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Biomedical subjects

M Lagerkranser

Publications and source records attributed to M Lagerkranser.

At least 19 recordsLinked to original sources
PubMed1998

Whitacre or Quincke needles--does it really matter.

BACKGROUND: Postdural puncture headache (PDPH) and backache are well known complications of spinal anaesthesia. The incidence of PDPH may be significant in young people (< 50 years). The present study was undertaken in order to compare the utility and complication rate of the Whitacre and Ouincke spinal needles. METHODS: During three years all patients who could comply, and who were to undergo spinal anaesthesia at the Department were asked to join this quality control study. Each one received a questionnaire including questions about discomfort and other possible side effects attributed to spinal anaesthesia. In each case, an extended anaesthetic record was filled out by the anaesthesiologist. About 50 anaesthesiologists at different educational levels were involved. RESULTS: The study includes 2598 cases, of which questionnaires were returned by 66%. Needles of the 25 G gauge size were used in over 90% of the cases. Multiple skin punctures were required more frequently in the Quincke than in the Whitacre group (P < 0.01). The number of insufficient blocks was also higher in the Quincke group (P < 0.01). There was a higher incidence of backache in the Quincke group (P < 0.05). In patients under 50 years, PDPH was more frequent following use of the Quincke needle (P < 0.05), whereas no difference between the needles in this regard was found among those over 50 years (P > 0.05). CONCLUSIONS: For routine clinical use the Whitacre needle appears to be associated with better performance and increased reliability. In younger patients the Whitacre needle have the additional advantage of decreasing the risk of postdural puncture headache.

Adolescent↗
PubMed1997

Effects of propofol on cerebral blood flow, metabolism, and cerebral autoregulation in the anesthetized pig.

We studied the effects of propofol on the cerebral circulation and flow/pressure autoregulation in eight anesthetized pigs. Regional cerebral blood flow (rCBF) was measured with a cerebral venous outflow technique. Autoregulation was tested with angiotensin infusions and gradual blocks of the caval vein for hyper- and hypotensive challenges, respectively. Propofol was given in a bolus of 2.5 mg.kg-1 followed by an infusion starting at 12 mg.kg-1.h-1 and gradually reduced to 8 mg.kg-1.h-1. As expected, propofol caused a substantial reduction in cerebral metabolic rate of oxygen, which was accompanied by an increase in cerebrovascular resistance and a decrease in CBF. In the control situation, i.e., during background anesthesia (low-dose isoflurane+nitrous oxide) only, the autoregulation was well preserved, and its lower limit was found at a mean arterial blood pressure (MABP) of 48 mm Hg. Propofol did not affect autoregulation in the group as a whole: the slope of the regression line of regional cerebrovascular resistance (rCVR) versus MABP during blood pressure reduction (caval test) was not significantly changed during propofol when compared to the control, neither was the lower limit of autoregulation (MABP, 54 mm Hg). All pigs but one followed this response pattern. The nonautoregulating pig had a completely pressure-dependent rCBF during propofol anesthesia, despite a perfectly intact auto-regulation in the control situation. It is concluded that propofol in clinical dosage does not affect autoregulation in this pig model, although individual animals may display a different response pattern.

Anesthetics, Intravenous↗
PubMed1994

Nimodipine does not affect the cerebral autoregulatory response in the anesthetized pig.

The effect of the calcium blocker nimodipine on the cerebral blood flow (CBF) and cerebral autoregulatory responses was examined in seven fentanyl/N2O/anesthetized pigs. CBF was measured continuously from the sagittal sinus by a venous outlet flow technique. Cerebral autoregulation tests were performed before, after 30 min of nimodipine infusion (0.5 microgram.kg-1.min-1), and at 30 min after the infusion. The autoregulatory response to a gradual blood pressure increase was tested by infusion of angiotensin, and to a gradual blood pressure decrease was tested by caval block. The slope of the relationship between the regional cerebral vascular resistance (rCVR) and mean arterial blood pressure (MABP) was used as a measure of the autoregulatory capacity. The lower limit of autoregulation was determined as the MABP at which rCVR did not further decrease. An i.v. bolus dose (10 micrograms.kg-1) of nimodipine resulted in a transient increase in rCBF during 3 min, together with an MABP reduction. After 1 h of nimodipine infusion, MABP was reduced (19%), while rCBF, rCVR, and cerebral metabolism were unaffected. In the control condition, a preserved cerebral autoregulatory response to the increase of MABP (+30 mm Hg) was indicated by an unaffected rCBF and determined by the slope of the rCVR/MABP regression line (0.053), not different from the slope during blood pressure decrease (0.063). The cerebral autoregulatory responses to increase or decrease in MABP were not attenuated by nimodipine infusion. The lower limit of autoregulation (48 +/- 6 mm Hg) was not altered by nimodipine.

