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Biomedical subjects

B A Henriksson

Publications and source records attributed to B A Henriksson.

At least 19 recordsLinked to original sources
PubMed2000

[Guidelines for management of patients with acute pancreatitis].

During recent years new concepts and methods have been introduced in the management of acute pancreatitis. Severity and risk of complications show wide variation. Outcome is also dependent on the physician's experience and on his local resources. In this light the Swedish Society of Upper Abdominal Surgery has elaborated national guidelines for management. Attention is paid to diagnosis, severity assessment and etiology. Furthermore, guidelines are offered for treatment of mild and severe pancreatitis, as well as for the management of pseudocysts. The role of multidisciplinary intensive care specialist teams in the management of severe disease is emphasized. The guidelines are supported by the Swedish Society of Gastroenterology, the Swedish Society of Gastroenterology, the Swedish Society of Anesthesiology and Intensive Care and by experts from other Nordic countries.

APACHE↗
PubMed1997

The effect of a heat and moisture exchanger on humidity in a low-flow anaesthesia system.

The heat and humidity in a low-flow breathing system was measured in order to study the inherent humidifying properties of the system at low fresh gas flows (< 1 and 21.min-1) and whether a heat and moisture exchanger could compensate for the loss of heat and humidification occurring at higher fresh gas flows (51.min-1) in these systems. Sixty patients were randomly divided into three groups (< 1, 2 and 51.min-1 fresh gas flows) with a heat and moisture exchanger and three groups without a heat and moisture exchanger in the breathing system. Thirty minutes after the start of anaesthesia a control measurement was performed, after which a heat and moisture exchanger was inserted into the breathing system of the three groups randomly allocated to have one. Three more measurements were performed at 10, 30 and 60 min after control. At low fresh gas flows the humidifying properties of the low-flow breathing system are adequate (i.e. provide an absolute humidity > 20 mg.l-1) but at a fresh gas flow of 51.min-1 there is a need for a heat and moisture exchanger for adequate humidification of the inspired gas.

Abdomen↗
PubMed1996

Effects of fentanyl, nitrous oxide, or both, on baroreceptor reflex regulation in the cat.

We have investigated the effects of fentanyl, nitrous oxide, or both, on carotid sinus baroreceptor reflexes in cats during basal chloralose anaesthesia. The bilaterally isolated carotid sinuses were perfused at prevailing systemic arterial pressure or at predetermined levels of pump-controlled pulsatile pressures of 50-200 mm Hg in steps of 25 mm Hg. Other major baroreceptor sites were denervated by bilateral vagotomy. Fentanyl decreased arterial pressure dose-dependently when the carotid sinuses were perfused at prevailing systemic arterial pressure and when the perfusion pressure was controlled artificially. High-dose fentanyl reduced significantly baroreceptor reflex responses in the sinus perfusion pressure range 50-125 mm Hg. Nitrous oxide increased arterial pressure in the carotid sinus perfusion range 75-125 mm Hg. There was no interaction between nitrous oxide and fentanyl for baroreceptor reflex responses. Our results indicated that baroreceptor reflexes, with and without nitrous oxide, were well preserved by moderate doses of fentanyl while high doses of fentanyl depressed baroreceptor reflexes.

Analgesics, Opioid↗
PubMed1996

Effects of desflurane on systemic, preportal and renal circulatory responses to infra-renal aortic cross-clamping in the pig.

BACKGROUND: Different pharmacological approaches have been used in the control of cardiovascular responses to surgical infra-renal aortic occlusion (AXC). The aim of the present study was to explore the modulatory effects of desflurane (DES) on these responses. METHODS: The study was performed in normoventilated chloralose-anesthetized pigs (n = 14). Measurements included cardiac output (CO), pulmonary vascular pressures, heart rate (HR) and mean arterial pressure proximal to the AXC site (MAPPROX). Renal arterial (QREN) and portal venous (QPORT) blood flows were measured ultrasonically. Systemic (SVR), preportal (RPORT) and renal (RREN) vascular resistances were derived. Sets of measurements were done a) prior to, b) during and c) 5 min after AXC. This was repeated, in a randomized fashion, at control (no DES) and with 4.9% and 9.8% DES, respectively. RESULTS: DES decreased MAPPROX, CO, HR, SVR, RREN and RPORT. At control, AXC increased MAPPROX (+27%), SVR (+27%), QPORT (+14%), RPORT (+12%) and RREN (+43%). DES 4.9% did not change this response pattern. With 9.8% DES, the AXC-induced increases in MAPPROX (+17%) and SVR (+21%) were attenuated. At this stage, AXC caused no demonstrable changes in RREN or RPORT, while both QREN (+16%) and QPORT increased (+9%). CONCLUSIONS: DES effectively controlled increases in proximal blood pressure during AXC. The increases in RREN and RPORT that were seen during AXC at control were inhibited by 9.8% DES. Consequently, at this DES dose, both QREN and QPORT increased during AXC.

Anesthetics, Inhalation↗
PubMed1995

Are the cardiovascular actions of dopamine altered by isoflurane?

