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Biomedical subjects

B A Henriksson

Publications and source records attributed to B A Henriksson.

At least 37 records · Page 2Linked to original sources
PubMed1990

Metabolic gas exchange during nitrous oxide anaesthesia with controlled ventilation.

A system for metabolic gas exchange has been used during nitrous oxide-opioid anaesthesia incorporating a Servo Ventilator 900 C and external analysers for oxygen and carbon dioxide. Oxygen consumption and carbon dioxide excretion were calculated as differences in content between inspired and expired minute ventilation. Nitrous oxide uptake was calculated similarly, assuming it was the only other gas present in addition to oxygen and carbon dioxide. The mean value for oxygen consumption was 3.25 ml kg-1 min-1, declining by 8% during the 2 h of anaesthesia. The formula for the best fit curve of nitrous oxide uptake was 18.3 . t-0.48 ml kg-1 min-1 when FIN2O was 0.7. To simplify measurement procedures and avoid measurements of expiratory volume, we also calculated metabolic gas exchange when expiratory minute ventilation was expressed as a function of inspiratory minute volume and nitrous oxide uptake. The latter value was obtained from the overall best fit curve for nitrous oxide uptake.

Adult↗
PubMed1989

Effects of isoflurane on feline intestinal blood flow during hemorrhage-induced hypovolemia.

The influence of isoflurane on intestinal reflex vasoconstriction during hemorrhage was investigated in cats (n = 10) during basal chloralose-nitrous oxide anesthesia. Intestinal blood flow (IBF) was studied in a model with controllable intestinal perfusion pressures to exclude local myogenic vascular responses related to changes in intraluminal pressure. A jejunal segment, which was dissected free in situ, was perfused via an extracorporeal arterial circuit which included a roller pump and a variable arterio-venous shunt. Intestinal perfusion pressure was controlled by adjusting the shunt flow. IBF was measured (optical drop-recording) before and after hemorrhage (8% of estimated blood volume). The protocol included steady-state recordings at defined perfusion pressures (50, 75, 100, 125 and 150 mmHg in a randomized order; 6.7, 10.0, 13.3, 16.7 and 20.0 kPa, respectively) with and without the addition of 0.7% (MAC 1.0) isoflurane. IBF levels were consistently higher during isoflurane anesthesia than during basal chloralose anesthesia in the perfusion pressure range 75-150 mmHg (10.0-20.0 kPa). During basal anesthesia, a hemorrhage-induced decrease in IBF was demonstrated throughout the perfusion pressure range 50 to 150 mmHg (6.7-20.0 kPa). The magnitude of the hemorrhage-induced decrease in IBF was not significantly influenced by the addition of isoflurane. Thus, IBF, following hemorrhage, was significantly higher during isoflurane anesthesia than during basal chloralose anesthesia at perfusion pressures 50, 100, 125 and 150 mmHg (6.7, 13.3, 16.7 and 20.0 kPa).

Anesthesia, Inhalation↗
PubMed1989

Whole body gas exchange: amino acid and lactate clearance as indicators of initial and early allograft viability in liver transplantation.

A method for the rapid assessment of liver allograft circulation and function after liver transplantation is described. In 12 patients undergoing liver transplantation continuous recording of whole body energy production was made on the basis of gas exchange measurements during the surgical procedure. Oxygen consumption decreased rapidly by 25% when the blood supply to the native liver was interrupted. After the anhepatic period, there was a sharp increase of oxygen consumption with successful reperfusion of the allograft. Carbon dioxide production fell by 14% and returned to preanhepatic values after successful declamping. In two cases with suboptimal reperfusion the return of gas exchange values was slow and incomplete. Results from the studies of whole body energy production were compared with biochemical measurements. No significant accumulation of amino acids occurred during the anhepatic period, but in the two patients with incomplete revascularization, clearance of amino acids, after the anhepatic phase, was impaired and plasma amino acids accumulated. The same pattern was found for plasma lactate levels. By the techniques described in this article, rapid and reliable assessment of initial and early graft function in hepatic transplantation is possible. This is of great value for the intraoperative and early postoperative assessment and planning of surgical and anesthesiologic strategies.

Adolescent↗
PubMed1988

Effects of halothane, enflurane, and isoflurane on coronary vascular tone, myocardial performance, and oxygen consumption during controlled changes in aortic and left atrial pressure. Studies on isolated working rat hearts in vitro.

