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Biomedical subjects

J M Bernard

Publications and source records attributed to J M Bernard.

At least 55 records · Page 3Linked to original sources
PubMed1991

Effects of enflurane and isoflurane on hepatic and renal circulations in chronically instrumented dogs.

Seven dogs were chronically instrumented for measurements of mean aortic blood pressure and cardiac output and for simultaneous measurements of hepatic, portal, and renal blood flows. Each animal was studied on two separate occasions, awake and during 1.2, 1.4, 1.75, and 2.0 MAC isoflurane and enflurane. Both anesthetics induced tachycardia; to a greater degree than isoflurane, enflurane lowered mean aortic blood pressure in a dose-dependent manner (-37, -45, -48, and -62% vs. -19, -25, -41, and -44%, respectively) and cardiac output (-20, -26, -41, and -48% vs. -3, -5, -11, and -15%, respectively). With isoflurane, cardiac output decreased only at 1.75 and 2.0 MAC, and portal blood flow did not change significantly, whereas hepatic arterial blood flow increased at 1.75 and 2 MAC (by 28 and 33%, respectively). With enflurane, no significant changes were recorded in hepatic arterial blood flow, whereas portal blood flow decreased in a dose-dependent manner. Except at 2 MAC, hepatic circulation did not differ between anesthetics. Likewise, neither anesthetic significantly changed renal blood flow, except for enflurane at 2.0 MAC, which was associated with a 35% reduction. Both anesthetics led to similar systemic, hepatic, and renal vasodilations. Our data suggest that high concentrations of enflurane are associated with decreases in portal, total hepatic, and renal blood flows, most likely as a result of an anesthetic-induced cardiac depression.

Animals↗
PubMed1991

Comparison of the effects of isoflurane and desflurane on cardiovascular dynamics and regional blood flow in the chronically instrumented dog.

Seven mongrel dogs were chronically instrumented for the measurement of aortic and left ventricular blood pressures, cardiac output, left ventricular wall thickening, left ventricular dP/dt, and circumflex coronary, renal, hepatic and portal blood flows under the influence of desflurane (D) and isoflurane (I). Administration of the two anesthetics, was randomized, as was the order of the concentrations administered. Each dog was studied awake and at 1.2, 1.4, 1.75, and 2.0 MAC of each anesthetic on different days. Both anesthetics decreased mean arterial pressure, stroke volume, systemic vascular resistance, left ventricular dP/dt, and wall thickness. The decreases were dose-dependent for mean arterial pressure (percent of awake values: D 78, I 85 at 1.2 MAC, and D 67, I 69 at 2.0 MAC); stroke volume (D 66, I 72 at 1.2 MAC, and D 52, I 57 at 2.0 MAC); dP/dt (D 61, I 64 at 1.2 MAC, and D 46, I 49 at 2.0 MAC); and WT (D 68, I 70 at 1.2 MAC, and D 47, I 60 at 2.0 MAC). Systemic vascular resistance decreased approximately the same at 1.2 MAC (D 71, I 87%) as at 2.0 MAC (D 71, I 79%). Heart rate increased but also not in a dose-dependent fashion (percent of awake values: D 177, I 145 at 1.2 MAC, and D 176, I 155 at 2.0 MAC). Coronary blood flow was increased by both anesthetics at all concentrations (percent of awake values: I 136 at 1.2 MAC and 161 at 2.0 MAC of awake, and D 131 at 1.2 MAC and 138 at 2.0 MAC.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Postoperative analgesia by intravenous clonidine.

Clonidine, an alpha 2 adrenoreceptor agonist, has nonopiate antinociceptive properties, which might be an alternative for postoperative analgesia free of opioid-induced side effects. To document the analgesic properties of intravenous clonidine during the postoperative period, 50 ASA physical status 1 patients, immediately after spinal fusion, were randomly assigned to two groups, blindly administered either clonidine (5 micrograms/kg infused the 1st h and then 0.3 microgram-1.kg-1.h-1 during 11 h) or a placebo. A visual analog scale graded from 0 (no pain) to 100 mm was used to assess pain before clonidine or placebo administration (T0), at the end of the loading dose (T1) and then every 2 h (T3, T5, T7, T9, and T11). Morphine (0.1 mg/kg) was administered intramuscularly after each pain measurement if the score was greater than 50 mm. No morphine was given at T0. Hemodynamics, blood gases and plasma clonidine concentrations were measured each time the pain score was measured. The pain score decreased from 42 +/- 5 to 26 +/- 3 mm (mean +/- standard error) in the clonidine group whereas it was unchanged in the placebo group despite a greater morphine requirement (dose for each patient: 3.8 +/- 1 vs. 10.8 +/- 1.2 mg). Clonidine delayed the onset of pain and the first request for morphine injection. Mean arterial pressure decreased to 74 +/- 2 mmHg in the clonidine group (-26 +/- 2 vs. -15 +/- 2% in the placebo group at T11) despite a significant increase in the cumulative fluid volume.(ABSTRACT TRUNCATED AT 250 WORDS)

Clonidine↗
PubMed1991

Effects of oral clonidine premedication and postoperative i.v. infusion on haemodynamic and adrenergic responses during recovery from anaesthesia.