Dopamine seems theoretically to be a rationale choice when adrenergic support is needed to counter undesired cardiovascular depressant effects of isoflurane. Although the cardiovascular effects of isoflurane (ISO) and exogenous dopamine (DA) are well documented, there are no reports on their pharmacological interaction. The effects of ISO 1.4% (MAC 1.0) on the cardiovascular response to exogenous DA were studied in dogs during chloralose anesthesia. Instrumentation included catheterizations of the femoral artery (for aortic pressures and heart rate, HR), the pulmonary artery (for thermodilution cardiac output, CO, and pulmonary arterial pressures) and the left ventricle (for tip-manometer measured left ventricular end-diastolic pressure, LVEDP). ISO per se decreased HR (-16%), mean arterial pressure (MAP; -33%), CO (-29%), left ventricular dP/dt (LV dP/dt; -51%), and increased pulmonary artery occlusion (PAOP; +64%) and LVEDP (+28%). Prior to ISO, DA increased MAP, CO stroke volume (SV), LV dP/dt and LV dP/dt/SAP (systolic arterial pressure) at the dose 10 micrograms.kg-1.min-1. At the dose 20 micrograms.kg-1.min-1 DA, besides these effects, increased PAOP and mean pulmonary artery pressure (MPAP). During ISO, DA at the dose 10 micrograms.kg-1.min-1 restored MAP, CO, and SV to pre-ISO control levels, while LV dP/dt was increased to +96% above the pre-ISO control level. At the dose 20 micrograms.kg-1.min-1, DA increased MAP (+33%), LV dP/dt (+172%), PAOP (+132%) and MPAP (+50%) above pre-ISO control levels. The cardiac effects of DA were similar to when it was given alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthetics, Inhalation↗
PubMed1993

Complement activation during liver transplantation.

Twelve patients with end-stage liver disease undergoing liver transplantation were studied regarding complement activation and formation of anaphylatoxins (C3a and C5a) and terminal C5b-9 complement complexes (TCC) after reperfusion of the grafted liver. Blood samples for complement variables (C1INH, C3, C4, C5, C3a, C5a, and TCC) were drawn preoperatively, before the anhepatic phase, 1 min before, and 2, 15, and 60 min after the start of reperfusion of the grafted liver. Activation of complement was observed during the operation. The C1INH, C3, C4, and C5 plasma concentrations decreased during the entire operation while the anaphylatoxin C3a and the terminal C5b-9 complement complex increased after the reperfusion of the grafted liver. Activation of complement with the formation of biologically active substances like anaphylatoxins and terminal C5b-9 complement complexes may be one explanation for circulatory complications often seen in patients undergoing orthotopic liver transplantation.

Adult↗
PubMed1992

Isolated hyperthermic liver perfusion with cytostatic-containing perfusate activates the complement cascade.

Eight patients with advanced liver malignancy undergoing isolated hyperthermic liver perfusion with melphalan and cisplatin were studied with regard to complement activation and formation of anaphylatoxins (C3a and C5a) and terminal C5b-9 complement complexes (TCCs). Blood samples for complement variables (C1-INH, C3, C4, C5, C3a, C5a and TCCs) were taken before surgery, 1 min before the start of perfusion, 1, 2 and 3 h after the start of perfusion, and 24 h after operation. Samples were drawn from the perfusate 1 h after the start of perfusion. Activation of complement was observed during perfusion. Raised plasma concentrations of C3a and TCCs were recorded and high levels of C3a and TCCs were found in the perfusate. In vitro tests indicated that melphalan and cisplatin may activate complement. This activation occurred at 37 and 42 degrees C but was more pronounced at 42 degrees C.

Adult↗
PubMed1992

Inspiratory to end-tidal oxygen difference during nitrous oxide anaesthesia.

In order to evaluate the value of the inspiratory to end-tidal oxygen concentration difference (Io2-E'o2) as a monitor during general anaesthesia, we studied 40 orthopaedic patients allocated randomly to four groups: anaesthesia with enflurane or isoflurane in nitrous oxide with either spontaneous or controlled ventilation. (Io2-E'o2) followed an asymptotically increasing curve because of decreasing uptake of nitrous oxide. At 1 h, (Io2-E'o2) approached the end-tidal carbon dioxide concentration (E'o2). During spontaneous ventilation, (Io2-E'o2) correlated best with E'co2. During controlled ventilation, there was a negative correlation between (Io2-E'o2) and nitrous oxide uptake rate. Changes in oxygen uptake rate were reflected in (Io2-E'o2), provided that the total ventilation volume was constant and the nitrous oxide uptake rate approached steady state conditions.

Adult↗
PubMed1992

The effects of propofol, methohexitone and isoflurane on the baroreceptor reflex in the cat.