The effects of equi-anesthetic concentrations of halothane (HAL, n = 11), enflurane (ENF, n = 11) and isoflurane (ISO, n = 10) on cardiac function were studied and compared with a control group (n = 12) in isolated paced rat hearts by means of an antegrade heart perfusion technique. Left atrial pressure (LAP) and mean aortic pressure (MAP) could be altered independently of each other, and aortic flow, coronary flow (CF), and po2 in venous coronary effluent were continuously recorded. Stroke volume (SV), myocardial oxygen consumption (MVO2), and myocardial oxygen extraction were calculated: 1) MAP was altered from 60 to 120 mmHg at a constant LAP (7.5 mmHg), and 2) LAP was varied from 4 to 12.5 mmHg at a constant MAP (80 mmHg). Left ventricular function curves (LVFC) were constructed and the maximal SV (SVmax) was obtained. The LAP needed to perform 75% of the maximal SV (LAP0.75) was estimated to assess the effect of the anesthetics on diastolic function. HAL ENF and ISO decreased SVmax significantly compared to control. This decrease was more pronounced for HAL (41%) compared to both ENF (26%) and ISO (26%). Accordingly, SV, at various levels of MAP, at a constant LAP, was significantly lower for HAL than for both ENF and ISO, while there was no significant difference between the latter two. None of the anesthetics shifted the LVFC to the right, i.e., did not affect diastolic properties. HAL induced the most pronounced decrease in MVO2, while there was no significant difference between ENF and ISO in this respect. Coronary flow (CF), at controlled perfusion pressures, decreased significantly with HAL but not with ENF or ISO compared to control. CF was significantly higher with ISO compared to both ENF and HAL. HAL and ISO, but not ENF, decreased myocardial oxygen extraction significantly compared to control and, thus, increased the myocardial oxygen supply-to-demand ratio.

Animals↗
PubMed1987

Propofol vs thiopentone as anaesthetic agents for short operative procedures.

In a randomized open study, 120 healthy female patients were included. For short gynaecological procedures they were anaesthetized with either propofol 2.5 mg X kg-1 (n = 60) or thiopentone 5 mg X kg-1 (n = 60) in combination with nitrous oxide/oxygen (67%/33%). Supplementary doses of propofol (10-20 mg) or thiopentone (25-50 mg) were given when necessary during the procedure. Induction characteristics for propofol and thiopentone 1 min after start of induction were similar. Propofol seemed to have a more depressant effect than thiopentone on the circulatory response to anaesthesia. Recovery times from the end of the operative procedure until the patients opened their eyes on command and were orientated were shorter in the propofol patients compared to the thiopentone patients. In the propofol group, patients recalled discomfort on injection more often than patients anaesthetized with thiopentone. Otherwise, the side-effects were similar in both groups. We conclude that propofol is similar to thiopentone in its anaesthetic qualities during induction and maintenance of short anaesthetic procedures. Propofol was associated with a more rapid emergence from anaesthesia than thiopentone.

Anesthesia, Intravenous↗
PubMed1985

Cardiovascular studies during controlled baroreflex activation in the dog: I. Effects of enflurane.

In chloralose-anaesthetized dogs the carotid sinuses were bilaterally perfused with blood from a femoral artery, either at systemic arterial pressure through a direct by-pass or with a pump in order to control the sinus pressure. Influences from cardiac receptors and aortic baroreceptors were eliminated by denervation. Administration of enflurane (1.6% end-tidal concentration) with the presence of barostatic modulation, i.e. the carotid sinuses were perfused at prevailing systemic arterial pressure, reduced cardiac performance (cardiac output, cardiac contractility, heart rate and left ventricular stroke work) and mean arterial pressure. When barostatic compensation of enflurane-induced circulatory changes was prevented by maintaining sinus perfusion pressure constant at the pre-enflurane level, these haemodynamic alterations, with the exception of cardiac output, were significantly more pronounced. Furthermore, systemic vascular resistance decreased. We conclude that barostatic reflexes significantly modify cardiovascular depressive effects of enflurane.

Animals↗
PubMed1985

Cardiovascular studies during controlled baroreflex activation in the dog: II. Effects of metoprolol and enflurane.