The effects of clonidine, a central alpha 2-adrenoreceptor agonist, on haemodynamic and catecholamine changes were assessed during emergence from anaesthesia, a period which is associated with increased sympathetic nervous discharge, hypertension and tachycardia. According to a double-blind randomized design, 32 patients received either clonidine, preoperatively given by oral route (3.5 micrograms.kg-1) and postoperatively by i.v. infusion (0.3 microgram.kg-1.h-1), or a placebo. Perioperative management was similar in both groups. Measurements were made in the recovery room, before starting clonidine or placebo infusions for evaluation of clonidine premedication, and then during infusion as follows: when core temperature reached 37 degrees C; then 2 h, and 6 h later. Prior to starting infusions, mean blood pressure (88 +/- 15 vs 103 +/- 14 mmHg) (11.7 +/- 2.0 vs 13.7 +/- 1.9 kPa), heart rate (67 +/- 8 vs 87 +/- 17 beats.min-1) and plasma norepinephrine levels (462 +/- 393 vs 615 +/- 361 pg.ml-1) were lower in the clonidine group. Only at the latest measurement (6 h after core temperature reached 37 degrees C) did clonidine elicit significant effects. The values during clonidine infusion compared to placebo were at this time: mean blood pressure (73 +/- 10 vs 86 +/- 13 mmHg) (9.7 +/- 1.3 vs 11.5 +/- 1.7 kPa), heart rate (71 +/- 6 vs 93 +/- 13 beats.min-1) and plasma norepinephrine levels (240 +/- 224 vs 451 +/- 111 pg.ml-1). Our results suggest that: 1) preoperative clonidine may improve the haemodynamic profile associated with anaesthetic discontinuation, but 2) i.v. infusion (0.3 microgram.kg-1.h-1) did not prolong this effect during the early postoperative period in the face of the sympathetic nervous discharge of recovery.

Administration, Oral↗
PubMed1991

Deliberate hypotension with nicardipine or nitroprusside during total hip arthroplasty.

To induce deliberate hypotension during anesthesia, nicardipine was administered to patients undergoing total hip arthroplasty and was randomly compared with nitroprusside. Hemodynamic measurements were performed before and 10, 20, 30, and 60 min after starting to administer either nicardipine (n = 12) or nitroprusside (n = 12) (B, T1, T2, T3, and T4, respectively); at the end of drug infusion (T5); and 10, 20, and 60 min later (T6, T7, and T8, respectively). Plasma renin activity and catecholamine levels were measured at B, T1, T5, T6, and T7. In addition, plasma nicardipine concentration was measured in five patients at T1, T2, T5, T7, and T8. As with nitroprusside, nicardipine administration (1-3 micrograms.kg-1.min-1, after a titration dose of 4.7 +/- 1.5 mg) resulted in hypotension (up to -34% +/- 3%), a decrease in systemic vascular resistances (up to -49% +/- 4%), and increases in heart rate (up to +17% +/- 6%), cardiac index (up to +37% +/- 8%), plasma norepinephrine (up to +63% +/- 17%) and epinephrine (up to +232% +/- 68%) levels, and plasma renin activity (up to +336% +/- 207%). Ten and 20 minutes after discontinuation of the hypotensive drug, nicardipine led to persistent vasodilation and hypotension, which differed significantly from the hypertensive rebound observed after nitroprusside discontinuation, despite a similar increase in plasma renin activity and catecholamine levels. Our results indicate that after the infusion was terminated, the nicardipine-induced vasodilation was opposed to the vasoconstrictive effects of angiotensin II and catecholamines, thus avoiding hypertensive rebound.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1990

Effects of sevoflurane and isoflurane on cardiac and coronary dynamics in chronically instrumented dogs.

