[How to achieve changes within health care services?].
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Biomedical subjects
Publications and source records attributed to M Andreen.
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One hundred and sixty-four patients scheduled for elective termination of pregnancy under general anaesthesia were randomly assigned to receive one of three different supplements to propofol and oxygen in nitrous oxide anaesthesia: 0.1 mg fentanyl, 0.5 mg alfentanil or placebo. Postoperative pain and nausea, as well as complications during anaesthesia were studied. There were no differences in complications or complaints by surgeons during anaesthesia, and no patient in any group reacted unsatisfactorily to surgery. The patients in the placebo group consumed significantly more propofol during the procedure (P less than 0.001). No differences were seen in time until hospital discharge between the three groups. Complaints about postoperative pain were significantly less frequent among patients receiving fentanyl (P less than 0.01). The number of patients requesting postoperative analgetics, however, did not differ. There was no difference in the frequency of nausea or vomiting, but postoperative pain was found significantly to increase complaints of nausea (P less than 0.01) and also time until hospital discharge (P less than 0.01). In conclusion, opioid supplementation lowered the amount of propofol needed for anaesthesia. Alfentanil 0.5 mg did not improve the postoperative course. Fentanyl 0.1 mg decreased the frequency of postoperative pain without increasing the time to hospital discharge.
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To study the effects on plasma proteins, blood coagulation and fibrinolysis of dextran-60, given as plasma volume substitute in a 3% solution, 57 patients were studied preoperatively and for 8 days postoperatively in conjunction with elective orthopaedic surgery. Three groups were formed according to the blood loss during the day of surgery: Group I (n = 22) less than 30%, Group II (n = 24) 30-50% and Group III (n = 11) greater than 50% of the estimated blood volume. Dilution to a haemoglobin concentration of 110 g.1-1 was intended and erythrocytes transfused accordingly. No platelets were transfused. All patients received similar amounts of crystalloids. Nine patients in Group III received plasma and/or albumin solution for further volume replacement once the maximum dose of dextran (1.5 g.kg-1) was reached. Dextran-70 was given on days 1 and 3 postoperatively for thromboprophylaxis. No patient exhibited clinical signs of thrombosis or embolism. Mean postoperative bleeding times were longer than preoperatively, but still within the normal range in all groups. They were both pre- and postoperatively slightly longer in Group III, compared to the other groups, perhaps due to mild haemostatic disorders and/or undisclosed antiphlogistic therapy. Postoperative colloid osmotic pressures decreased by 11-19% in the three groups. Dilution of plasma constituents was also seen in the postoperative fall of platelet counts and of albumin, antithrombin and Factor X levels, most marked in Group III. Albumin levels on day 8 were still only 77-83% of preoperative values. IgG and IgM were decreased and the IgG level was still only 75% of preoperative on day 8.(ABSTRACT TRUNCATED AT 250 WORDS)
One hundred and one patients undergoing outpatient abortion using local anesthesia were randomly allocated to one of three different premedications: morphine-scopolamine, pethidine or midazolam. The incidence of pain, anxiety, emetic (nausea-vomiting) and patient cooperation was analyzed. Discomfort was frequently noticed, 79 patients reported pain, 57 nausea and 26 vomited at least once during the postoperative period which lasted 2.6 h (mean value). There were no major differences in complaints among the different premedication groups. Nausea, though, was correlated to pain. Symptoms of pain, nausea and vomiting were frequent after abortion under paracervical block. These complaints were not found to be related to the type of premedication or other circumstances in the perioperative period.
The acrylic bone cement has been regarded as a very potent activator of the hemostatic mechanisms. A battery of coagulation, fibrinolytic, and kallikrein variables were studied perioperatively in 21 patients undergoing hip arthroplasty with fixation of the prosthesis either with (Charnley) or without (HP-Garches) cement. Epidural analgesia was used and dextran 6 per cent as thromboprophylaxis. The HP-Garches procedure was shorter and caused less blood loss. No differences were found between the two surgical procedures regarding the activation of the cascade systems. The coagulation and fibrinolytic systems were activated early, but a week postoperatively the latter seems to predominate. A marked activation of the kallikrein system was apparent. Our study shows that despite thromboprophylaxis a marked activation of the coagulation, fibrinolytic, and kallikrein systems occurs in relation to hip arthroplasty irrespective of the use or nonuse of cement and irrespective of the volume of blood loss during surgery. It may be the reaming of the bone marrow that initiates the activation of the cascade systems.
