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Biomedical subjects

L Irestedt

Publications and source records attributed to L Irestedt.

At least 37 records · Page 2Linked to original sources
PubMed1996

Lack of analgesic effect of systemically administered morphine or pethidine on labour pain.

OBJECTIVE: To evaluate the true analgesic effect of morphine and pethidine on labour pain. DESIGN: The analgesic and sedative effects of intravenous morphine or pethidine and their effect on anxiety were compared in a prospective, double-blind, randomised dose-response study. SETTING: A Stockholm teaching hospital obstetric unit. PARTICIPANTS: Ten healthy nulliparous parturients in active labour were included in each group. RESULTS: Even after repeated doses (up to 0.15 mg/kg body weight morphine and up to 1.5 mg/kg body weight pethidine) the findings were uniform, with very high pain scores maintained in each group as assessed with visual analogue scale. The parturients were all significantly sedated and several fell asleep but were awakened by pain during contractions. CONCLUSION: It is concluded that labour pain is not sensitive to systemically administered morphine or pethidine. These drugs only cause heavy sedation. It therefore seems unethical and medically incorrect to meet parturients' requests for pain relief by giving them sedation. Considering the well documented negative effects on newborn infants we also believe systemic pethidine should be avoided in labour.

Adult↗
PubMed1989

Cerebral blood flow and metabolism during adenosine-induced hypotension in patients undergoing cerebral aneurysm surgery.

The effects of adenosine-induced hypotension on cerebral blood flow (CBF), cerebral metabolic rate of oxygen (CMRO2), and cerebral lactate production, together with systemic haemodynamics, were studied in 10 patients undergoing cerebral aneurysm surgery in neurolept anaesthesia with controlled hyperventilation. CBF changes were determined in six of the patients with a retrograde thermodilution technique in the jugular vein. Hypotension was induced with a continuous infusion of adenosine in the superior vena cava. The dose range was 0.06-0.35 mg/kg/min, and this caused a 42% reduction in mean arterial blood pressure (MABP) from 79 +/- 4 to 46 +/- 1 mmHg (10.5 +/- 0.5 to 6.1 +/- 0.1 kPa) through a profound reduction in systemic vascular resistance (SVR), which amounted to 61%. No significant change occurred in CBF. Whole body AV-difference of oxygen was decreased by 37%, and cerebral AV-difference by 28%, corresponding to reductions in whole body oxygen uptake and CMRO2 of 16 and 17%, respectively. Cerebral AV-difference of lactate did not change. In the posthypotensive period MABP was increased by 10%, together with a minor increase in CBF (15%). It is concluded, that adenosine-induced hypotension at MABP levels between 40-50 mmHg (5.3-6.7 kPa) does not affect cerebral oxygenation unfavourably, and may even offer a protective effect by reducing cerebral oxygen demand. The slight CBF increase in the posthypotensive period was probably secondary to an increase in MABP together with a blunted autoregulation, but in no case was this effect considered to be harmful for the patient.

Adenosine↗
PubMed1989

Adenosine concentration in umbilical cord blood of newborn infants after vaginal delivery and cesarean section.

Umbilical blood was collected immediately at birth (less than 30 s) in full-term infants after vaginal deliveries (n = 33) and elective cesarean sections (n = 11). Blood gases, plasma adenosine, hypoxanthine, and catecholamine concentrations were determined. In vaginally born infants the median arterial adenosine concentration was found to be 0.46 microM (range 0.13-2.06) and the venous 0.48 microM (0.09-1.62). These levels were significantly higher (p less than 0.01) than in infants delivered by elective cesarean section; 0.16 microM (0.04-0.42) in the artery and 0.17 microM (0.02-0.56) in the vein. Vaginally born infants showed about a 4-fold higher level of umbilical arterial catecholamines than infants born by elective cesarean section. There was a strong inverse correlation between arterial hypoxanthine concentration and pH (r = -0.81, p less than 0.01). It is suggested that increased adenosine release at vaginal delivery modulates the stress response elicited by the strong catecholamine surge and may furthermore exert protective effects in perinatal asphyxia.