To assess the hemodynamic properties of the new inhalational anesthetic sevoflurane, 22 dogs were chronically instrumented for measurement of heart rate, aortic, left ventricular and left atrial pressures, cardiac output, and coronary blood flow. Dogs were randomly assigned to two groups, receiving either 1.2 and 2 MAC of sevoflurane (n = 11) or isoflurane (n = 11). At 1.2 and 2 MAC, sevoflurane produced an increase in heart rate (+60 +/- 12% and +54 +/- 9%, respectively), dose-dependent aortic hypotension (-22 +/- 4% and -38 +/- 4%, respectively), systemic vasodilation (-22 +/- 5% and -19 +/- 5%, respectively), dose-dependent decrease in stroke volume (-31 +/- 6% and -48 +/- 4%, respectively), and left ventricular dP/dt (-40 +/- 4% and -61 +/- 10%, respectively). Cardiac output decreased only at 2 MAC (-17 +/- 6%). Finally, coronary blood flow increased at 1.2 MAC of sevoflurane (+29 +/- 8%). Except for heart rate, sevoflurane and isoflurane produced similar effects. At 1.2 MAC, sevoflurane produced a greater increase in heart rate than isoflurane (+60 +/- 12% vs. +33 +/- 9%). The authors conclude that, except for heart rate, the effects of sevoflurane on cardiac function and coronary blood flow are almost identical to those induced by isoflurane in the chronically instrumented dog.

Anesthetics↗
PubMed1989

[Baroreflex activity in carotid endarterectomy during general anesthesia].

The baroreceptor reflex was studied in eleven patients, aged 69 +/- 6 years, scheduled for carotid endarterectomy under general anaesthesia. Nine were hypertensive. The anaesthetic protocol was the same for all the patients: premedication with morphine and scopolamine, induction with 5 mg.kg-1 thiopentone, 6 micrograms.kg-1 fentanyl and 0.01 mg.kg-1 pancuronium bromide. All the patients were intubated and ventilated with a mixture of nitrous oxide and oxygen. Fentanyl, 100 micrograms, was routinely given at the time of incision. Baroreflex sensitivity was tested using Smyth's method, with a bolus of 75 micrograms trinitrin and plotting changes in heart rate against those in systolic blood pressure. Electrocardiogram, invasive arterial blood pressure and airway pressure were simultaneously recorded. PaCO2 and PaO2 were measured during arterial clamping. The tests were carried out before clamping, 2 min later and 10 to 20 min after the last injection of fentanyl. In the seven patients for whom clamping lasted more than 15 min, a further test was carried out after administration of 0.4 +/- 0.05 vol% halothane (Datex analyser) for 5 min. During anaesthesia, baroreflex sensitivity was low (1.8 +/- 0.3 ms.mmHg-1). After clamping, there was only a significant change in Pasys, with no changes in heart rate or blood gas values (129 +/- 8 mmHg before clamping; 167 +/- 12 mmHg after clamping; n = 8; p less than 0.01). After halothane administration, the sensitivity slope decreased, but not significantly. Moreover, halothane decreased the R-R intervals (1140 +/- 84 after clamping; 963 +/- 76 under halothane; n = 6; p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1989

Hypotensive anesthesia with isoflurane and enflurane during total hip replacement: a comparative study of catecholamine and renin angiotensin responses.

Catecholamine and renin-angiotensin responses to enflurane- or isoflurane-hypotensive anesthesia were compared in a randomized study. Two groups of 10 patients undergoing total hip arthroplasty were premedicated with morphine hydrochloride (0.1 mg/kg). Anesthesia was induced with thiopental and the trachea intubated after pancuronium. Equal concentrations of each volatile agent (1.3 MAC) were administered until mean arterial blood pressure decreased to 50-60 mm Hg. Hemodynamic data and blood samples for measurements of plasma renin activity (PRA) and plasma epinephrine (E) and norepinephrine (NE) concentrations were collected 1) after induction and intubation but before the start of isoflurane or enflurane; 2) 15 min (T15) after the start of isoflurane or enflurane administration; and 3) 45 min (T45) after the start of isoflurane or enflurane administration. The desired level of hypotension was achieved at T15 with isoflurane and at T45 with both anesthetics. When hypotension was achieved, cardiac index and stroke index were significantly lower in the enflurane group while systemic vascular resistance index was lower in the isoflurane group. Increases in E and NE levels above baseline levels were significantly greater in the isoflurane group than in the enflurane group. Use of isoflurane to induce hypotension is associated with more rapid induction of hypotension, less depression of cardiac output, and better preservation of homeostatic responses than is use of enflurane.

Enflurane↗
PubMed1988

Effects of systemic morphine and epidural bupivacaine on postoperative oxygen consumption during rewarming.

The alterations in hemodynamics and oxygen consumption as a consequence of continuous epidural infusions of bupivacaine at room temperature and conventionally administered morphine were studied during recovery from general anesthesia for total hip replacement. Twenty-four patients were randomized to receive either bupivacaine or morphine in the recovery room. The bupivacaine group received from 6 to 12 ml per hour of 0.25% bupivacaine epidurally. Patients in the morphine group received 0.1 mg/kg of morphine intramuscularly no more frequently than every 4 hours. A pulmonary artery flotation catheter was inserted into each patient to determine hemodynamics and oxygen consumption at three instances: before analgesia, when pulmonary artery blood temperature reached 36 degrees C, and when it reached 37 degrees C. During the rewarming there was a decrease in mean arterial blood pressure and the systemic vascular resistance index and an increase in heart rate. The whole body oxygen consumption index increased in the bupivacaine group at the last measuring point but was stable in the morphine group. There was no effect on the arterial-venous oxygen content difference in either group. At 37 degrees C, the cardiac index and oxygen consumption index were significantly higher in the bupivacaine group than in the morphine group. In contrast to regional analgesia, systemic morphine administration can partially antagonize cardiovascular response to postoperative rewarming because it induces a stable oxygen demand.

