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Biomedical subjects

A Sollevi

Publications and source records attributed to A Sollevi.

At least 109 records · Page 6Linked 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↗
PubMed1989

Evidence for co-transmitter role of neuropeptide Y in the pig spleen.

1. The possible involvement of neuropeptide Y (NPY) in relation to noradrenaline (NA) and adenosine triphosphate (ATP) mechanisms in the sympathetic nervous control of the vascular tone and capsule contraction in the blood perfused pig spleen was investigated in vivo. 2. Local injections or infusions of NA, NPY and alpha-, beta-methylene ATP (mATP) caused vasoconstriction (perfusion pressure increase) and capsule contraction (increased venous blood flow). ATP only evoked vasodilatation. NPY was about 50 fold more potent than NA as a vasoconstrictor, and the NPY response was more long-lasting. Reserpine treatment did not change the effects of NPY. 3. Electrical stimulation of the splenic nerves in control animals caused a frequency-dependent, guanethidine-sensitive output of both NPY-like immunoreactivity (-LI) and NA, suggesting co-release. The output of NPY-LI relative to NA was enhanced at high frequency stimulation. Furthermore, alpha-adrenoceptor blockade by phentolamine enhanced both the output of NPY-LI and NA while inhibition of the neuronal uptake of NA with desipramine reduced the low frequency stimulation-evoked overflow of NPY-LI. Preganglionic denervation did not change the output of NPY-LI or NA. 4. Reserpine treatment reduced both the splenic content of NA and NPY-LI. Preganglionic denervation inhibited the reserpine-induced depletion of the NPY content but not of NA in terminal areas. The stimulation-evoked NPY overflow was markedly enhanced, especially at low-frequency stimulation after reserpine, and the plasma levels of NPY-LI in the venous effluent were then in the nmolar range (i.e. where exogenous NPY induced vasoconstriction). The perfusion-pressure increase upon stimulation in reserpine-treated, preganglionically-denervated animals was highly correlated (r = 0.91) to the NPY overflow. The functional 0.5 Hz responses were reduced after reserpine, while at higher frequencies the functional effects were of similar magnitude to controls but longer-lasting. 5. Tyramine induced a release of NA but not of NPY-LI. Furthermore, the increase in perfusion pressure induced by tyramine was absent after reserpine. 6. After tachyphylaxis to the vasoconstrictor effects of mATP, the nerve stimulation-evoked, functional response as well as the NA and NPY-LI overflow were unchanged. After reserpine treatment, both the perfusion-pressure increase and NPY-LI overflow to nerve stimulation were reduced after mATP tachyphylaxis. 7. In conclusion, release of NPY rather than ATP may explain the long-lasting, non-adrenergic, splenic functional responses in reserpinized animals upon sympathetic stimulation. However, NA is most likely the main splenic transmitter when low-frequency stimulation is used under control conditions.

Adenosine Triphosphate↗
PubMed1989

The role of adenosine and prostacyclin in coronary flow regulation in healthy man.

Coronary flow regulation in man is incompletely understood. We addressed the hypothesis that endogenous adenosine and prostacyclin (PGI2) affect basal coronary tone and/or the coronary flow response to increased myocardial work. In healthy volunteers coronary sinus flow and cardiac oxygen extraction were measured at rest and during leg exercise (40-50 W), before and after i.v. administration of theophylline (to block adenosine receptors) and oral administration of ibuprofen (to inhibit prostaglandin synthesis). Before drug, the basal coronary flow was 118 +/- 23 ml min-1 and the cardiac extraction of oxygen 122 +/- 3 ml l-1. Leg exercise elevated coronary flow by 89 +/- 16 ml min-1. Theophylline, at a dose blocking the coronary flow response to dipyridamole (an adenosine-dependent mechanism), induced a moderate increase in myocardial oxygen extraction (by 11%, P less than 0.05), but failed to affect either the basal coronary flow (105 +/- 16 ml min-1) or the increase during exercise (88 +/- 25 ml min-1). Ibuprofen inhibited the urinary excretion of PGI2 metabolite by about 90%, but did not affect basal coronary tone or the coronary response to exercise. These data indicate that endogenous adenosine is of limited importance for normal coronary regulation in man, and that PGI2 has no effect.

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↗
PubMed1989

The effect of diclofenac sodium on renal function.

The effects of diclofenac sodium on the kidneys were studied during 4 1/2 hours in eight patients with normal renal function. Urinary output decreased within 10 min after the injection, and maximally by 80%. The renal plasma flow and the glomerular filtration rate initially diminished significantly, by 35%, but began to increase after only 2 hours. The dominant and persistent effect was reduction of free water clearance, with maximum fall from 5.9 to 0.08 ml/min after 2 1/2 hours. The long-lasting increased tubular reabsorption of water probably is important for the lowered intrapelvic pressure that is associated with good analgetic effect of diclofenac in ureteral colic.