An experimental model was designed to study circulatory drug effects with or without barostatic reflex influences. In dogs anaesthetized with chloralose, both carotid sinuses were perfused from a femoral by-pass either with systemic arterial pressure or with a pump in order to control the sinus pressure. Cardiac and aortic baroreceptors were denervated. I.v. metoprolol (240 micrograms X kg-1 + 102 micrograms X kg-1 X h-1) with constant carotid sinus pressure and thereby constant baroreceptor activation reduced cardiac output, heart rate, cardiac contractility and left ventricular stroke work index. Systemic vascular resistance increased. This response was independent of the degree of baroreflex activation. During the combined administration of enflurane (1.6% end-tidal concentration) and metoprolol, cardiac performance (cardiac output, stroke volume, heart rate, cardiac contractility and left ventricular stroke work index) was depressed independent of the degree of baroreflex activation. Barostatic reflexes, however, counteracted an observed decrease in systemic vascular resistance. This reflex vascular response was, during metoprolol-enflurane administration, associated with an increased left ventricular end-diastolic pressure.

Animals↗
PubMed1985

Vasodilator responses to enflurane in the small intestine.

Local effects of enflurane on intestinal vascular resistance were studied in vivo in cats. A jejunal segment was prepared and perfused at constant flow with blood from the femoral arteries. The intestine was either: (1) left with intact sympathetic innervation, (2) denervated and exposed to electrical post-ganglionic vasoconstrictor nerve stimulation, or (3) excluded from neurogenic remote control by post-ganglionic denervation. Enflurane dissolved in lipid and intra-arterially administered to the jejunal segment in doses comparable to those clinically encountered, decreased intestinal vascular resistance in relation to the intra-arterial concentration of the drug. The vasodilator response was, at the highest enflurane doses studied (blood concentration: 400 and 800 mg X 1(-1], most pronounced in the intestine with intact sympathetic innervation. Otherwise, no differences were observed in vasodilator responses between the three different investigated modes of neurogenic influence on the intestine. In vitro enflurane (-in-lipid) did not affect the vasoconstrictor response to electrical field stimulation in the rat mesenteric arterioles. Enflurane, however, dose-dependently reduced spontaneous contractile activity in the rat portal veins.

Animals↗
PubMed1985

Intestinal vascular effects of inhaled and locally administered enflurane in the cat.

The effects of enflurane on intestinal vascular resistance and blood flow in the intestine were studied in cats during basal chloralose anaesthesia. A jejunal segment was prepared and perfused with blood from both femoral arteries, allowing control of intestinal inflow pressure. Mesenteric venous blood flow was measured with an optical drop recorder. During constant intestinal arterial pressure (75 mmHg; 10 kPa), intestinal vascular resistance was calculated during enflurane inhalation at MAC 0.5 and 1.0 before and after postganglionic denervation of the jejunal segment. Inhalation of enflurane reduced intestinal vascular resistance in a dose-dependent fashion. The decrease in vascular resistance was attenuated but not abolished by post-ganglionic denervation, indicating both peripheral and central nervous sites of action for enflurane. Furthermore, with the intestinal segment perfused at systemic arterial pressure, the effects of locally intraarterially infused enflurane dissolved in a fat emulsion was studied. A vasodilator response was elicited in the intestine when exposed to local arterial enflurane concentrations in the same range as encountered during surgical anaesthesia in man, supporting the hypothesis of a peripheral site of action.

Anesthesia, Inhalation↗
PubMed1985

Cardiovascular effects of enflurane and asphyxia during long-term beta 1-adrenoceptor blockade.

The haemodynamic effects of enflurane (1.7% and 3.4% expiratory concentrations) were investigated in sheep (n = 6) pretreated with an infusion of metoprolol (0.2 mg X kg-1 X h-1 for 5 days) and in control animals (n = 6). Chloralose was used as basal anaesthetic. A 90 s apnoea period was included in the experiment to evaluate further the possible side-effects of long-term metoprolol treatment in combination with enflurane anaesthesia. MAC 1.0 for enflurane in the sheep was found at 1.45% end-tidal concentration by separate measurements. Before enflurane administration, the only significant differences between the two groups of animals were a lower systemic vascular resistance and a higher stroke volume during metoprolol treatment. Enflurane abolished these discrepancies in a dose-dependent fashion and similar cardiovascular depression was observed in both groups of animals at 3.4% expiratory concentration of enflurane. Metoprolol did not significantly affect the hypertensive response to apnoea during chloralose anaesthesia alone. At enflurane 1.7% expiratory concentration the apnoea response was small and only the metoprolol-treated animals showed a significant increase in left ventricular end-diastolic pressure. We conclude that 5 days of pretreatment with metoprolol in the sheep model does not significantly impair cardiovascular performance during enflurane anaesthesia.