Adenosine↗
PubMed1988

Cardiac function and sympathoadrenal activity in the newborn after cesarean section under spinal and epidural anesthesia.

Left ventricular systolic time intervals, bupivacaine concentrations, adrenaline and noradrenaline levels were determined in 19 neonates delivered by elective cesarean section. Ten of the cesarean sections were performed under spinal and nine under epidural anesthesia. Plain bupivacaine 0.5% was used for the epidural anesthesia and bupivacaine 0.5% in glucose 8% for the spinals. The noradrenaline and adrenaline levels were higher in the neonates whose mothers received epidural anesthesia. The differences in catecholamine and bupivacaine concentrations were not associated with differences in left ventricular dynamics, or the timing of postnatal circulatory changes. The significant exposure of the neonate to bupivacaine, at maternal epidural anesthesia, seems to have no negative effect on early neonatal circulation in the healthy term infant.

Anesthesia, Epidural↗
PubMed1986

Per- and postoperative changes in coagulation and fibrinolytic variables during abdominal hysterectomy under epidural or general anaesthesia.

Blood coagulation and fibrinolysis were studied in 20 premenopausal women undergoing abdominal hysterectomy under general anaesthesia (GA) or high epidural analgesia (EDA). As expected, the adrenocortical stress response was suppressed in the EDA group. The Factor VIII complex (F VIII:C, F VIII R:Ag = von Willebrand factor), known to be related to adrenocortical activity and/or vessel wall reactivity, was found to increase less in the EDA group. With regard to all the other variables analysed there were no significant differences between the groups. With both anaesthetic procedures activation of coagulation could be demonstrated by a decrease in prekallikrein, F X and antithrombin as well as by an increase in fibrinopeptide A levels. A decrease in plasminogen and alpha 2-antiplasmin suggested activation of the fibrinolytic system and a decrease in prekallikrein and kallikrein inhibition activity (C-1-esterase inhibitor) an activation of the kallikrein system. In this study only the differences in F VIII complex could explain the previously reported higher thromboembolic frequency after GA as compared to EDA.

Adult↗
PubMed1986

Hemostasis in cold-knife conization. Effects and side effects of Glypressin, a long-acting analogue of lysine-vasopressin.

In a double-blind, randomized study, 50 patients undergoing conization were treated with either lysine-vasopressin (LVP) or its longer-acting analogue Glypressin. Bleeding during the operation and side effects were studied. The hemostatic effect appeared better with LVP than with Glypressin. One postoperative bleeding occurred in the whole series, in a patient treated with Glypressin. The effect on the general circulation, especially with respect to pallor of the skin, was less prominent with Glypressin than with LVP (with the concentrations used in this study).

Adult↗
PubMed1985

Effects of prenalterol and volume loading with dextran on haemodynamics and oxygen consumption in dogs during high epidural block with special reference to the splanchnic region.

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.

Animals↗
PubMed1985

Renin release during controlled hypotension with sodium nitroprusside, nitroglycerin and adenosine: a comparative study in the dog.

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.

Adenosine↗
PubMed1984

Neonatal left ventricular performance after vaginal delivery and cesarean section under general or epidural anesthesia.

Left ventricular systolic time intervals, plasma norepinephrine concentration, hematocrit, and blood pressure were recorded in infants delivered vaginally and by cesarean section from mothers under epidural or general anesthesia. Each group comprised 12 infants. Left ventricular ejection time and the preejection period were longer in infants delivered vaginally, although the concentrations of norepinephrine found were greater than those found in the cesarean section groups. Hematocrit and blood pressure were unrelated to the mode of delivery or the anesthetic technique. The isovolumic contraction time, however, was significantly shorter after epidural anesthesia 15.6 +/- 7.6 msec (mean +/- 1 SD) than after general anesthesia 20.5 +/- 8.0 msec at 30 minutes (p less than 0.05), 14.8 +/- 6.2 msec, and 20.9 +/- 5.7 msec at 2 hours respectively (p less than 0.001). These differences in left ventricular dynamics are probably related to the effects of anesthetics that have traversed the placenta rather than to mode of delivery.

Anesthesia, Epidural↗
PubMed1984

Central and splanchnic hemodynamics in the dog during controlled hypotension with adenosine.