Adult↗
PubMed1989

Adenosine-induced increase in graft flow during coronary bypass surgery.

The influence of systemic adenosine infusion (30-50 micrograms/kg/min) on peroperative coronary graft flow was investigated in 16 patients undergoing bypass surgery. The central hemodynamic and graft flow (electromagnetic flow determination) responses were studied after 5-min, and in nine patients also after 30-min infusion. The low-dose adenosine infusion had little effect on the central hemodynamic parameters, while the graft flow increased in all patients (mean 84 +/- 12%, total 22 grafts). The adenosine-induced increase in graft flow was maintained when the infusion was prolonged. It is concluded that adenosine can produce marked coronary vasodilation in man at infusion rates that exert only minor systemic hemodynamic effects.

Adenosine↗
PubMed1989

Early circulatory and metabolic events in island skin flaps of the pig.

Circulatory and metabolic skin-flap events were studied prior to and up to 6 hours after elevation of buttock island flaps in pigs. During the elevation, significant reductions in superficial skin blood flow, measured by laser Doppler flowmetry (LDF) and dermal flap temperature, were seen. Significant correlations were found between blood flow and temperature. Total flap blood flow, measured as venous outflow, also showed an initial transient decrease, but 2 hours after flap construction, venous outflow had returned to preoperative values. A significant increase in lactate release, together with increased oxygen consumption and glucose uptake, was seen 4 hours after the surgical intervention. Hypoxanthine release, indicating ischemia, was seen only during the first hour after flap elevation. Noradrenaline outflow was noted after 4 and 6 hours, but there was no parallel reduction in flap blood flow. A great deal of the flow reduction in acutely elevated island flaps may thus be due to primary hypothermia rather than to the degenerative release of noradrenaline, which seems to have no early effect on skin flap blood flow. On the other hand, the noradrenaline release may be linked to an increased metabolic activity in the skin flaps.

Animals↗
PubMed1988

Neuropeptide Y- and alpha-adrenergic receptors in pig spleen: localization, binding characteristics, cyclic AMP effects and functional responses in control and denervated animals.

The localization of neuropeptide Y binding sites in the pig spleen, as revealed by [125I]Bolton-Hunter-labelled porcine neuropeptide Y and alpha 1-adrenergic receptor binding sites, as revealed by [125I](2-beta/4-hydroxy-phenyl/-ethylaminomethyl)-tetralone as radioligand, was compared with the distribution of neuropeptide Y and noradrenaline nerves, the latter revealed by tyrosine hydroxylase and dopamine-beta-hydroxylase, using immunohistochemistry. A large degree of codistribution was obtained between [125I]neuropeptide Y and alpha 1-binding sites in the capsule, trabeculae, blood vessels and the red pulp of the spleen. Neuropeptide Y and tyrosine hydroxylase as well as dopamine-beta-hydroxylase-positive nerves were identical in the spleen and had a similar gross distribution pattern as the [125I]neuropeptide Y and alpha 1 binding sites. In functional studies using the isolated blood-perfused spleen from pentobarbital-anaesthetized pigs, neuropeptide Y, noradrenaline and the alpha 1-selective agonist phenylephrine contracted the capsule and induced vasoconstriction in the spleen in vivo. However, the selective alpha 2-adrenoceptor agonists clonidine and azepexole had no effects on blood flow or perfusion pressure, suggesting that postjunctional alpha-receptors were of the alpha 1 type. Neuropeptide Y inhibited the forskolin-evoked, cyclic adenosine monophosphate formation in vitro. The [125I]neuropeptide Y binding, with an equilibrium-dissociation constant of 503 +/- 73 pM and a maximal number of specific binding sites of 23 +/- 3 fmol/mg protein, the neuropeptide Y-induced perfusion-pressure increase in vivo and the inhibition of forskolin-evoked cyclic adenosine monophosphate formation in vitro were dependent on the amidation of the C-terminal portion of the peptide molecule. Furthermore, the effects of neuropeptide Y were not changed by alpha- and beta-adrenoceptor blockade using prazosin and propranolol. Two weeks after postganglionic denervation the neuropeptide Y and the noradrenaline contents of the pig spleen were reduced by 97% and 99%, respectively. These changes were associated with a selective supersensitivity for the noradrenaline-induced perfusion-pressure increase in vivo compared with the effect of neuropeptide Y. However, a similar potentiation of the noradrenaline effect was induced by the monoamine-uptake blocker desipramine in the absence of denervation, and there was no change in the functional response to phenylephrine after denervation.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1988

Effects of adenosine-induced hypotension on myocardial hemodynamics and metabolism in fentanyl anesthetized patients with peripheral vascular disease.