Anesthesia↗
PubMed1991

Nitroprusside-induced hypotension and cerebrovascular autoregulation in the anesthetized pig.

The influence of sodium nitroprusside (SNP) on cerebral blood flow and cerebrovascular autoregulation at doses that produced 36% +/- 3% (slight) and 52% +/- 4% (moderate) reductions of mean arterial blood pressure (MABP) was evaluated in mechanically ventilated fentanyl/N2O-anesthetized pigs. The blood flow of the frontal hemispheres was evaluated by sagittal sinus outflow, which was determined by an electromagnetic method. Integrity of cerebral autoregulation was evaluated by two formal tests: one hypertensive challenge with an angiotensin infusion (n = 12) and one hypotensive challenge with reduced venous return to the heart (blockade of the vena cava, n = 7). The tests were performed before, during, and after hypotension. Cerebral blood flow tended to increase during hypotension, but this change was not significant. Impaired autoregulation was seen in both tests during slight hypotension (MABP = 89 +/- 3 mm Hg) with an SNP infusion of 12 +/- 3 micrograms.kg-1.min-1. Cerebral autoregulation was completely abolished at both tests during moderate hypotension (MABP = 61 +/- 2 mm Hg with an SNP infusion of 38 +/- 7 micrograms.kg-1.min-1). Despite a posthypotensive increase in cerebral blood flow without rebound hypertension, the autoregulatory response to angiotensin-induced hypertension was restored within 15-25 min. The autoregulatory response to a decrease in MABP was impaired for more than an hour after discontinuation of the SNP infusion. No acidosis was observed. The authors conclude that during slight and moderate SNP-induced hypotension, there was a dose-dependent impairment of cerebral autoregulation. Further, the autoregulatory response to the hypotensive challenge after SNP hypotension was markedly delayed, whereas the response to hypertension was rapidly restored.

Animals↗
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

Effects of adenosine-induced hypotension on cerebral blood flow and metabolism in the pig.

The cerebral and systemic effects of hypotension induced by adenosine (0.61 +/- 0.07 mg.kg-1.min-1) were studied in eight pigs anesthetized with droperidol, phenoperidine and nitrous oxide. Mean arterial blood pressure (MABP) was reduced by 58%, from 17.2 kPa (128 mmHg) to 6.9 kPa (53 mmHg) during a 30-min period. The hypotension was caused by a decrease in systemic vascular resistance (58%) while the cardiac output was unaffected. Cerebral blood flow (CBF), as determined by microsphere distribution, and the cerebral metabolic rate for oxygen (CMRO2) remained unchanged. Cerebral vascular resistance decreased by 61%. There were no signs of cerebral lactate release. After discontinuation of adenosine infusion, the MABP returned to control levels within 5 min. Thirty minutes later the CBF was increased by approximately 60% in comparison to the control, while the CMRO2 was unchanged. It is concluded that adenosine-induced hypotension in pigs is associated with preserved CBF and CMRO2, whereas cerebral hyperperfusion is present in the early post-hypotensive period.

Adenosine↗
PubMed1989

Effect of adenosine-induced hypotension on the cerebral autoregulation in the anesthetized pig.

The influence on cerebral blood flow (CBF) and autoregulation of systemic adenosine infusion, at doses that produced a 29 +/- 4% (0.28 +/- 0.06 mg/kg/min) or a 55 +/- 2% (0.49 +/- 0.07 mg/kg/min) reduction of mean arterial blood pressure (MABP), was evaluated in 12 normoventilated fentanyl/N2) anesthetized pigs. CBF was determined as sagittal sinus outflow and recorded continuously by an electromagnetic technique. Autoregulation was evaluated by two formal tests: infusion of angiotensin for elevation of MABP, and reduction of myocardial filling pressure by caval block for graded MABP decrease before, during and after adenosine infusion. CBF as well as cerebral metabolic rate of oxygen were unaffected during both levels of hypotension and were not significantly altered after the hypotension. Signs of impaired autoregulation were found during the angiotensin test as well as during the caval block at light hypotension (92 +/- 3 mmHg, 12.3 +/- 0.4 kPa), while autoregulation was completely abolished at moderate hypotension (59 +/- 2 mmHg, 7.9 +/- 0.3 kPa). After termination of adenosine-induced hypotension, autoregulation was restored in all animals within 60 min. It is concluded that systemically administered adenosine preserves CBF, even at low MABP levels, by a direct cerebral vasodilatory effect. However, the cerebral autoregulatory mechanisms are impaired or abolished in a dose-dependent and reversible manner.

