Biomedical subjects

M Lagerkranser

Publications and source records attributed to M Lagerkranser.

36 records · Page 2Linked to original sources

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↗

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↗

PubMed1985

Blood coagulation and fibrinolytic factors as well as their inhibitors in trauma.

Tests generally accepted in the diagnosis of DIC were evaluated in 13 patients with multiple trauma. The blood samples were drawn on admission before treatment with blood, blood products or heparin. The tests included platelet count, prothrombin complex (Normotest/Thrombotest), Factor V, Factor VIII:C, fibrinogen, fibrinogen degradation products (FDP), thrombin and Reptilase times as well as the ethanol gelation test (fibrin monomer). Based on the results of the tests, the patients were categorized into DIC, suspected DIC and no DIC groups. It was found that those patients who were referred to the DIC group were also those who later developed the most severe organ dysfunction and who stayed the longest time in the Intensive Care Unit. Thus, the clinical and laboratory findings agreed. The Normotest/Thrombotest ratio, thrombin times and Reptilase times, and presence of fibrin monomers were of limited value for the diagnosis of DIC. To make a correct diagnosis, the results of several of the conventional tests had to be combined. Additional tests were then evaluated. An increase of the fibrinopeptide A (FPA) level and the Factor VIIIR:Ag (vWF:Ag)/Factor VIII:C ratio in all the DIC patients as well as a decrease of the antithrombin (AT) level in some DIC patients indicated thrombin activity and a risk of thromboembolic events. A decrease of plasminogen and alpha 2-antiplasmin indicated activation of the fibrinolytic system. It is concluded that these new tests are useful in the diagnosis and treatment of DIC and similar proteolytic states.

Adolescent↗

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

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↗

PubMed1983

Effects of mannitol on blood volume and central hemodynamics in patients undergoing cerebral aneurysm surgery.

The effects on hemodynamics and blood volume of 500 ml of 20% mannitol administered intravenously in 15 min at the beginning of cerebral aneurysm surgery have been studied in 10 patients. Measurements were made before the infusion of mannitol (control) and at 15-min intervals for 1 hr. Control measurements showed normal hemodynamic data, while blood volume was lower than normal (P less than 0.001). Immediately after the mannitol infusion cardiac index (25%; P less than 0.01), pulmonary capillary wedge pressure (48%; P less than 0.001), and blood volume (43%; P less than 0.001) increased. Thirty minutes after the mannitol infusion, blood volume had returned to control levels, while the cardiac index and pulmonary capillary wedge pressure decreased 21% (P less than 0.01 and P less than 0.05, respectively) below control levels. Forty-five minutes after the mannitol infusion, serum osmolality and urine volume remained high. Our data confirm the presence of hypovolemia in patients with subarachnoid hemorrhage and a transient increase in blood volume associated with the infusion of mannitol. The data emphasize, however, that the hemodynamic response is biphasic, with an initial increase in pulmonary capillary wedge pressure and cardiac index, followed by a hypokinetic circulatory pattern with pulmonary capillary wedge pressure and cardiac index below control levels. The hypokinetic state occurred in spite of return of blood volume to control levels, suggesting that redistribution of blood from central to peripheral circulatory compartments had occurred.

Adult↗

PubMed1982

Cardiovascular effects of nitroglycerin as a hypotensive agent in cerebral aneurysm surgery.

The cardiovascular effects of nitroglycerin (TNG) were studied in 20 patients undergoing cerebral aneurysm clipping under controlled hypotension. Total oxygen consumption was also calculated in 15 patients. Mean arterial blood pressure was reduced by 36% from 91 to 58 mmHg (12.1 to 7.7 kPa) by TNG due to decrease in both total peripheral resistance (16%) and cardiac output (24%). Right atrial and pulmonary capillary wedge pressures were reduced during hypotension, indicating a decrease in venous return to the heart. There were no significant changes in total oxygen consumption. It is concluded that the fall in cardiac output results from a reduction in central blood volume due to venous pooling of blood, and that TNG has no major overall metabolic effects.

Adult↗

PubMed1982

Neurogenic pulmonary oedema. A review of the pathophysiology with clinical and therapeutic implications.

Five cases of neurogenic pulmonary oedema (NPE) are described. The causes were mechanical trauma to the skull, subarachnoid haemorrhage and epileptic seizure. In every case a frank pulmonary oedema was diagnosed that resolved within a few days. Treatment of the underlying disease resulted in a favourable outcome. The literature has been reviewed. The basic mechanism seems to be an increased intracranial pressure (ICP) precipitating an increased central sympathetic nerve activity mediated via peripheral alpha- or beta-adrenergic discharge. NPE results from a predominant alpha-receptor stimulation with massive increase in pre- and afterload. The major therapeutic efforts should be directed towards the underlying cause and, in addition, mechanical ventilation with passive hyperventilation is vital. High positive end-expiratory pressure should not be used without strict monitoring of ICP.

Adult↗

PubMed1980

Cardiovascular effects of sodium nitroprusside in cerebral aneurysm surgery.

Cardiovascular effects of sodium nitroprusside (SNP) were studied in 17 patients undergoing cerebral aneurysm surgery under controlled hypotension. In 10 patients oxygen uptake was also calculated. Mean arterial blood pressure was decreased from 91 to 58 mmHg by SNP due to reductions in both total peripheral resistance (29%) and cardiac output (15%). Mean right atrial and pulmonary capillary wedge pressures were reduced during hypotension. Total oxygen uptake remained constant throughout the procedure. There was no significant change in arterial oxygen tension in the hypotensive period, but after discontinuation of SNP infusion it was significantly increased. The haemodynamic effects of SNP in patients with a recent subarachnoid haemorrhage and its effect on blood oxygenation are discussed. It is concluded that the fall in cardiac output is related to a reduction of central blood volume and might be more pronounced in these patients than in normal subjects.

Adult↗

PubMed1979

Sodium nitroprusside as a hypotensive agent in intracranial aneurysm surgery.

Sodium nitroprusside (SNP) was used to induce hypotension during intracranial aneurysm surgery in 67 patients. The effects of SNP infusion (0.1 mg/ml) on blood pressure were rapid and it was easy to adjust blood pressure to desired levels in most patients. When SNP was stopped, the blood pressure returned instantly to the initial level. In eight patients an increase to about 25% or more above prehypotensive level was seen, counteracted in two patients by administration of small doses of halothane. There was a mean increase of 36% in heart rate. Total doses of SNP were 0.05--120 mg (mean: 10.8), corresponding to 0.08--6.8 micrograms/kg/min (mean: 1.9). No metabolic acidosis indicating cyanide intoxication was observed. Tachyphylaxis was seen in three patients, and SNP had to be discontinued in one. It is concluded that SNP gives a rapid and effective hypotension but tachyphylaxis and subsequent danger of cyanide intoxication exist. Therefore, in some cases SNP has to be replaced by or combined with some other hypotensive agent to achieve the desired effect. As there is a risk of impairment of cerebral autoregulation after the use of SNP, it is important to avoid sudden and prolonged blood pressure fluctuations, and to continue with controlled hyperventilation in the postoperative period to reduce the risk of brain oedema and high intracranial pressure.

Adolescent↗