PubMed Health⌕ Search

Biomedical subjects

A Sollevi

Publications and source records attributed to A Sollevi.

At least 55 records · Page 3Linked to original sources
PubMed1996

Effects on skeletal muscle oxygenation and capillary blood flow by adenosine-, sodium nitroprusside- and acetylcholine-induced hypotension.

BACKGROUND: Adenosine (ADO)-induced hypotension during diethyl ether anesthesia has been shown to increase skeletal muscle oxygenation. Whether this beneficial effect of ADO hypotension is present also during another anesthetic technique was tested in the present study using ketamine-xylazine anesthesia, and its actions were compared with sodium nitroprusside (SNP) and acetylcholine (ACh) induced hypotension in rabbits. METHODS: Local oxygen pressure and capillary blood flow were measured with a multiwire microelectrode which was placed on the surface of the left vastus medialis muscle. The experiments were performed in three groups, in which either ADO, SNP or ACh was infused into a central vein in a dose that produced a reduction of the mean arterial pressure by 20-25%, to approximately 60 mmHg. RESULTS: In the ADO group (60-170 micrograms kg-1 min-1) the tissue oxygen pressures increased by 23% while capillary blood flow decreased by 38%. During SNP administration (1-3 micrograms kg-1 min-1) the oxygen pressures decreased by 21% and an increase of 31% in capillary flows was seen. When ACh was infused (1-4 micrograms kg-1 min-1) the oxygen pressures decreased by 21% and, in parallel, capillary blood flow decreased by 50%. During hypotension no low tissue oxygen pressure values (< 1.5 kPa) were found in the ADO group, whereas they were present in both the SNP and ACh group. CONCLUSION: Compared to sodium nitroprusside and acetylcholine, adenosine appears to have an oxygen-sparing effect in the skeletal muscle during pharmacologically induced hypotension.

Acetylcholine↗
PubMed1996

Splanchnic homeostasis during endotoxin challenge in the pig as assessed by microdialysis and tonometry.

The splanchnic region is particularly susceptible to shock. The purpose of this study was to evaluate microdialysis of the liver and small intestine as a monitor of splanchnic metabolic deterioration (elevation of lactate and hypoxanthine) in porcine endotoxic shock. Tonometry of the small intestine was used as a reference. Microdialysis probes (liver, ileum, and artery), tonometer, and pulmonary artery catheter were inserted. Eight animals were given Escherichia coli lipopolysaccharide endotoxin (20 micrograms kg-1 h-1 for 2 h). Five animals served as controls. Measurements were made every half-hour. Three hours after onset of endotoxin challenge, there were significant differences between endotoxin and control groups in intestinal lactate and hypoxanthine, as well as liver lactate, in addition to mucosal pH obtained by tonometry. Lactate elevation in blood was first seen at 4 h, while there was no significant hypoxanthine elevation in arterial blood over 5 h. Hence, data obtained from the splanchnic region became significantly different early, when compared with data obtained from arterial blood. Microdialysis of liver and small intestine as well as intestinal tonometry are sensitive tools for detection of splanchnic metabolic deterioration during endotoxin shock.

Animals↗
PubMed1995

Systemic adenosine attenuates touch evoked allodynia induced by mustard oil in humans.

The effect of adenosine on tactile allodynia (secondary hyperalgesia) was studied in 6 healthy volunteers, using a double-blind, placebo controlled, cross-over design. Tactile allodynia was induced by topical application of mustard oil on the skin of the volar aspect of the forearm. Adenosine (50 micrograms kg-1 min-1) or saline was given intravenously for 20 min before the mustard oil application and continued for another 50 min. The tactile allodynic areas for brush and von Frey filament stimulation were both significantly reduced by approximately 50% during adenosine infusion, compared with placebo. The threshold for eliciting allodynia with von Frey filaments was not influenced by adenosine. The study shows that adenosine can reduce the area of mustard oil induced tactile allodynia.

Adenosine↗
PubMed1995

Peroperative adenosine infusion reduces the requirements for isoflurane and postoperative analgesics.