Central and splanchnic hemodynamic effects during controlled hypotension induced by the administration of the endogenous vasodilator adenosine were studied in ten artificially ventilated dogs under neurolept anesthesia. Adenosine was administered as a continuous infusion in the aorta (n = 3), in the inferior vena cava (n = 3), and after pretreatment with dipyridamole (which inhibits the cellular uptake of adenosine) (n = 4) in a dose sufficient to maintain a mean arterial blood pressure (MABP) level of approximately 50 mmHg. Observations were made before and after 20 min of controlled hypotension. Basal arterial plasma levels of adenosine were in the 10(-7) M range (means = 0.4 microM). The hemodynamic response was similar in all three settings. Adenosine caused a profound decrease in systemic vascular resistance (SVR) (52%, P less than 0.01) and preportal vascular resistance (PPR) (64%, P less than 0.01), while hepatic arterial vascular resistance ( HAR ) increased by 49% (P less than 0.05). Cardiac output increased (22%, P less than 0.05) through increase of stroke volume (77%, P less than 0.01), while heart rate decreased (28%, P less than 0.01). Whole-body oxygen uptake decreased (14%, P less than 0.01). Portal venous blood flow increased by 28% (P less than 0.05), whereas hepatic arterial blood flow decreased by 70% (P less than 0.01). In the preportal tissues, oxygen uptake decreased by 21% (P less than 0.01). In contrast, hepatic oxygen consumption increased (53%, P less than 0.05). Adenosine-induced hypotension was not associated with changes in plasma renin activity or the plasma concentration of norepinephrine. It is concluded that adenosine causes a rapidly induced and easily maintained hypotension and may be a potentially useful agent for controlled hypotension in patients.

Adenosine↗
PubMed1984

Controlled hypotension with adenosine in cerebral aneurysm surgery.

The cardiovascular effects of adenosine-induced controlled hypotension were studied in 10 patients undergoing cerebral aneurysm surgery. Adenosine and its metabolites were measured in arterial plasma using high-pressure liquid chromatography. Whole body and cerebral arteriovenous oxygen content differences (AVDO2), arterial lactate levels, and arteriojugular lactate differences were determined. In order to reduce the dose requirement of adenosine, the patients were pretreated with the adenosine uptake inhibitor, dipyridamole (0.3-0.4 mg . kg-1). During the infusion of adenosine (0.14 +/- 0.04 mg . kg-1 . min-1) the mean arterial blood pressure decreased by 43%, from 82 to 46 mmHg, during a mean hypotensive period of 32 min, without signs of tachyphylaxis. The arterial adenosine level increased from 0.15 +/- 0.02 to 2.45 +/- 0.65 microM (P less than 0.01). Hypotension was caused by a profound decrease in peripheral vascular resistance (61 +/- 3%, P less than 0.01), which was accompanied by an increase in cardiac output (44 +/- 9%, P less than 0.01). Heart rate increased moderately by 16 +/- 5% (P less than 0.01). Pulmonary vascular resistance and central venous pressures were unaffected. Arterial lactate and PaO2 were unchanged, while whole body oxygen consumption was decreased by 13 +/- 4% (P less than 0.05). The AVDO2 across the brain was decreased by 37 +/- 5% (P less than 0.05) without signs of lactate formation. The authors conclude that adenosine rapidly induces a stable and easily controlled hypotension in humans by dilation of arterial resistance vasculature.

Adenosine↗
PubMed1984

Central and splanchnic haemodynamics in the dog during controlled hypotension with sodium nitroprusside.

The effects of controlled hypotension induced by sodium nitroprusside (SNP) on central and splanchnic haemodynamics were studied in ten artificially ventilated dogs under neurolept anaesthesia. SNP was given intravenously as a continuous infusion in order to maintain a mean arterial blood pressure (MABP) of about 50 mmHg. Observations were made before (control) and at 20 and 60 min after the start of the SNP infusion. The mean SNP dosage was 13.7 micrograms X kg-1 X min-1. Systemic vascular resistance (SVR) decreased by 47%. After 20 min there was a 17% decrease in cardiac output, while the hepatic arterial blood flow was diminished by 39%, and portal venous blood flow by 16%. Cardiac output and portal venous blood flow tended to return towards control values at 60 min, while the hepatic arterial blood flow remained depressed. The total oxygen uptake was unaltered after 20 min, but slightly decreased after 60 min. There were no changes in hepatic or preportal tissue oxygen consumption, nor in hepatic lactate uptake. It is concluded that SNP-induced hypotension was achieved primarily by a profound reduction of SVR, and initially also by a slight decrease in cardiac output. Although splanchnic and hepatic blood flows decreased, there were no signs of hypoxia in the preportal tissues or in the liver.

