia in treated and untreated hypertensive patients.

Hypertensive patients were monitored for myocardial ischaemia during anaesthesia and surgery with the V5 lead of a standard electrocardiograph. Myocardial ischaemia was detected in 11 of 39 untreated hypertensive patients and in four of seven receiving therapy with a diuretic, but in none of 44 receiving atenolol. Fourteen of the atenolol-treated patients were receiving the drug on a long-term basis and the remaining 30 were treated acutely only on the morning of surgery. When myocardial ischaemia was observed, it was always associated with noxious stimulation and tachycardia, but a conspicuous increase in arterial pressure was not usually present. We conclude that myocardial ischaemia is prevalent during anaesthesia in untreated hypertensive patients, and that pretreatment with atenolol, but not diuretics, provides prophylaxis.

Anesthesia↗
PubMed1988

Myocardial ischemia in untreated hypertensive patients: effect of a single small oral dose of a beta-adrenergic blocking agent.

In a non-double-blind, prospective, randomized study, the intra-operative electrocardiograms of 128 mildly hypertensive surgical patients were examined in order to determine the incidence of myocardial ischemia during anesthesia. No patient had been receiving chronic antihypertensive therapy prior to the study, but a single small oral dose of a beta-adrenergic blocking agent (labetalol, atenolol, or oxprenolol) was given to 89 of them along with premedication. Forty-four per cent of the untreated control patients and 61% of the patients pretreated with a beta-adrenergic blocking agent had normal preoperative electrocardiograms and no risk factors for coronary artery disease other than hypertension (this difference between groups was not statistically significant). During tracheal intubation and/or emergence from anesthesia, a brief, self-limited episode of myocardial ischemia was detected in 11 of 39 untreated control patients, and in two of 89 patients pretreated with a beta-adrenergic blocking agent (P less than 0.001). Tachycardia always accompanied the ischemic events, but a conspicuous increase in blood pressure did not. The authors conclude that mild hypertension, when untreated prior to the induction of anesthesia, is associated with a high incidence of myocardial ischemia; and that a single small oral dose of a beta-adrenergic blocking agent, given with pre-medication, can significantly reduce that risk.

Administration, Oral↗
PubMed1988

Intravenous diltiazem worsens regional function in compromised myocardium.

The effect of intravenous diltiazem on regional myocardial function was assessed in a canine model of critical constriction of the left anterior descending coronary artery (LAD). Maintenance anesthesia with fentanyl (1.5 micrograms.kg-1.min-1), 60% inspired nitrous oxide, and 0.7% inspired halothane resulted in regional dysfunction, measured as postsystolic shortening (20.6 +/- 10.7%), which was significantly worsened after 0.1 mg/kg (48.7 +/- 12.5%, P less than 0.05) and after 0.2 mg/kg (68.8 +/- 11.7%, P less than 0.05) intravenous diltiazem. Systolic shortening in the compromised LAD territory was substantially depressed after 0.1 mg/kg diltiazem (8.2 +/- 0.6% to 5.3 +/- 1.3%, P less than 0.05) and was essentially abolished after 0.2 mg/kg diltiazem (8.2 +/- 0.6% to 0.7 +/- 2.3%, P less than 0.05). At the higher dose of diltiazem, cardiac output was substantially decreased (1.37 +/- 0.23 L/min to 0.88 +/- 0.30 L/min, P less than 0.05) and LV dP/dtmax significantly depressed (1090 +/- 90 mm Hg/sec to 744 +/- 80 mm Hg/sec, P less than 0.05). These results demonstrate significant depression of regional systolic shortening and substantial worsening of regional dysfunction in myocardium with a compromised blood supply, in association with significant depression of left ventricular performance, with intravenous diltiazem administration during anesthesia.

Anesthesia, Inhalation↗
PubMed1988

Gradual or abrupt nitrous oxide administration in a canine model of critical coronary stenosis induces regional myocardial dysfunction that is worsened by halothane.

