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Biomedical subjects

A Sollevi

Publications and source records attributed to A Sollevi.

At least 73 records · Page 4Linked to original sources
PubMed1994

The influence of adenosine, ketamine, and morphine on experimentally induced ischemic pain in healthy volunteers.

Adenosine, intrathecally administered, produces antinociception in experimental studies on animals. The effect of intravenous (i.v.) adenosine on experimentally induced pain in humans has not been studied. The present single-blind, randomized, placebo-controlled study was conducted in nine healthy volunteers. The pain-reducing effects of adenosine (70 micrograms.kg-1.min-1 i.v.), morphine (0.1 mg/kg i.v.), ketamine (0.1 mg/kg i.v.), adenosine + morphine, and adenosine + ketamine were compared to each other and to placebo in random order. Ischemic pain was induced by the submaximum effort tourniquet technique. Pain was assessed using the visual analog scale (VAS, 0-100 mm). The sums of pain scores (SPS) were compared and found significantly 30%-40% lower for adenosine as well as for the other compounds and combinations (P < 0.03), compared to placebo. The number of subjects who reached VAS 100 within 30 min was significantly lower (P < 0.03) when receiving adenosine + morphine (0/9) and adenosine + ketamine (2/9) than when receiving placebo (7/9). This may indicate an additive effect on pain reduction when adenosine is given in combination with morphine or ketamine. In conclusion, the results indicate that i.v. adenosine, as well as morphine and ketamine, can reduce experimentally induced ischemic muscle pain in healthy volunteers.

Adenosine↗
PubMed1993

Effects of low-dose adenosine on myocardial performance after coronary artery bypass surgery.

The effect of a non-hypotensive dose of adenosine infusion on myocardial performance after coronary artery bypass surgery was examined. Upon arrival at the intensive care unit, 16 patients (14 males, 2 females; mean age 64.5, range 46-71) were randomized to a blinded infusion of either low-dose adenosine (n = 8) or placebo (n = 8). The infusion continued at a rate corresponding to 30 micrograms.kg-1.min-1 of adenosine into the right ventricle over 4 h. Data were collected from the arterial line, thermodilution pulmonary artery catheter, transoesophageal echocardiogram (TEE), and 12-lead ECG on six occasions: before infusion, hourly during the infusion, and 1 h after terminating the infusion. Mean arterial blood pressure did not differ between the adenosine and placebo groups at any measurement point. Heart rate increased by approximately 15% during the first hour of adenosine infusion. Cardiac index increased by approximately 50% during infusion of adenosine and cardiac index remained higher while systemic vascular resistance remained lower in the adenosine-treated group during infusion. The E/A ratio (ratio between peak left ventricular inflow blood velocities during early filling and atrial contraction) was significantly higher in the adenosine-treated group after treatment for 1 h while the area injection fraction did not differ between groups at any time. The number of patients with ischaemic events as judged from ECG and from left ventricular regional wall motion abnormalities (RWMA) as visualized by TEE did not differ between groups (ECG: one patient in the adenosine group and one patient in the placebo group-RWMA: four patients in the adenosine group versus three in the placebo group).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1993

Renal effects of i.v. adenosine infusion in humans.

The effects of systemic intravenous (i.v.) infusion of adenosine on renal blood flow and glomerular filtration in eight healthy, awake females have been examined. Renal blood flow and glomerular filtration rate were measured as the clearance of para-aminohippuric acid (PAH) and inulin, respectively. Following basal sampling adenosine was infused i.v. at successive rates of 60 and 80 micrograms kg-1 min-1 for 30 min at each rate. Plasma clearance of PAH showed a minor, but non-significant, increase from 697 +/- 41 to 775 +/- 97 ml min-1. However, the arterial plasma concentration of PAH decreased by 17 +/- 4% (P < 0.001), indicating that there was a small increase in renal blood flow. Inulin clearance was reduced from 123 +/- 14 to 88 +/- 11 ml min-1 1.73 m-2 (P < 0.01). The resulting filtration fraction was reduced from 18 +/- 1 to 11 +/- 1 (P < 0.001). The K+/Na+ excretion ratio increased from a basal value of 10 +/- 1 to 42 +/- 11 (P < 0.01) at the highest dose of adenosine, and renal oxygen consumption decreased from 17 +/- 2 to 9 +/- 1 ml min-1 (P < 0.001). In conclusion, i.v. infusion of adenosine in healthy, awake subjects causes a minor increase in total renal blood flow and a marked reduction in glomerular filtration. This shows that adenosine also exerts a vasodilatory effect in the renal circulation, primarily on postglomerular arterioles. In addition, adenosine may produce an aldosterone-like effect on salt excretion, and a reduction in renal oxygen consumption.