Adenosine↗
PubMed1988

Use of mannitol during neurosurgery: interpatient variability in the plasma and CSF levels.

An i.v. infusion of mannitol was given over 15 min to 12 patients before they underwent intracranial surgery under general anesthesia. Samples of blood, CSF and urine were taken over 4 h. Mannitol disappeared from plasma in a bi-exponential manner. The mean maximal plasma concentration was 4.08 mg/ml at 15 min, and at 4 h it had declined to 0.53 mg/ml. The mean distribution rate constant was 11.2 h-1, corresponding to a plasma distribution half-life of 0.11 h. The mean elimination rate constant was 0.41 h-1, the plasma half-life was 2.2 h, the central distribution volume was 16.3 l, and total plasma clearance was 100.4 ml/min. The mean concentration of mannitol in CSF during the 4 h period increased up to 0.10 mg/ml. There were marked interindividual differences in the concentration ratio blood/CSF, and the CSF concentration varied 7.5 fold between patients. Optimal use of mannitol during neurosurgery requires further prolonged study of its pharmacokinetics.

Adult↗
PubMed1988

The effect of isoflurane on cerebrospinal fluid pressure in patients undergoing neurosurgery.

Ten patients with intracerebral tumours (TC) and 13 patients with subarachnoid haemorrhage (SAH) from a ruptured cerebral arterial aneurysm were studied before intracranial surgery, and during a 3-h postoperative period. Cerebrospinal fluid pressure (CSFP) determined by an intraventricular (TC group) or intraspinal (SAH group) catheter, and mean arterial blood pressure (MABP) were recorded under neurolept anaesthesia (control) followed by isoflurane inhalation. These two measurements were performed during normocapnia. A third measurement was made during hypocapnia, with unchanged isoflurane concentration. After the experimental period, isoflurane remained the main anaesthetic agent throughout the surgical procedure. After recovery from anaesthesia, the patients were monitored with CSFP and blood pressure during the first postoperative hours, and the quality of breathing was assessed by hourly blood-gas analyses. The results show that isoflurane causes a 10-14% reduction of MABP with no further changes during hyperventilation. Mean CSFP increased 27% in the TC group, and 12% in the SAH group after isoflurane induction and decreased from these levels by 29% during hyperventilation in both groups. Consequently, the impact on cerebral perfusion pressure (CPP) by isoflurane was a 19% and 21% mean decrease in the TC and SAH group, respectively. Controlled hyperventilation reduced this effect by partially restoring control CPP values, with 8% and 14% increase, respectively. In the postoperative follow-up, all patients had normal breathing and blood pressure with low values of CSFP. It is concluded that isoflurane can be used in intracranial surgery with adequate safety if combined with controlled hyperventilation.

Adult↗
PubMed1988

Effects of adenosine-induced hypotension on myocardial hemodynamics and metabolism during cerebral aneurysm surgery.

The effects of adenosine-induced hypotension on central as well as myocardial hemodynamics and metabolism were studied in five neurolept-anesthetized patients without known heart or lung diseases, who were undergoing cerebral aneurysm surgery. Adenosine (217 +/- 32 micrograms.kg-1.min-1) decreased mean arterial pressure 30% from 77 +/- 5 to 54 +/- 3 mm Hg. Cardiac filling pressures and heart rate remained unchanged during hypotension. Adenosine decreased systemic vascular resistance 50 +/- 5% while cardiac index increased 39 +/- 10%. Coronary sinus blood flow increased by 73 +/- 13% from 128 +/- 18 to 224 +/- 36 ml/min with a concomitant decrease in calculated coronary vascular resistance (66 +/- 4%). Both systemic and myocardial arteriovenous oxygen content differences decreased, and myocardial oxygen consumption decreased 42 +/- 9%. There were no alterations in myocardial fractional lactate extraction. Arterial plasma renin activity and arterial catecholamine levels were unaffected by hypotension. It is concluded that adenosine hypotension in this group of patients produced a hyperkinetic circulation in the systemic as well as in the myocardial vascular bed. Cardiac output and coronary sinus blood flow increased at the same time as myocardial oxygen consumption decreased.