High lumbar epidural block was induced in seven dogs, causing a fall in mean arterial blood pressure (AP) from 24.5 +/- 2.9 to 12.0 +/- 3.1 kPa owing to reductions in cardiac output (QT) and systemic vascular resistance (SVR) to 67% and 68% of the pre-epidural values. Volume loading with dextran 10 ml X kg-1 b.w. increased QT nearly to the pre-epidural value. SVR decreased further to 61% of the pre-epidural value and AP was only slightly increased to 14.9 +/- 2.7 kPa. Subsequent administration of prenalterol 20 micrograms X kg-1 b.w. caused a further increase in QT to 17% above the pre-epidural value due to an increase in heart rate of 51 beats/min. AP did not change since SVR decreased further to 49% of the pre-epidural value. The hepatic arterial blood flow (QHA) was essentially unchanged during epidural block as well as during volume loading, while the portal venous blood flow (Qpv) was changed concurrently with (QT). In spite of the decrease in SVR, the preportal and hepatic arterial vascular resistances were not diminished following prenalterol. The increase in OT must therefore have favoured other vascular beds. Hepatic and pre-portal tissue oxygen uptakes were unchanged during the experimental procedure, while whole-body oxygen uptake decreased by 20% following the epidural block and increased nearly to the pre-epidural level following volume loading in combination with prenalterol.
The haemodynamic effects of i.v. infusions of sodium nitroprusside (SNP), nitroglycerin (TNG), and adenosine were studied in dogs in parallel with quantitative determinations of plasma renin activity (PRA) by radioimmunoassay. The drugs were given for controlled hypotension, and the mean arterial blood pressure (MABP) was decreased to approximately 50 mmHg (6.7 kPa). Arterial blood samples for PRA were collected at 10-min intervals. During the last interval the dogs were subjected to haemorrhagic shock. SNP-induced hypotension could be maintained only with a stepwise increase in infusion rate, from 11.8 to 16.0 micrograms X kg-1 X min-1 (P less than 0.05). TNG could not produce the desired blood pressure level, but gradually increasing doses induced a gradually decreasing MABP (80-60 mmHg) (10.7-8.0 kPa). During adenosine-induced hypotension, a perfectly stable blood pressure level was maintained without dose adjustments. Both SNP and TNG induced blood pressure-dependent increases in PRA, while no changes in PRA were seen during adenosine-induced hypotension. Nor could haemorrhagic shock, which induced further increases in PRA during SNP- and TNG-induced hypotension, alter PRA during adenosine infusions. We conclude that adenosine differs markedly from conventional hypotensive drugs such as SNP and TNG with respect to stability of action and dose requirements, and that this stability is related to an inhibited increase in renin release.
The effects of neurolept anaesthesia (NLA) on central circulation, total oxygen uptake and splanchnic circulation and oxygen uptake were studied in 12 artificially ventilated dogs, basally anaesthetized with thiopental and nitrous oxide. Hepatic arterial, superior mesenteric arterial and portal venous blood flows were measured with electromagnetic flowmetry. Cardiac output was measured by thermodilution. Determinations of oxygen contents were made in arterial, pulmonary arterial, portal venous and hepatic venous blood. NLA was induced with droperidol 0.5 mg . kg-1 b.w. and fentanyl 0.01 mg . kg-1 b.w. Arterial blood pressure decreased to 63% of control value due to reductions of cardiac output to 78% and of total peripheral vascular resistance to 81% of control values. Hepatic arterial, superior mesenteric arterial and portal venous blood flows all diminished to 75% of control values. Hepatic arterial, superior mesenteric arterial and preportal tissue vascular resistances all decreased. Total oxygen uptake declined to the same extent as cardiac output, leaving the arterio-venous oxygen difference unchanged. Oxygen uptake of the preportal tissues was unaffected and hepatic oxygen uptake was not significantly reduced, although there were decreases of hepatic oxygen uptake in some of the individual dogs. It is suggested that the cardiovascular depression following NLA was due to adaptation to a lowered total oxygen uptake. It is further concluded that splanchnic circulation was well preserved due to decreases in splanchnic vascular resistances, and that splanchnic oxygen consumption was maintained by means of increased oxygen extraction.
The effects of enflurane anaesthesia on central circulation, total oxygen uptake, splanchnic circulation and splanchnic oxygen uptake were studied in 10 artifically ventilated dogs, basally anaesthetized with thiopental and nitrous oxide. Hepatic arterial, superior mesenteric arterial and portal venous blood flows were measured with electromagnetic flowmetry. Cardiac output was measured by thermodilution. Determinations of oxygen contents were made in arterial, pulmonary arterial, portal venous and hepatic venous blood. The end-tidal enflurane concentration was kept at about 1 MAC (= 2.2%). Arterial blood pressure diminished 54% of control value due to decreases of cardiac output to 65% and of total peripheral vascular resistance to 81% of control values. Hepatic arterial, superior mesenteric arterial and portal venous blood flows decreased to 65-70% of control levels and the corresponding vascular resistances all declined to about 80-85% of control values. Total oxygen uptake decreased, but less than cardiac output, leading to an increased arterio-venous oxygen content difference. Oxygen uptake of the preportal tissues was unchanged and hepatic oxygen uptake was not significantly altered, although there were decreases in hepatic oxygen uptake in some of the individual experiments. It is suggested that the cardiovascular depression following enflurane anaesthesia in the dog was due, to a great extent, to a primary myocardial depression. It is further concluded that the splanchnic blood flows were relatively well preserved, due to decreases in splanchnic vascular resistances, and that hepatic and preportal tissue oxygen consumptions were maintained by increased oxygen extraction.