Adenosine↗
PubMed1993

Effect of systemic adenosine infusion on capillary flow and oxygen pressure distributions in skeletal muscle of the rabbit.

The aim of this study was to investigate the effect of systemic adenosine (ADO) infusion on blood flow and oxygenation at the capillary level in skeletal muscle in order to estimate oxygen demand. In anesthetized rabbits, a multiwire microelectrode was placed on the left vastus medialis muscle surface, and was used for capillary flow (determined by hydrogen clearance) as well as for oxygen pressure (PtO2) measurements. Laser Doppler flowmetry (LDF) was also used on the contralateral muscle surface for regional microcirculatory blood flow measurements. ADO infusion (50-100 micrograms/kg/min) was given in a central vein. During the ADO infusion the mean arterial blood pressure decreased from 81 +/- 5 (mean +/- SD) to 64 +/- 4 mmHg (a 21% decrease) (p < 0.001), while capillary flow decreased by 37% from a mean value (relative units) of 1.0 +/- 0.84 during control to 0.63 +/- 0.72 (p < 0.001). During ADO infusion there was an increased flow heterogeneity. The mean PtO2 increased by 29% from 5.6 +/- 2.3 to 7.2 +/- 2.2 kPa (p < 0.001) associated with decreased oxygen heterogeneity. A 43% reduction of the relative calculated local oxygen consumption was found during ADO infusion (p < 0.05). The LDF flux decreased by 7% (p < 0.05). We conclude from these results that systemic adenosine infusion decreases skeletal muscle capillary blood flow and in parallel increases the oxygen pressures. This can be explained by a redistribution of the capillary blood flow as well as a reduction in skeletal muscle oxygen demand.

Adenosine↗
PubMed1992

Evidence against endogenously released adenosine as modulator of the pressor response to hypoxia in isolated rat lungs.

Unlike other vascular beds, lung vessels constrict when exposed to hypoxia. However, a marked difference has been noticed as regards the elicitability of hypoxic pulmonary vasoconstriction (HPV) in vivo as compared to in vitro models, like a preparation of isolated rat lungs; in the latter, HPV cannot be evoked from the onset of perfusion, but might be triggered gradually by repeated hypoxic challenges. The formation of adenosine, a potent dilator of most vascular beds, is enhanced during conditions of hypoxia or ischemia. Our hypothesis therefore was that pulmonary vasoconstriction was initially antagonized by tissue-adenosine accumulating during the circulatory arrest necessary for lung isolation, and then, gradually invigorated along with the elimination of adenosine during periods of perfusion with normally oxygenated blood. In a first series of isolated rat lungs, we studied release of adenosine in connection with the third and the sixth hypoxic challenges. Although the vascular responses were of significantly different size, there was no sign of increased adenosine formation during any of the two provocations, as assessed by release of its more stable metabolites hypoxanthine, xanthine and uric acid. In a series of tissue preparations taken at the height of a fully developed hypoxic pressor response and immediately frozen, we could not find significant changes in tissue level of adenosine, hypoxanthine and inosine as compared to controls that had never been exposed to hypoxic challenges. Further, we found no correlation between the size of pressor responses and concentrations of adenosine and its metabolites, in either blood or in lung tissue.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1992

Adenosine infusion during isoflurane-nitrous oxide anaesthesia: indications of perioperative analgesic effect.