The effects of propofol (P), methohexitone (M) and isoflurane (I) on the baroreceptor reflex were studied in a cat model in which the blood pressure in a bilateral isolated carotid sinus preparation was artificially varied between 50-200 mmHg. The influence from aortic and cardiopulmonary baroreceptors was excluded by vagotomy. With basal chloralose anaesthesia as control, the investigated anaesthetics were used in doses corresponding to MAC 0.5 and 1.0. The maximum change in systemic mean arterial pressure (MAP) and heart rate (HR) following a defined increase in carotid sinus pressure was used as an index of baroreceptor reflex sensitivity. Compared to control, M and I anaesthesia were associated with significant depression of baroreceptor reflex sensitivity at the high dose (corresponding to MAC 1.0), and during I anaesthesia also at the low dose (MAC 0.5). The baroreceptor reflex sensitivity was maintained during propofol anaesthesia. The carotid sinus pressure interval at which the maximum changes in MAP could be elicited, was significantly higher during M than during P. This indicates resetting of the baroreflex.

Animals↗
PubMed1991

Metabolic gas exchange during aortocoronary bypass surgery using a double pump system and mechanical ventilation. A comparison between indirect calorimetry and invasive blood gas measurements using Fick's principle.

Oxygen uptake and carbon dioxide excretion during aorto-coronary bypass surgery were studied in seven patients by indirect calorimetry and compared to blood-gas based measurements. Medium-high dose fentanyl, droperidol and midazolam were used for maintaining anaesthesia. During the period of extracorporeal circulation no external oxygenator was used. Circulation was maintained by two pumps by-passing the left and right heart respectively and the patient's lungs were ventilated with O2/N2 using a Servo 900C ventilator. For indirect calorimetric measurements gas concentrations were analysed by Beckman instruments and gas volumes were measured by the Servo 900C ventilator. Oxygen uptake and carbon dioxide excretion decreased by 31% and 39%, respectively. For invasive measurements during extracorporeal circulation, arterial and venous blood gases and pump flow were used. Using pump flow instead of cardiac output when calculating oxygen uptake circumvented errors in thermodilution measurements. There was a good correlation (r = 0.88) between the invasive and the indirect calorimetric measurements. Further, there was a good correlation between naso-pharyngeal temperature and indirect calorimetric measurements of oxygen uptake (r = 0.87).

Blood Gas Analysis↗
PubMed1991

Effects of thoracic epidural anesthesia and adrenoceptor blockade on the cardiovascular response to dopamine in the dog.

The cardiovascular effects of dopamine are different before and during thoracic epidural anesthesia (TEA). To evaluate underlying adrenoceptor-mediated mechanisms, dopamine effects were investigated in nine chloralose-anesthetized dogs. The circulatory response to dopamine (0-40 micrograms.kg-1.min-1) was studied before and during TEA, and during TEA after introducing the alpha 1-antagonist prazosin (0.3 mg.kg-1), the alpha 2-antagonist rauwolscine (0.3 mg.kg-1), and the beta 1-antagonist metoprolol (0.5 mg.kg-1). TEA decreased mean arterial pressure (MAP) by 29%, cardiac output (CO) by 36%, heart rate (HR) by 27%, and the maximum rate of change of left ventricular pressure (LVdP/dt) by 52%. Systemic vascular resistance, pulmonary vascular resistance and mean pulmonary artery pressure (MPAP) remained unaltered by TEA. Dopamine-induced increases in MAP and HR were augmented by TEA. Both MAP and LVdP/dt increased above pre-TEA levels at 10 micrograms.kg-1.min-1. Prazosin attenuated the increases in MAP and MPAP by dopamine. Adding rauwolscine almost abolished the dopamine response in MAP and MPAP. Metoprolol almost eliminated the dopamine effects on CO and LVdP/dt. Only minor alterations in cardiac filling pressures were observed during the study. Plasma norepinephrine (NE) concentration was lower during than before TEA at corresponding dopamine infusion rates. NE was reduced by the beta 1-blockade. During TEA, the plasma dopamine levels were generally higher, and they were further increased by adding beta 1-blockade. In conclusion, myocardial contractility and arterial pressure were restored to pre-TEA values by dopamine at 5-10 micrograms.kg-1.min-1.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗
PubMed1991

Local vascular effects of isoflurane during regional intestinal hypothermia in cats.

The influence of isoflurane on intestinal blood flow (IBF) during regional intestinal hypothermia (28 degrees C intraluminal temperature) was investigated in cats (n = 12) during basal chloralose-nitrous oxide anesthesia. A jejunal segment, which was dissected free in situ and intermittently cooled in a saline bath, was perfused via an extracorporeal arterial circuit which included a roller pump and a variable arterio-venous shunt. Intestinal perfusion pressures were controlled by adjusting the shunt flow. IBF was measured (optical drop-recording) during regional normothermia and hypothermia. 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% isoflurane. During normothermia, IBF levels were higher during isoflurane anesthesia than during basal chloralose anesthesia. Regional intestinal hypothermia induced no significant changes in IBF during basal chloralose anesthesia. However, the intestinal vasodilator effects of isoflurane, as shown during normothermia, were efficiently countered by regional cooling of the intestinal segment to 28 degrees C. Accordingly, hypothermia IBF levels were similar, regardless of whether isoflurane was administered or not. This could have an impact on the choice of anesthetic techniques.

Anesthesia, Inhalation↗
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↗