Aged↗
PubMed1988

[Can isoflurane be advised for controlled hypotension?].

Since 1983, many papers tell of the usefulness of isoflurane for induced hypotension. It can induce and maintain stable arterial hypotension during neurosurgery, or any other surgical procedure requiring induced hypotension. Its use has proved to be simple. Although other hypotensive techniques are possible, especially if only moderate hypotension is required, the mechanism of action of isoflurane is very appealing: it reduces arterial pressure by reducing the peripheral resistances, without reducing the output, unlike halothane or trinitrin. Moreover, as it is anaesthetic, it reduces the overall oxygen consumption, such that if there were a fall in output one could assume that it was related to the level of oxygen consumption. When there is no severe hypocapnia, isoflurane, quite unlike sodium nitroprusside, lowers cerebral oxygen consumption without affecting cerebral blood flow rate. It does however increase intracranial pressure, like all the other hypotensive agents used. It does not increase filling pressures and has no effect on blood gas movements, unlike sodium nitroprusside and trinitrin which increase filling pressures and the intrapulmonary shunt. It is not toxic either, unlike sodium nitroprusside. The expensiveness of the drug is balanced by its many advantages, all the more so as this cost can be reduced by using a filter-system for some cases (e.g. middle ear surgery), or by using some drug combinations which need yet to be defined. However, there exist some disadvantages which may, in fact, be due to experimental conditions: failure of induced hypotension, coronary ischaemia, doubtful cerebral protection in case of focal areas of ischemia, different degrees of organ vasodilation.(ABSTRACT TRUNCATED AT 250 WORDS)

Cerebrovascular Circulation↗
PubMed1988

Pharmacokinetics and haemodynamic effects of prolonged methohexitone infusion.

1. The use of continuous infusion anaesthesia has only been of interest since the development of short-acting, less cumulative and less toxic drugs. 2. This study aimed to compare pharmacokinetics and haemodynamic effects during and after long time methohexitone constant rate infusion. Sixteen patients were given either 60 or 90 micrograms kg-1 min-1 methohexitone during 14 h. Blood samples were taken hourly during this time and 12 h following the end of infusion. 3. Infusion period was analysed by a single exponential model; post-infusion time showed a three compartment model, the intermediate phase parameters corresponding to those of the infusion period. 4. Methohexitone was haemodynamically well tolerated; prolonged infusion decreases oxygen consumption, mainly by a decrease in oxygen demand. 5. Many patients remained unconscious for unacceptably long periods of time after post-operative sedation by methohexitone.

Hemodynamics↗
PubMed1988

Impact of surgical stress on the haemodynamic profile of isoflurane-induced hypotension.

It has been suggested that stimulation of adrenoreceptors could be responsible for some of the haemodynamic effects of isoflurane. But there are no solid data demonstrating the role of sympatho-adrenal stimulation induced by pain during isoflurane administration. The impact of surgical stress on the haemodynamic profile of isoflurane-induced hypotension has been investigated in 28 patients (47-76 years), scheduled for total hip arthroplasty. After premedication with morphine hydrochloride (0.1 mg/kg), patients were randomly assigned to receive either no fentanyl (control group) or fentanyl (5 micrograms/kg before tracheal intubation, 5 micrograms/kg before skin incision, and 2 micrograms/kg each 15 min during the 1st hour). Isoflurane was given to maintain mean arterial blood pressure in the range 6.7-8 kPa in both groups. Haemodynamic data and blood samples for determination of plasma renin activity (PRA) and epinephrine (E) and norepinephrine (NE) levels were collected before and during hypotension. The fentanyl group and the control group differed significantly during hypotension: heart rate, cardiac index, oxygen consumption and E, NE and PRA were lower (P less than 0.01) in the fentanyl group than in control group. Fentanyl lowered the required concentration of isoflurane to achieve the same degree of hypotension (end-tidal concentration: 0.8 +/- 0.2% in the fentanyl group and 1.4 +/- 0.15% in the control group; P less than 0.001). Our results demonstrate that the cardiovascular effects of higher isoflurane concentrations in the absence of narcotic analgesia are counterbalanced by adrenergic stress stimulation of released epinephrine and norepinephrine. Among the likely reasons for catecholamine release during isoflurane administration, inadequate analgesia may be considered.

Aged↗