The effects of adenosine on central and myocardial hemodynamics and metabolism were evaluated during fentanyl anesthesia (100 micrograms.kg-1) in six patients with peripheral vascular disease. Adenosine was intravenously infused, at a rate of 90 +/- 20 (SEM) micrograms.kg-1.min-1, to reduce mean arterial blood pressure by approximately 20% (23 +/- 2% SEM, from 82 +/- 3 to 63 +/- 3 SEM mmHg) during a 20-min period. Systemic and pulmonary vascular resistance indices decreased by 36 +/- 3 and 32 +/- 6% (SEM), and cardiac index increased by 18 +/- 5%. Heart rate, ventricular filling pressures, and whole body oxygen consumption were not affected by adenosine. Despite the reduced mean arterial blood pressure, coronary sinus flow increased by 128 +/- 26% (SEM) in parallel with a 96 +/- 11% (SEM) increase in coronary sinus oxygen content. Left and right ventricular stroke work indices, as well as myocardial oxygen consumption, were maintained. ECG (12-lead) demonstrated signs of ischemia in one subject, while myocardial lactate uptake was unchanged in all subjects. In conclusion, adenosine-induced hypotension in patients with peripheral vascular disease increased cardiac index without affecting myocardial work, whole body, and myocardial oxygen consumptions. The marked increase in coronary sinus blood flow, indicating coronary vasodilation, was not related to increased myocardial work. Further information regarding myocardial effect of adenosine in patients with ischemic heart disease is warranted.

Adenosine↗
PubMed1988

Influence of adenosine-induced hypotension on the canine myocardium rendered acutely ischaemic by artificial stenosis.

An open-chest preparation was carried out in 14 pentobarbitone anaesthetized dogs in order to evaluate the myocardial effects of controlled hypotension induced by adenosine in the presence of a severe coronary stenosis that caused ischaemia of the left anterior ventricular wall. Myocardial performance, blood flow and metabolism were studied before and during a 78 +/- 3% reduction of flow in the left anterior descending coronary artery (LAD) and during adenosine-induced hypotension (approximately 40% reduction of the mean arterial pressure) in the presence of the LAD stenosis. The LAD stenosis decreased the myocardial lactate uptake (P less than 0.01), increased ST-T segment depression (P less than 0.05) of the left ventricular subendocardial ECG, and reduced cardiac output by 10% (P less than 0.05). In the presence of stenosis, the mean arterial pressure was reduced by adenosine from 10.4 +/- 0.6 kPa to 6.3 +/- 0.2 kPa for 15 min. Heart rate decreased by 22% (P less than 0.01). There was no change in cardiac output during hypotension, while the rate-pressure product decreased by 47% (P less than 0.01) and myocardial oxygen consumption decreased by 30 +/- 7%. Adenosine increased the coronary sinus blood flow by 52% (P less than 0.01), while the LAD flow distal to the stenosis was not significantly reduced. Myocardial lactate uptake was not further reduced and subendocardial ECG signs of ischaemia were not aggravated by the hypotension. In conclusion, adenosine-induced hypotension did not aggravate the subendocardial ECG signs of acute poststenotic myocardial ischaemia. Nor did myocardial lactate determinations indicate aggravation of myocardial ischaemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1988

Hypotensive anesthesia and blood loss.

Controlled hypotension reduces blood loss during defined major surgical procedures, which in turn will minimize transfusion needs and thereby the risks of transmission of infectious diseases. There is no evidence that hypotension below 8 kPa (60 mmHg) (MAP) is associated with better blood-sparing effects than a more moderate hypotension, but it will probably increase the risk of cardiovascular complications. Therefore, controlled hypotension, being a sophisticated technique, requires handling by an experienced anesthetist well aware of contraindications and the need for adequate monitoring for prevention of tissue ischemia. Large randomized and prospective studies are still warranted, especially for further evaluation of the risk-benefit with controlled hypotension.

Anesthesia↗
PubMed1988

Increased IMP content in glycogen-depleted muscle fibres during submaximal exercise in man.

To study the relationship between glycogen depletion and IMP accumulation in different fibre types, single fibres were dissected from biopsies taken at rest and after one hour of exercise at 70% of maximal oxygen uptake. These fibres were analysed histochemically for glycogen and fibre types and pooled into classes of type I or type II fibres with low, medium or high glycogen content, in a total of six classes. These pools were analysed for ATP, ADP, AMP and IMP contents by high performance liquid chromatography. The contents of ATP, ADP and AMP at rest, and immediately after exercise, were not significantly different between the six fibre classes. The IMP content in glycogen-depleted fibres obtained after exercise was, however, higher than in pools of glycogen-filled fibres obtained both at rest and after exercise. In conclusion, the elevated IMP content in glycogen-depleted but not in glycogen-filled type I and type II muscle fibres during prolonged submaximal exercise indicates a decreased ATP regeneration rate in glycogen-depleted fibres, which may be a factor limiting exercise duration during prolonged submaximal exercise.