Adenosine↗
PubMed1987

Effect of adenosine on human cerebral blood flow as determined by positron emission tomography.

The effect of intravenous infusion of adenosine on CBF was studied in seven patients with cerebral arteriovenous malformation. The patients were examined with positron emission tomography with controlled ventilation using [15O] water and [11C] fluoromethane as tracers. Total and regional CBF were determined before and during infusion of adenosine at rates producing a reduction of the MABP by approximately 10-40%. Six patients were normoventilated, and one was hyperventilated. Mean CBF in areas with normal brain tissue was 54 ml/100 g/min before adenosine infusion under normoventilation. Adenosine infusion increased mean CBF with 23-85%. Mean CVR was decreased with 43-65% and exceeded the percentage reduction of MABP in all normoventilated subjects. In the hyperventilated patient, the reduction of CVR was similar to the reduction of MABP, and CBF was unaffected, except for the 30% increase in the thalamus. It is concluded that intravenous administration of adenosine produces marked cerebral vasodilation in normoventilated subjects and that this response can be counteracted by hyperventilation.

Adenosine↗
PubMed1987

Clinical experience with adenosine for controlled hypotension during cerebral aneurysm surgery.

The cardiovascular effects of adenosine-induced hypotension were studied in 47 patients undergoing intracranial vascular surgery under neurolept anesthesia. Adenosine infusion (214 +/- 18 micrograms X kg-1 X min-1) decreased mean arterial pressure (MAP) by 42 +/- 1% from 80 +/- 1 to 46 +/- 1 mm Hg for an average of 29 +/- 5 min of hypotension. Hypotension was associated with a minor increase in heart rate (13 +/- 2%) and with prolongation of the PR interval (9 +/- 2%). ST-T depression did not occur except in one patient with a previous history of myocardial infarction. The adenosine-induced increase in cardiac index (42 +/- 9%, n = 7) was associated with a 63 +/- 10% decrease in systemic vascular resistance index (n = 7) while the pulmonary capillary wedge pressure remained unchanged. Adenosine metabolism was limited and there was no accumulation of the end metabolite, uric acid. Serum creatinine levels were normal in all patients postoperatively. We conclude that adenosine rapidly induces a stable and easily controlled hypotension in man without tachyphylaxis or rebound hypertension. There were no signs of renal or myocardial dysfunction except for dysrhythmias that occurred in two patients with a history of myocardial infarction.

Adenosine↗
PubMed1986

Effect of hypotension induced by sodium nitroprusside on catecholamine overflow in the canine kidney.

The overflow of noradrenaline (NA) and dopamine (DA) to plasma in the kidney in response to hypotension induced by sodium nitroprusside were studied in barbiturate-anaesthetized dogs in order to evaluate the possible existence of separately regulated renal noradrenergic and dopaminergic nerve fibres. When mean arterial blood pressure was lowered to 55 +/- 5 mmHg, arterial plasma NA, DA and adrenaline concentrations were increased and renal blood flow decreased. Renal sympathetic nerve activity was assessed by measuring the renal overflow of catecholamines to plasma. To obtain more accurate estimates of the renal contribution to catecholamines in renal venous plasma we corrected for the renal extraction of arterial catecholamines, assessed by the extraction of endogenous adrenaline. The corrected renal NA overflow to plasma increased from 164 +/- 52 to 419 +/- 137 pmol min-1 (P less than 0.05) during sodium nitroprusside induced hypotension. The renal overflow of DA to plasma was, however, not influenced significantly. The DA/NA ratio for renal venous plasma concentration as well as for renal overflow to plasma was decreased (P less than 0.05) by sodium nitroprusside induced renal nerve activation. In contrast, electrical renal nerve stimulation has previously been shown to enhance the overflows of DA and NA in parallel. One possible interpretation of these findings is that sodium nitroprusside selectively activated renal noradrenergic but not the putative dopaminergic nerve fibres while electrical stimulation activated both types of fibres.

Animals↗