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Biomedical subjects

A Sollevi

Publications and source records attributed to A Sollevi.

At least 91 records · Page 5Linked to original sources
PubMed1990

Haemodynamic and metabolic effects of infused adenosine in man.

1. Haemodynamic and metabolic effects of intravenous infusion of adenosine, an endogenous vasodilator, were studied in healthy humans. 2. Catheters were inserted into pulmonary and brachial arteries and into the hepatic and subclavian veins. Cardiac output was determined according to the Fick principle, and splanchnic blood flow was measured by using extraction of Indocyanine Green. Skin blood flow was estimated by a laser Doppler technique, calf blood flow by venous occlusion plethysmography and skeletal muscle and adipose tissue blood flow by a local isotope clearance technique. 3. Adenosine (infused in steps from 40 to 80 micrograms min-1 kg-1 into a central vein) elicited a gradual reduction in the peripheral vascular resistance to less than 50% of the basal level. There was a slight increase in the systemic blood pressure, but the pulmonary arterial and the ventricular filling pressures were unchanged. Cardiac output was doubled, accomplished by a combination of a positive chronotropic effect and an increase in stroke volume, which may be secondary to diminished peripheral resistance. 4. Skin blood flow increased by 100% at 50 micrograms of adenosine min-1 kg-1, whereas splanchnic blood flow rose significantly at 60 micrograms of adenosine min-1 kg-1. Blood flow in the calf, gastrocnemius muscle and adipose tissue did not change significantly. 5. Arterial concentrations of noradrenaline and adrenaline increased by 62 and 43%, respectively, during infusion of adenosine. Arterial levels of glycerol were depressed by more than 50%, but those of glucose and pyruvate were unchanged. 6. In conclusion, exogenous adenosine caused a marked systemic vasodilatation, with different responsiveness in the investigated vascular beds.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1990

Plasma neuropeptide Y on admission to a coronary care unit: raised levels in patients with left heart failure.

STUDY OBJECTIVE - The aim of the study was to measure plasma neuropeptide Y, which is related to sympathetic nerve stimulation, in patients admitted to a coronary care unit and to relate the findings to clinical information. DESIGN - Plasma neuropeptide Y was measured on admission and the results were related to the cause of admission and to clinical information collected prospectively and retrospectively. SUBJECTS - Plasma subjects were obtained from 377 consecutive daytime admissions to the coronary care unit at Södersjukhuset. Results of only the first sample in each patient are included in this study, so 45 cases observed more than once (readmitted patients) were omitted. Six samples were abandoned because of technical failures. The study therefore comprises 326 patients. Clinical diagnoses were defined as acute myocardial infarction, arrhythmia, angina pectoris, and miscellaneous (all other diagnoses). Heart failure was defined according to a modified Killip scheme. MEASUREMENTS and RESULTS - Neuropeptide Y like immunoreactivity was measured by radio-immunoassay. Plasma concentrations above normal (greater than 30 pmol.litre-1) were found in association with: increased age, female sex, diuretic treatment, tachycardia, arterial hypotension, increased respiratory rate, and mortality in the unit. There was a strong relationship between high neuropeptide Y concentrations and: moderate left heart failure (63%), pulmonary oedema (90%), and cardiogenic shock (100%). Of patients without heart failure only 25% had raised neuropeptide Y. In multivariate analysis, the severity of heart failure (Killip class), heart rate and respiratory rate were the only variables that were significantly and independently related to plasma neuropeptide Y. CONCLUSIONS - The presence and degree of circulatory disturbance, in particular tachycardia and left heart failure, were strongly related to increased plasma concentrations of neuropeptide Y in coronary care patients.

Aged↗
PubMed1990

Release of neuropeptide Y and noradrenaline from the human heart after aortic occlusion during coronary artery surgery.