Adenosine Diphosphate↗
PubMed1988

Influence of infused adenosine on bronchial tone and bronchial reactivity in asthma.

Adenosine has been found to contract human bronchial smooth muscle in vitro and to induce bronchoconstriction in asthmatic patients when administered by inhalation. The aim of the present study was to investigate if elevation of circulating levels of adenosine influence bronchial tone or bronchial reactivity. Seven patients with bronchial asthma in whom bronchial hyperreactivity had been confirmed in a pretrial bronchial histamine challenge (PC20 FEV1 0.064 to 2.45 mg/ml) received intravenous infusions of adenosine in increasing doses (10, 30 and 50 micrograms/kg/min, 6 min on each dose step) or placebo (saline solution) on two different days in a randomized, single-blind manner. Heart rate, blood pressure and lung function (lung volumes, flow-volume loops and airway conductance) were measured on each dose step. Infusion rate was held constant (at 50 micrograms/kg/min) throughout the trial and a bronchial methacholine challenge was performed during the infusion of adenosine or placebo. Infusions of adenosine and placebo did not influence heart rate, blood pressure or bronchial tone on either day and bronchial reactivity was similar on both days. We conclude that bronchial tone and bronchial reactivity in asthmatic patients are not increased by intravenously administered adenosine at a dose level which, in other studies, has been shown to induce regional effects in the systemic arterial circulation.

Adenosine↗
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

Evidence for an anti-aggregatory effect of adenosine at physiological concentrations and for its role in the action of dipyridamole.

The effects of physiological adenosine concentrations on platelet aggregation in vitro were studied. Furthermore, we evaluated the effect of elevated adenosine levels in vivo, produced by the administration of dipyridamole, on platelet aggregation in whole blood. Platelet aggregation in plasma was significantly inhibited in vitro by adenosine at all concentrations tested in the physiological range (0.1-1.0 microM, 14-63% inhibition). Dipyridamole by itself had no effect at a therapeutic plasma concentration in vitro. Ten patients with ischaemic cerebrovascular disease were given 100 mg dipyridamole orally, and the level of adenosine increased from 0.22 to 0.29 microM (p less than 0.05). This was accompanied by a decrease in ADP-induced platelet aggregation in whole blood (17 to 15 ohms, p less than 0.05). When dipyridamole was infused in 11 healthy subjects, the adenosine level was not significantly elevated but the platelet aggregation was inhibited (from 13 to 11 ohms, p less than 0.05). It is concluded that adenosine may be of importance in the physiological regulation of platelet aggregation. Furthermore, dipyridamole treatment is associated with an anti-aggregatory effect that is probably mediated by its effect on endogenous adenosine levels.

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

Adenine nucleotide degradation in the human myocardium during cardioplegia.

The tissue content of adenine nucleotides and their metabolites, inosine monophosphate, adenosine, hypoxanthine, and uric acid, were determined in biopsy specimens from the left ventricle of six patients during cardioplegia for open heart surgery. Biopsy specimens were collected immediately after the induction and at the end of cardioplegia (51-82 min) and were analysed by high performance liquid chromatography. After the induction of cardioplegia (cold potassium enriched solution) the left coronary artery was continuously perfused with cold (10 degrees C), potassium enriched, diluted blood. The adenosine triphosphate concentration decreased from 13 to 8 mmol.kg-1 dry muscle (p less than 0.01) during cardioplegia. Adenosine diphosphate and adenosine monophosphate concentrations were 6 and 3 mmol.kg-1 dry muscle respectively and remained unaffected. The adenosine concentration (0.3 mmol.kg-1 dry muscle) was three times higher than that of inosine monophosphate. Inosine concentrations increased from 0.8 to 2.7 mmol.kg-1 dry muscle (p less than 0.01) in parallel with the increase in hypoxanthine from 0.1 to 0.4 mmol.kg-1 dry muscle (p less than 0.01). The total adenine nucleotide pool decreased by 5 mmol.kg-1 dry muscle (p less than 0.01), whereas the corresponding increase in nucleotides and bases only was 2 mmol.kg-1 dry muscle. In conclusion, the adenosine triphosphate content and the adenine nucleotide pool were appreciably reduced during continuous cold blood cardioplegia as used in the present study. The tissue content of adenosine and further metabolites was considerably increased.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenine Nucleotides↗