Adenosine, an endogenous compound with a known antinociceptive effect when administered into the CNS, was applied in nine patients (21-65 years) by the peripheral intravenous route (70-130 micrograms.kg-1.min-1) as a replacement for peroperative opioids during inhalation anaesthesia for surgical procedures not requiring muscle relaxation. Lorazepam was given as premedication, thiopentone was used for induction, and succinylcholine facilitated intubation of the trachea. Anaesthesia was maintained with isoflurane [initial surgery endtidal concentration (ET) 0.88% (range 0.7-1%)] and nitrous oxide (60-70%) in oxygen. Adenosine infusion was initiated 5-10 min prior to surgery, and stopped close to or when isoflurane was terminated at the end of surgery. The duration of anaesthesia, adenosine infusion, and surgery were 120 min (range 80-165), 90 min (range 70-145), and 90 min (range 60-135), respectively. Spontaneous unassisted ventilation was maintained in all patients. Mean heart rate increased 10 beats.min-1 (range 0-35) upon induction of surgery, while systolic blood pressure was unaffected at 105 mmHg (range 85-120) (14 kPa (range 11.3-16.0)). Spo2 and ETCO2 were in the normal range. The isoflurane concentration was gradually reduced in most cases [mid-surgery ET 0.63% (range 0.5-0.8) and end-surgery ET 0.57% (range 0.3-0.8)]. Extubation and verbal communication were rapidly achieved after anaesthesia. The mean postoperative (24 h) opioid requirement was 4 mg (range 0-10 mg). These pilot cases suggest that systemic adenosine infusion may replace opioids during inhalation anaesthesia, and that adequate spontaneous ventilation can be achieved.

Adenosine↗
PubMed1992

Splanchnic and renal vasoconstrictor and metabolic responses to neuropeptide Y in resting and exercising man.

The local clearance of neuropeptide Y (NPY) and whether NPY influences splanchnic and renal metabolism in man have not been investigated previously. The influence of NPY on splanchnic and renal blood flows at physiologically elevated levels has also not been investigated. The effects of a 40-min constant NPY infusion (3 pmol kg-1 min-1) at rest and during 130 min of exercise (50% of VO2max) were studied in six healthy subjects and compared with resting and exercising subjects receiving no NPY. Blood samples were drawn from arterial, hepatic and renal vein catheters for the determination of blood flows (indicators: cardiogreen and para-aminohippuric acid [PAH]), NPY, catecholamines, glucose, lactate and glycerol. NPY infusion was accompanied by: (1) significant fractional extraction of NPY-like immunoreactivity (NPY-Li) by splanchnic tissues at rest (58 +/- 5%) and during exercise (53 +/- 6%), while no arterial-venous differences could be detected across the kidney; (2) a reduction in splanchnic and renal blood flows of up to 18 and 13% respectively (P less than 0.01-0.001) at rest without any additional changes during exercise; and (3) metabolic changes as reflected in: (a) a more marked fall in arterial glucose during exercise compared to the reference group (P less than 0.05); (b) a 35% lower splanchnic glucose release (P less than 0.01) during exercise due to diminished glycogenolysis (P less than 0.01); and (c) a lower arterial lactate level (18% P less than 0.05) together with unchanged splanchnic lactate uptake during exercise, suggesting reduced lactate production by extrahepatic tissues. The disappearance of plasma NPY-Li after the infusions was biphasic with two similar half-lives at rest (4 and 39 min) and during exercise (3 and 43 min).

Adult↗
PubMed1991

Effect of dipyridamole-like compound (R-E 244) on aggregation and cyclic AMP accumulation in human platelets.