STUDY OBJECTIVE: The aim was to study the influence of complete myocardial ischaemia during aortic occlusion on release of neuropeptide Y and noradrenaline from the human myocardium. DESIGN: Coronary sinus neuropeptide Y and noradrenaline were measured after 46(SEM 7) min of aortic occlusion with cold cardioplegia in patients undergoing coronary artery surgery. Patients - Seven patients (all male), aged 64(SEM 3) years, were studied. All were undergoing coronary artery bypass grafting. MEASUREMENTS AND MAIN RESULTS: Reperfusion was associated with an increase in coronary sinus blood flow as determined by thermodilution. Simultaneously there was cardiac release of both neuropeptide Y and noradrenaline during the first two sampling periods: 3(0.6) and 7(0.6) min after the start of reperfusion. The outflow of neuropeptide Y and noradrenaline returned to preischaemic values by 14(1) min after reperfusion. Coronary sinus blood lactate and pyruvate concentrations were also increased at the start of reperfusion, while the lactate/pyruvate ratio remained unchanged. Myocardial oxygen uptake was not influenced by cardiac ischaemia. CONCLUSIONS: Ischaemia of the human heart in vivo is associated with an enhanced outflow of neuropeptide Y and noradrenaline from the heart. Since arterial blood concentrations of these substances were also increased on reperfusion, their release is probably due to increased sympathetic nerve activity, though other mechanisms such as temperature change and local metabolite formation could also participate. Local release of neuropeptide Y during cardiac ischaemia may be involved in the regulation of coronary vascular tone as well as in the release of noradrenaline and acetylcholine.

Aorta, Thoracic↗
PubMed1990

Elevation of plasma neuropeptide Y-like immunoreactivity and noradrenaline during myocardial ischaemia in man.

Plasma levels of neuropeptide Y-like immunoreactivity (NPY-LI) and noradrenaline were studied for 25 h in 22 patients with acute ischaemic heart disease. On admission, NPY-LI levels were above normal in 16 patients, and 20 patients had increased noradrenaline levels. The initial plasma NPY-LI did not differ between patients with acute myocardial infarction (AMI) and angina pectoris. Initial plasma noradrenaline levels were higher in patients with AMI than in those with angina pectoris. Plasma levels of noradrenaline remained elevated in AMI patients, but decreased towards normal values in patients with angina pectoris. Levels of NPY-LI returned to normal within 25 h in all patients. Tachycardia and left ventricular failure were related to high NPY-LI and noradrenaline levels. A positive correlation was found between noradrenaline and NPY-LI in plasma. It is suggested that neuropeptide Y (NPY), an endogenous vasoconstrictor peptide, should be considered as one of the mediators involved in the cardiovascular response to sympathetic activation induced by myocardial ischaemia.

Aged↗
PubMed1990

Controlled hypotension with adenosine or sodium nitroprusside during cerebral aneurysm surgery: effects on renal hemodynamics, excretory function, and renin release.

Adenosine, a potent vasodilator both in animals and in humans, has been used to produce controlled hypotension in patients, especially during cerebral aneurysm surgery. However, in animals adenosine by intrarenal infusion decreases renal blood flow (RBF), glomerular filtration rate (GFR), urine flow, and causes an inhibition of renin secretion. In this study we evaluated the effect of adenosine on RBF in patients (n = 15) scheduled for cerebral aneurysm surgery who had been anesthetized with a modified neurolept-anesthesia during controlled hyperventilation. Perioperative hypotension was achieved with infusion of adenosine (252.8 +/- 55.8 micrograms.kg-1.min-1) (n = 8) or sodium nitroprusside (2.5 +/- 0.8 micrograms.kg-1.min-1) (n = 7). Mean arterial pressure was lowered by 25%-30%, to approximately 60-70 mm Hg, in both groups. Glomerular filtration rate and RBF were measured using standard renal clearance methods for 51Cr-ethylenediaminetetraacetic acid and paraaminohippuric acid. Urine and blood samples were collected during normotension before and after a bolus dose of hypertonic mannitol, during hypotension, and during normotension after clipping of the aneurysm. Adenosine induced a marked decrease in GFR (-91%) and RBF (-92%), and a pronounced increase in renal vascular resistance. Sodium nitroprusside caused a significantly (P less than 0.01) less pronounced decrease in GFR (-24%) and RBF (-36%), but did not affect renal vascular resistance. After discontinuation of the hypotensive agents, GFR returned to baseline levels in both groups. Renal blood flow, however, increased above baseline after discontinuation of adenosine (+93%) but not after sodium nitroprusside. Sodium nitroprusside increased renin secretion, which was not seen with adenosine. Four patients in the adenosine group developed reversible atrioventricular conduction disturbances.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1989

Pharmacological characterization of neuropeptide Y and noradrenaline mechanisms in sympathetic control of pig spleen.