The existence of a dose-response relation between nitrous oxide concentration and regional dysfunction in compromised myocardium, and whether or not halothane-induced myocardial depression alleviated this regional dysfunction was examined. Nitrous oxide was administered to eight dogs with experimentally induced left anterior descending coronary artery (LAD) critical stenosis during fentanyl (100 micrograms/kg bolus plus 1.5 micrograms.kg-1.min-1) anesthesia. Two modes of nitrous oxide administration were employed: gradual (in steps of 20% inspired, i.e., 0%, 20%, 40%, and 60% inspired) and abrupt (0-60% inspired). Regional myocardial function was assessed by sonomicrometry. Regional dysfunction in the compromised myocardium, in the form of postsystolic shortening (PSS), increased above baseline levels during 40% (4.2 +/- 2.3% to 12.1 +/- 3.9%, P less than 0.05) and 60% (4.2 +/- 2.3% to 12.5 +/- 3.6%, P less than 0.05) inspired nitrous oxide (gradual administration) and also during abrupt 60% nitrous oxide administration (6.4 +/- 2.6% to 9.9 +/- 3.2%, P less than 0.05). After abrupt 60% inspired nitrous oxide administration, halothane (0.7% inspired) was introduced and caused decreases in mean arterial pressure (106.1 +/- 4.5 mm Hg to 76.2 +/- 5.5 mm Hg, P less than 0.05) and peak LV dP/dt (1700 +/- 150 mm Hg/sec to 1100 +/- 100 mm Hg/sec, P less than 0.05). Halothane caused a marked increase in PSS (9.9 +/- 3.2% to 30.8 +/- 12.6%, P less than 0.05). Thus nitrous oxide administration caused regional dysfunction in myocardium supplied by a critically narrowed LAD whether administered gradually or abruptly and at concentrations as low as 40% inspired.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Differences in ischaemic dysfunction after gradual and abrupt coronary occlusion: effects on isovolumic relaxation.

The effects of both gradual and abrupt coronary occlusion on regional wall function (sonomicrometry) and left ventricular relaxation were studied in the intact dog heart. The ischaemic dysfunction observed in the two interventions as assessed by pressure-length loops showed considerably different patterns. The regional ischaemia after abrupt occlusion of the left anterior descending coronary artery was characterised by a bulge during isovolumic relaxation in contrast to the pattern observed during gradual occlusion, which was characterised chiefly by early systolic lengthening and post-systolic shortening. The effect of regional dysfunction on left ventricular relaxation was evaluated using peak negative dP/dt and tau, the time constant of isovolumic pressure decline. Abrupt occlusion had a more profound effect on relaxation than did gradual occlusion, though there were no significant changes in either pressure or flow derived indices of systolic ventricular function with abrupt occlusion of the left anterior descending artery. Two distinct patterns of regional dysfunction were produced at zero coronary flow depending on the time course of the occlusion. The regional dysfunction observed during abrupt occlusion may in part be explained by the mechanical effect of abrupt cessation of coronary flow, which in turn influences relaxation. With gradual occlusion tau was less affected even though substantial regional dysfunction was observed. This may reflect the development of collateral flow. Thus the patterns of regional dysfunction and ventricular relaxation depend on the time course of ischaemia.

Animals↗
PubMed1987

Isoflurane causes regional myocardial dysfunction in dogs with critical coronary artery stenoses.

The effects of isoflurane-induced hypotension to mean aortic pressures of 70 and 55 mmHg on global and regional right and left ventricular performance (ultrasonic dimension technique) and on coronary hemodynamics (electromagnetic flow probes) were studied in 12 open-chest dogs (anesthetized and paralyzed by continuous infusions of fentanyl and pancuronium) with critical coronary artery stenoses (micrometer-controlled snares) of the right and left anterior descending coronary arteries. The stenoses reduced resting coronary blood flow by approximately 10% without affecting global or regional myocardial performance. During subsequent isoflurane administration, coronary blood flow fell markedly. In the areas supplied by the stenosed coronary arteries, segment length shortening decreased by 70% (P less than 0.01), and regional akinesis, paradoxical motion, or postsystolic shortening developed in 9 of 12 animals. In contrast, in the areas supplied by normal coronary arteries, myocardial segment length shortening decreased significantly less and did not show signs of dysfunction. In these non-ischemic areas at both concentrations of isoflurane, end diastolic and systolic dimensions were greater in the right than in the left ventricle, probably related to differences in right (unchanged) and left (reduced) ventricular afterloads. The data indicate that in the presence of coronary artery stenoses, isoflurane-induced hypotension may cause regional myocardial dysfunction suggestive of ischemia.

Animals↗
PubMed1987

The association isoflurane-verapamil causes regional left-ventricular dyssynchrony in the dog.

In ten dogs anesthetized with 1% inspired isoflurane, the effect of low-dose verapamil on global and regional myocardial function was studied. The administration of verapamil resulted in no change in heart rate or blood pressure, but left ventricular stroke work, peak power, LV dP/dt max, and aortic blood acceleration were significantly reduced, while coronary blood flow remained unchanged. End-diastolic length increased in territory supplied by both left anterior descending (LAD) and left circumflex (LC) artery, but a significant decrease in systolic shortening occurred in the LAD segment only. Dyssynchrony of wall motion, characterized by post-systolic shortening, accompanied in three animals by a small amount of systolic lengthening, appeared with the administration of verapamil and was more pronounced in the LAD segment. Such patterns of wall motion have usually been attributed to myocardial ischemia. In the absence of significant reduction in coronary blood flow, and in the presence of a delay in onset of shortening and lengthening, these patterns of wall motion are more likely to reflect dyssynchrony of regional function than ischemia.

Anesthesia, Inhalation↗