The aim of this in vitro study was to evaluate the effect of a clinical concentration (2 microM) of dipyridamole alone or in combination with adenosine, 5'-N-ethyl-carboxamido-adenosine (NECA), or prostaglandin E2 on ADP-induced whole blood aggregability. Cyclic AMP accumulation in platelet-rich plasma was also evaluated. For comparison, R-E 244 (a dipyridamole analogue with low phosphodiesterase inhibition) was examined. In whole blood, dipyridamole (2 microM), but not R-E 244 (2 microM), had a small inhibitory effect (16% +/- 5%, p less than 0.01) on aggregation. Adenosine (1 or 5 microM) had an inhibitory effect that was enhanced by the combination with dipyridamole or R-E 244. Adenosine + dipyridamole produced an inhibition almost equal to that of adenosine + R-E 244. Dipyridamole and R-E 244 had no influence on the antiaggregatory effect of NECA and prostaglandin E2. In platelet-rich plasma, dipyridamole and R-E 244 did not enhance cyclic AMP, nor did they reinforce the cyclic AMP production during treatment with adenosine, NECA, and prostaglandin E2. Our results suggest that inhibition of the uptake of adenosine into red blood cells may play a more important role than the inhibition of phosphodiesterase as the pharmacological mechanism for the antiaggregatory effect of dipyridamole in clinical treatment.

Adenosine↗
PubMed1991

Plasma accumulation of hypoxanthine, uric acid and creatine kinase following exhausting runs of differing durations in man.

During exhausting exercise adenylate kinase in the muscle cells is activated and a degradation of adenosine 5'-diphosphate occurs. Consequently, degradation products of adenosine 5'-monophosphate including hypoxanthine and uric acid, accumulate in plasma. The aim of this study was to compare the concentration changes of hypoxanthine and uric acid in plasma following running of varying duration and intensity. In addition, plasma creatine kinase activity was measured to assess the possible relationship between metabolic stress and protein release. Four groups of competitive male runners ran 100 m (n = 7), 800 m (n = 11), 5000 m (n = 7) and 42,000 m (n = 7), respectively, at an exhausting pace. Subsequent to the 100 m event (mean running time 11 s) plasma concentrations of hypoxanthine and uric acid increased by 364% and 36% respectively (P less than 0.05), indicating a very high rate of adenine nucleotide degradation during the event. Following the 800-m event (mean running time 125 s), hypoxanthine and uric acid concentrations had increased by 1598% and 66%, respectively (P less than 0.05). Both the events of longer duration, 5000 m and 42,000 m, also caused a significant increase in plasma concentration of hypoxanthine (742% and 237% respectively, P less than 0.05) and plasma uric acid (54% and 34% respectively, P less than 0.05). Plasma activities of creatine kinase were significantly increased at 24 h only following the 5000 m and 42,000 m events (64% and 1186% respectively, P less than 0.05). Changes in plasma creatine kinase activity showed no correlation with changes in plasma concentration of either hypoxanthine or uric acid for the 5000 m and 42,000 m events (r = 0.00-0.45, P greater than 0.05).

Adenosine Triphosphate↗
PubMed1991

Anti-aggregatory effects of physiological concentrations of adenosine in human whole blood as assessed by filtragometry.

1. The anti-aggregatory effect of adenosine (0.3-10 mumol/l), alone or in combination with the adenosine-uptake inhibitor dipyridamole (2 mumol/l), was studied in vitro in whole blood from 11 healthy subjects by filtragometry. 2. ADP (0.05-0.1 mumol/l) was used to reduce the filter occlusion time (tA, a measure of platelet aggregate formation in blood) from approximately 600 s to 71-101 s in the absence of other agents. 3. Adenosine was infused into the tubing system of the filtragometer, yielding a contact time of approximately 25 s with the blood before the filter. Adenosine did not influence the aggregatory response to ADP significantly at 0.3 mumol/l in plasma, whereas tA was prolonged by 19 +/- 6% (P less than 0.02) at 1 mumol/l adenosine and by 259 +/- 78% (P less than 0.02) at 3 mumol/l adenosine. 4. When the rapid elimination of adenosine from plasma was prevented by 2 mumol/l dipyridamole, adenosine caused marked prolongation of ADP-induced tA, with significant effects at 0.3 mumol/l (+143 +/- 72%, P less than 0.05). Dipyridamole per se did not affect tA values. 5. The present results suggest that adenosine has a transient anti-aggregatory effect in whole blood at about 0.3 mumol/l, as this is the highest possible calculated concentration of adenosine at the filter of the apparatus when 1 mumol/l adenosine is infused in the absence of dipyridamole or when 0.3 mumol/l adenosine is infused in its presence. 6. It is concluded that adenosine has anti-aggregatory effects at submicromolar (physiological) concentrations in human whole blood.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1991