The mechanisms underlying the functional effects of neuropeptide Y (NPY)-like immunoreactivity (LI) and noradrenaline (NA) and their release evoked by nerve stimulation were studied with the blood-perfused pig spleen in vivo. Infusion of selective agonists and antagonists suggested the presence of alpha 1- and beta 2-adrenoceptors mediating vasoconstriction and vasodilatation, respectively. NPY caused a slight inhibition of stimulation-evoked [3H]NA release and a clearcut non-adrenergic vasoconstriction. Local pretreatment with phentolamine and prazosin as well as with clonidine and UK 14304 reduced the perfusion pressure response to nerve stimulation. Phentolamine, yohimbine and idazoxan enhanced while clonidine and UK 14304 decreased the output of [3H]NA or NA and NPY-LI. The subsequent addition of propranolol to the alpha-adrenoceptor antagonists was followed by reappearance at a considerable portion of the perfusion pressure response while the output of [3H]NA or NA and NPY-LI was slightly reduced. It is concluded that NPY exerts pre- and post-junctional actions in pig spleen that regulate both NA release and vascular tone. alpha 1-Adrenoceptors are mainly involved in vasoconstriction, and prejunctional alpha 2 mechanisms inhibit both NA and NPY release at a low frequency of stimulation. beta 2-Adrenoceptors mediate vasodilatation when NA release is enhanced with a minor effect on mediator secretion.

Animals↗
PubMed1989

Co-release of neuropeptide Y and noradrenaline from pig spleen in vivo: importance of subcellular storage, nerve impulse frequency and pattern, feedback regulation and resupply by axonal transport.

The importance of subcellular storage, nerve impulse rate and pattern, and feedback regulation, as well as resupply by axonal transport for the release of noradrenaline and neuropeptide Y-like immunoreactivity, was studied in the blood perfused pig spleen in vivo. Vasoconstrictor responses were recorded as perfusion pressure changes. Subcellular fractionation experiments using sucrose density gradients showed a bimodal distribution of noradrenaline (peak concentrations at 0.8 and 1.1 M sucrose) while only one main peak of neuropeptide Y was present (at 1.1 M sucrose). Overflow suggesting release of noradrenaline and neuropeptide Y-like immunoreactivity could be detected after 10 s stimulation at 10 Hz. The ratio for the output of noradrenaline and neuropeptide Y upon continuous nerve stimulation in control animals decreased with frequency. After inhibition of noradrenaline reuptake by desipramine the vasoconstrictor response and noradrenaline output were enhanced while the corresponding overflow of neuropeptide Y was reduced by 50% at 0.5 Hz. Stimulation with the irregular or regular bursting patterns at high frequencies caused larger perfusion pressure increase and relative enhancement of neuropeptide Y output compared to noradrenaline than a continuous stimulation both before and after desipramine treatment. A similar fractional release per nerve impulse was calculated both for [3H]noradrenaline (5.6 +/- 1.0 x 10(-5) and neuropeptide Y (7.3 +/- 0.3 x 10(-5). After reserpine treatment combined with preganglionic denervation the vasoconstrictor responses were more long-lasting, neuropeptide Y release was enhanced while noradrenaline content and release were reduced by 99%. The difference in neuropeptide Y overflow between continuous and bursting types of stimulation was smaller after reserpine treatment. After prolonged intermittent stimulation with regular bursts (20 Hz) for 1 h the splenic content of neuropeptide Y was reduced by 58%, while no change was observed for noradrenaline. The maximal perfusion pressure increase upon prolonged nerve stimulation after reserpine was similar in control and reserpine-treated animals, but after reserpine the vasoconstrictor response and neuropeptide Y release were subjected to fatigue. Ligation experiments of the splenic nerves revealed the splenic neuropeptide Y content was resupplied by axonal transport with a calculated total tissue turnover time of 11 days. In contrast, axonal transport contributed only to a marginal extent for the resupply of noradrenaline.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1989

Circulatory and metabolic events in pig island skin flaps after arterial or venous occlusion.

After 1 hour of arterial or venous occlusion, the circulatory and metabolic events in island skin flaps of the pig were studied. Both occlusion types showed significant but transient increases in glucose uptake and a parallel release of lactate, hypoxanthine, and potassium. Oxygen uptake and noradrenaline release were not significantly affected. No significant difference between the arterial and venous occlusions was seen in the metabolic parameters. The flap blood flow, measured by total venous outflow and laser Doppler flowmetry, was significantly lower after venous than after arterial occlusion. This long-lasting difference in flow response may help to explain the observation that venous occlusion is more deleterious to skin flaps than arterial occlusion. A mechanism underlying these results may be more pronounced microthrombotization and/or edema formation after venous occlusion than after arterial occlusion.

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↗
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↗