Adrenergic beta-Antagonists↗
PubMed1985

Successful vasoconstrictor therapy of anaphylactoid reactions during induction of anaesthesia. A report of two cases.

Anaphylactoid reactions were evoked during intravenous induction of anaesthesia in two patients on three occasions. In the first patient the reaction occurred during the first anaesthetic on propranolol and hydrochlorthiazide medication due to hypertension. Since the major target organ for the anaphylactoid reaction in this patient was the pulmonary circulation, the cardiovascular collapse at his first anaesthetic was misinterpreted as a nonspecific reaction to anaesthesia reinforced by the beta-receptor blocking therapy. At the second anaesthetic central haemodynamics, plasma adrenaline (A) and noradrenaline (NA) were measured. Following injection of thiopentone sudden decreases of mean arterial blood pressure (60%), cardiac output (60%), and systemic vascular resistance (20%) were observed. Thirty minutes later, still during circulatory shock, the concentration of A had increased whereas that of NA was normal. In the second patient the anaphylactogenic drug was supposed to be thiopentone, suxamethonium or alcuronium. In this patient, the fall in arterial blood pressure was associated with bronchospasm and the sudden appearance of peripheral oedema. In both cases initial resuscitation comprised volume replacement and beta 1-agonist therapy but the cardiovascular state was not normalized until vasoconstricting agents were infused.

Adult↗
PubMed1984

The relationship between circulating catecholamines and ST waveform in the fetal lamb electrocardiogram during hypoxia.

Previous studies from this laboratory have shown that changes in the ST waveform in the fetal electrocardiogram are a sign of fetal asphyxia. In the present study, seven chronically instrumented fetal lambs between 117 and 143 days' gestation were studied during 16 one-hour periods of maternally induced hypoxia. The aim was to test the hypothesis of a relationship between the concentration of circulating catecholamines and T-wave amplitude. The response to hypoxia was aged-dependent. Fetuses below 126 days of gestation did not react with electrocardiographic changes and output of epinephrine unless acidosis occurred. In more mature fetuses, hypoxia per se would induce a surge of epinephrine and changes in the ST waveform. Overall there was a strong correlation between the T/QRS ratio and the level of circulating epinephrine. During normoxia, epinephrine was undetectable (less than 0.1 nmol/L) in most fetuses; norepinephrine showed an increase at term. The analysis showed one fetus with chronic changes in the ST waveform (T/QRS ratio greater than 0.30) related to a marked increase in the plasma level of epinephrine in spite of normal blood gas values. These findings complement previous results in the acute and chronically instrumented fetal lamb and suggest that changes in the ST waveform expressed as T/QRS ratio identify a change to anaerobic myocardial metabolism mediated by beta-adrenergic stimulation.

Acidosis↗
PubMed1982

Long-term beta-receptor blockade--adrenergic and metabolic response to surgery and neurolept anaesthesia.

Twenty-six patients on chronic (greater than 3 months) beta-receptor blocking therapy due to ischaemic heart disease and/or hypertension were randomly distributed to a 4-day gradual withdrawal (n = 13) or a continuation of ordinary therapy until a planned cholecystectomy under neurolept anaesthesia (n = 13). Plasma-adrenaline, -noradrenaline, -potassium, -glycerol, -FFA, -insulin and b-glucose were determined perioperatively. The metabolic response to surgery was as expected with hyperglycaemia and depressed insulin levels, which did not differ significantly between the two groups of patients. Plasma-catecholamines showed the highest mean values during emergence from anaesthesia. Plasma-adrenaline and -potassium were constantly highest in the beta-receptor-blocked patients, who also showed indices of a relatively depressed lipolysis compared to patients in whom beta-receptor blockers had been withdrawn. These discrepancies between withdrawal versus continuation of preoperative beta-receptor blockade seemed to be of small clinical importance and did not oppose the present view that beta-receptor blockers should generally be continued during surgery. However, findings in individual patients suggest that beta-receptor blockade may maintain hypoglycaemia in catabolic patients.