Animals↗
PubMed1984

Effects of ephedrine on haemodynamics and oxygen consumption in the dog during high epidural block with special reference to the splanchnic region.

High lumbar epidural block was induced in seven dogs with 0.5% bupivacaine, causing a fall in mean arterial blood pressure (AP) from 19.2 +/- 3.2 to 10.5 +/- 3.2 kPa, owing to equal reductions in cardiac output (QT) and systemic vascular resistance (SVR). After the administration of ephedrine (a single injection of 200-300 micrograms X kg-1 b.w. followed by a continuous infusion of 10-20 micrograms X kg-1 b.w. X min-1) AP, QT and SVR rose to pre-epidural values. Furthermore, the hypokinetic circulation following the epidural block returned to normokinetic levels. Portal venous blood flow was increased from 16.5 +/- 6.2 to 25.5 +/- 4.3 ml X kg-1 b.w. X min-1 by ephedrine, while the hepatic arterial blood flow was unchanged and remained at its pre-epidural level. In spite of a slight rise in hepatic oxygen consumption from 1.2 +/- 0.4 to 1.6 +/- 0.6 ml X kg-1 b.w. X min-1, the percentages of oxygen extracted from the portal vein and the hepatic artery decreased significantly. It is concluded that ephedrine restores central and splanchnic haemodynamics in a desirable manner during high epidural anaesthesia.

Anesthesia, Epidural↗
PubMed1984

Catecholamine surge and metabolic adaptation in the newborn after vaginal delivery and caesarean section.

The immediate postnatal metabolic adaptation and sympatho-adrenal activation were studied in infants delivered vaginally or by elective caesarean section. Vaginally delivered infants showed high catecholamine levels at birth compared to infants born by caesarean section under epidural or general anaesthesia. Umbilical arterial glucose levels were significantly higher in the vaginal group than in both caesarean section groups. At 30 min, all groups showed a marked decrease with several infants showing asymptomatic hypoglycaemia in the caesarean section group. C-peptide levels showed no difference at birth but later became significantly higher in the vaginal group. Although the levels of free fatty acids and glycerol were low at birth, they were significantly higher in the vaginal group. In all groups they increased substantially with time. Considering the marked differences in catecholamine levels, the differences in metabolic adaptation were unexpectedly small. This implies an attenuated metabolic response to sympatho-adrenal stimulation in the newborn.

Adaptation, Physiological↗
PubMed1984

Relationship between arterial and venous adenosine levels and vasodilatation during ATP- and adenosine-infusion in dogs.

The hemodynamic effects of ATP and adenosine (i.v. infusions) were studied in dogs in parallel with quantitative determination of purines in plasma by HPLC. In two experiments, infusion were performed during treatment with dipyridamole, an uptake inhibitor of adenosine. A 50-60% reduction of mean arterial blood pressure (MABP) was induced by both ATP and adenosine at infusion rates ranging between 17-290 mumoles/min. Cardiac output was unaffected by the purine infusions, indicating that the reduction of MABP was caused by a reduction of the systemic vascular resistance. Elevated ATP and adenosine concentrations were seen in venous plasma (pulmonary artery) during infusion, while only approximately 10% recovered ATP had been degraded to adenosine. On the other hand, in arterial plasma, virtually all nucleotides had been eliminated whereas the adenosine concentrations in plasma ranged between 5 and 20 microM. The magnitude of the vasodilatation was strictly related to the arterial plasma adenosine level irrespective of whether ATP or adenosine was infused. Thus, adenosine probably mediates the vasodilatory effect of ATP.

Adenosine↗