Myocardial effects of adenosine- and sodium nitroprusside-induced hypotension: a comparative study in patients anaesthetized for abdominal aortic aneurysm surgery.

The effects of adenosine and sodium-nitroprusside (SNP) on central and myocardial haemodynamics and metabolism were evaluated during fentanyl anaesthesia (100 micrograms.kg-1) in six patients with peripheral vascular disease. The investigation was performed during stable anaesthesia, before scheduled abdominal aortic graft surgery. Adenosine and SNP were infused intravenously in random order over 20 min, leaving a 30-min control period in between. The vasodilators were titrated in order to reduce mean arterial pressure by approximately 25%. Adenosine (90 +/- 20 micrograms.kg-1.min-1) reduced mean arterial pressure from 10.9 +/- 0.3 to 8.4 +/- 0.4 kPa (82 +/- 3 to 63 +/- 3 mmHg), and SNP (0.7 +/- 0.1 micrograms.kg-1.min-1) from 11.0 +/- 0.2 to 8.4 +/- 0.3 kPa (83 +/- 3 mmHg to 63 +/- 3 mmHg), during the hypotension period. Cardiac index remained unaffected during induced hypotension with both vasodilators, while heart rate increased during SNP infusion (8 +/- 3%) and remained unaffected with adenosine. Left ventricular stroke work index and myocardial oxygen consumption decreased during SNP infusion (33 +/- 3% and 17 +/- 5%, respectively), while these parameters were unchanged with adenosine. Adenosine hypotension increased coronary sinus flow 1-2 fold (128 +/- 26%), together with increased coronary sinus oxygen content (96 +/- 11%). In contrast, coronary sinus flow decreased during SNP hypotension (-15 +/- 4%) with unaffected coronary sinus oxygen content. It is concluded that adenosine, in contrast to SNP, is associated with a hyperkinetic myocardial circulation.

Adenosine↗
PubMed1991

Influence of adenosine and prostacyclin on hypoxia-induced pulmonary hypertension in the anaesthetized pig.

The effects of adenosine and prostacyclin (PGI2) infusions on hypoxia-induced pulmonary hypertension in the pulmonary and systemic circulatory systems of nine pigs were compared. The animals received the drugs in random order, and they were allowed to recover between each experimental sequence. Hypoxia was induced by reducing FiO2 to 0.12-0.13 so as to result in an arterial PO2 of approximately 6 kPa. Dose rates of adenosine or PGI2 during hypoxia were individualized in order to achieve a maximal reduction of 15% in the mean arterial blood pressure. Adenosine and PGI2 produced a fall in pulmonary vascular resistance of 36 +/- 4% (s.e.mean P less than 0.01) and 37 +/- 6% (P less than 0.01), respectively. The mean pulmonary artery pressure was reduced by 19 +/- 3% (P less than 0.01) during adenosine infusion and by 36 +/- 4% (P less than 0.01) during PGI2 infusion. The systemic haemodynamic responses to the two drugs were similar but adenosine produced a 7 +/- 2% (P less than 0.01) increase in cardiac output. Arterial PO2 during hypoxia and vasodilator treatment did not differ from the hypoxic situation without drug infusion. It is concluded that adenosine and PGI2 counteract hypoxia-induced increases in pulmonary vascular resistance similarly, but the reduction in pulmonary artery pressure was greater with PGI2 at infusion rates, causing minor systemic haemodynamic changes.

Adenosine↗
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↗
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↗