A brief summary of the anatomy and physiology of the splanchnic circulation is presented. The influence of 1 MAC enflurane anaesthesia on splanchnic circulation and oxygenation was studied in 10 dogs. Superior mesenteric arterial, portal venous and hepatic arterial blood flows decreased less than mean arterial blood pressure, due to reductions in superior mesenteric arterial, preportal vascular and hepatic arterial resistances. It is suggested that these reactions within the splanchnic circulation are mainly dependent on normal autoregulative responses elicited by the fall in blood pressure. Oxygen consumption of the preportal tissues and the liver was unchanged as a result of increased extraction of oxygen.
Five anaesthetized dogs were given 20 infusions of 1--9 min duration of somatostatin in a dosage of 0.2--15 micrograms.kg-1.min-1. Cardiac output was measured by thermodilution. Electromagnetic blood flow measurements were simultaneously performed in the hepatic artery proper, the left gastric artery, the superior pancreatico-duodenal artery, the superior mesenteric artery and in the portal vein. Mean arterial blood pressure was recorded continuously. Somatostatin reduced all splanchnic blood flows measured by 15--35%, except for the hepatic artery flow, which was increased by 5% or unaffected. Cardiac output and mean arterial pressure were unchanged. Somatostatin was thus demonstrated to exert a specific vasoactivity in the splanchnic area without influencing central circulation. It is suggested that somatostatin acts directly on the vascular smooth muscle.
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Six dogs were subjected to halothane anaesthesia under hypoxic and non-hypoxic conditions. Plasma fluoride levels in hepatic venous and arterial blood, as well as blood flow to the liver, were measured during anaesthesia. The amount of fluoride released by the liver could thus be calculated. Release of fluoride took place in all animals during non-hypoxic halothane anaesthesia. The amount released varied between the individual animals and in three of them it rose further during hypoxic anaesthesia. The occurrence of defluorination of halothane, even under nonhypoxic conditions, may indicate a reductive metabolism in at least some parts of the liver. The significance of this hypothesis is discussed.
Ten dogs were subjected to a period of hypovolaemia (bleeding volume: 2% of body weight) and to a period of halothane anaesthesia (end-tidal halothane concentration: 1%). Mean arterial blood pressure decreased to 79% of control value during hypovolaemia and to 58% of control value during halothane anaesthesia. Mean total peripheral and preportal vascular resistances increased during hypovolaemia and were unchanged during halothane. Mean hepatic arterial and portal venous blood flows decreased to 82% and 55% of control values, respectively, during hypovolaemia, and to 41% and 56% of control value, respectively, during exposure to halothane. Mean hepatic arterial resistance was unchanged during hypovolaemia, but increased during halothane. Mean hepatic oxygen consumption did not change significantly during hypovolaemia, but decreased during halothane anaesthesia, in spite of an increased extraction of oxygen from both the hepatic arterial and the portal venous blood. Possible mechanisms which may maintain oxygen supply to the liver by increasing the hepatic arterial fraction of total liver blood flow when portal venous blood flow is reduced are discussed. It is concluded that this mechanism is upset or inhibited during halothane anaesthesia.
The uptake of bupivacaine in the liver and lung of the dog was studied 10,20,30 and 60 min after intramuscular injection of the drug. It was possible to quantify this uptake by combining measurements of concentrations and flows. The administration of bupivacaine (0.75 mg/kg b.w.) did not result in any significant circulatory changes. Arterial bupivacaine concentrations showed major variations, indicating interindividual differences in absorption rate. Lung uptake after 10 min was high in two dogs with initially high blood concentrations of bupivacaine, but low after 20 min or longer. The other dogs showed little or no uptake. Mean hepatic bupivacaine uptake was about 50% of the total dose during the first hour after injection, this indicates the central role of the liver in eliminating bupivacaine even during the initial period following administration. The hepatic extraction ratio showed interindividual variations, but the mean value of about 55% was constant throughout the observation period. This is in agreement with earlier findings indicating a first-order elimination of bupivacaine.
The effects of occlusion of the hepatic artery on total and regional splanchnic oxygen consumption were studied in lightly anaesthetized dogs. Mean whole body oxygen uptake (+/- S.D.) was 4.72 +/- 0.55 ml/kg b.w. min-1, mean liver oxygen uptake (+/- S.D.) 1.18 +/- 0.42 ml/kg b.w. min-1 and mean oxygen uptake of the portally-drained tissues (+/- S.D.) was 0.80 +/- 0.54 ml/kg b.w. min-1 during the control period. The hepatic artery contributed 45 +/- 24% of the total liver oxygen uptake. The duration of occlusion was 45 min. Mean liver oxygen uptake was found to decrease to 64% of control values. The extraction of oxygen from the portal blood increased slightly. Mean whole body oxygen uptake and mean oxygen uptake of the portally-drained tissues were unchanged. 45 min after release of the hepatic artery occlusion, liver oxygen consumption had returned to control values. It is concluded that oxygen uptake in the liver is correlated to oxygen tension.