Adrenergic beta-Antagonists↗
PubMed1982

beta-Receptor blockade and neurolept anaesthesia. Withdrawal vs continuation of long-term therapy in gall-bladder and carotid artery surgery.

Forty-eight chronically (greater than 3 months) beta-receptor-blocked patients with ischaemic heart disease and/or hypertension were studied on 49 occasions after random distribution to a 4-day, gradual preoperative withdrawal (n = 26) or a continuation (n = 23) of beta-receptor blockers. The patients were scheduled for either a cholecystectomy (n = 28) or a carotid thrombendarterectomy (n = 21) under neurolept anaesthesia. Three patients were excluded from the randomized part of the study due to complications (tachycardia, hypertension, severe angina) after therapy withdrawal. In subgroups, central haemodynamics (beta-receptor blockers withdrawn n = 6, continued n = 8) and creatinine-kinase B (beta-receptor blockers withdrawn n = 9, continued n = 11) were studied. Withdrawal of beta-receptor blockers was associated with high heart rates, supraventricular tachyarrhythmias and a hyperkinetic circulation during pain stimuli. Significantly more postoperative ECG changes (P less than 0.02) indicative of myocardial ischaemia were found than in beta-receptor blocked patients. These patients had low heart rates but also pronounced increases in pulmonary capillary wedge pressures, which in single patients could be associated with myocardial damage. These results imply that beta-receptor blockers should be continued before surgery and that a concomitant vasodilatatory therapy is likely to avoid the drawbacks of an increased cardiac afterload.

Adrenergic beta-Antagonists↗
PubMed1982

Beta-receptor blocker withdrawal. A preoperative problem in general surgery?

A prospective randomized study was performed in 91 patients scheduled for general surgery on 99 occasions. The patients were chronically (greater than 3 months) treated with beta-receptor blockers because of ischaemic heart disease and/or hypertension and the beta-receptor blockade was either gradually withdrawn (n = 51) during 4 days preoperatively or continued until surgery (n = 48). The effects on arterial blood pressure (BP), heart rate (HR) and rate-pressure product (RPP) at rest and the incidence of chest pain during daily activities were registered. A withdrawal of the beta-receptor blockade was associated with increases of HR (in eight patients greater than 30 beats min-1) and RPP and in patients treated for hypertension there were also increases of systolic and diastolic BP (in five patients greater than or equal to 30/15 mmHg). Patients who continued the beta-receptor blockade until surgery showed no changes. Nine out of 23 patients with a previous history of ischaemic heart disease had an increase of chest pain after withdrawal of the beta-receptor blockers, whereas none of the corresponding 25 patients who continued the therapy suffered from an increased chest pain. Due to the severity of symptoms after beta-receptor blocker withdrawal, surgery had to be postponed in 4 patients. The observations suggest that a 4-day preoperative withdrawal of long-term beta-receptor blockade is potentially hazardous in ischaemic and/or hypertensive patients.

Adrenergic beta-Antagonists↗
PubMed1982

Beta-receptor blockade and spinal anaesthesia. Withdrawal versus continuation of long-term therapy.

A prospective study was performed in 43 men scheduled for transurethral resections under spinal anaesthesia. All patients were on chronic beta-receptor blockade because of hypertension and/or ischaemic heart disease. The patients were randomly subjected to either a gradual preoperative withdrawal or a continuation of the beta-receptor blockade. Haemodynamics were measured non-invasively. Spinal anaesthesia was performed and an i.v. injection of atropine given. The patients were then placed in a lithotomy position. Mean anaesthetic level included T6. After beta-receptor blocker withdrawal consistently elevated heart rates, a high incidence of arhythmias, angina pectoris and postoperative ST-T changes indicating myocardial ischaemia were seen. These changes were not seen in patients with continued beta-receptor blockade. Withdrawal of beta-receptor blockers was also associated with an increased total peripheral vascular resistance in connection with spinal anaesthesia. These results suggest that patients on long-term beta-receptor blockade should continue the therapy during and after spinal anaesthesia.

Adrenergic beta-Antagonists↗