The aims of this study were to investigate the influence of adenosine infusion, firstly, on postoperative analgesic requirements, and secondly, on peroperative isoflurane requirements. Seventy-five women, aged 18-70 yrs, ASA grades I and II, scheduled for breast surgery, were randomly assigned to peroperatively receive a double-blind intravenous infusion of either adenosine, 80 micrograms.kg-1.min-1, or placebo, during surgery under isoflurane/N2O/O2 anesthesia. The peroperative isoflurane requirements were significantly reduced at 30 and 90 min of surgery during adenosine treatment. The number of patients reporting pain when regaining consciousness after surgery was reduced by 57% in the adenosine group, 8/31 vs 19/32 (P < 0.02). Further, the postoperative 24-h opioid requirements were reduced by 27% in the adenosine group (P < 0.03). In conclusion, we found that a peroperative infusion of a small dose of adenosine during breast surgery, reduces the peroperative anesthetic requirements, and the demand for post-operative analgesics.

Adenosine↗
PubMed1995

Systemic adenosine infusion alleviates spontaneous and stimulus evoked pain in patients with peripheral neuropathic pain.

In seven patients with peripheral neuropathic pain, the effect of systemic adenosine infusion on pain symptoms was evaluated in a double-blind, placebo controlled, cross-over study. The study infusions, adenosine (50 micrograms.kg-1.min-1) or placebo, were given intravenously (IV) during 45-60 min at two separate occasions. Before and during infusions, bedside examination of sensibility and quantitative sensory testing (QST), i.e., assessments of perception thresholds for touch, touch-evoked pain, cold, warmth, painful heat, and cold, were performed. In the neuropathic area, sensation magnitude was rated by a visual analog scale (100 mm VAS) using a pin and at perception threshold for touch-evoked pain using von Frey filaments. Adenosine infusion reduced spontaneous pain (P < 0.05), and caused an increase of the touch-evoked pain threshold from 10.8 +/- 5.3 to 22.2 +/- 6.9 g (P < 0.05), whereas placebo had no effect. Pain intensity at perception threshold for touch-evoked pain was, however, unaltered. Pinprick-evoked pain in the neuropathic areas was reduced from 53 +/- 11 to 29 +/- 10 mm (P < 0.05). No other sensory modality was consistently changed during adenosine infusion. In conclusion, the present study demonstrates that adenosine infusion alleviates spontaneous neuropathic pain, tactile allodynia, and pinprick hyperalgesia in patients with peripheral neuropathic disorders, probably by a central mechanism of action.

Adenosine↗
PubMed1995

Adenosine for per-operative blood pressure control in an infant with neuroblastoma.

We describe a child with a localised pelvic neuroblastoma and a hypertensive crisis during the first weeks of life due to elevated systemic norepinephrine of tumoural origin. In spite of treatment with high doses of alpha-blockers, blood pressure did not respond fully and the boy had a very unstable circulation. Surgery was performed at one month of age. Adenosine, a potent short-acting vasodilator, was used for peroperative blood pressure control to protect the patient from an uncontrolled hypertensive crisis. During tumour manipulation the child became hypertensive with systolic pressure exceeding 130 mm Hg and adenosine infusion (100 micrograms.kg-1.min-1) was started with a prompt normalisation of the blood pressure. Adenosine infusion could be discontinued after tumour removal. Norepinephrine, dopamine, homovanillic acid and vanillylmandelic acid in urine were elevated preoperatively and normalised at follow up. Plasma concentrations of norepinephrine and dopamine were elevated preoperatively. Norepinephrine increased during hypertension due to tumour manipulation. Plasma neuropeptide Y increased during tumour manipulation but still within the normal range for infants. It is concluded that adenosine can be used peroperatively in children with severe hypertension and in this case no adverse effects of adenosine were noted. Furthermore, tumour synthesis and systemic release of norepinephrine, but not neuropeptide Y, contributed to hypertension in this child with neuroblastoma.

Adenosine↗
PubMed1995

Adenosine increases the cutaneous heat pain threshold in healthy volunteers.

Adenosine is an endogenously produced substance which in animal experiments exerts anti-nociceptive effects. In humans, algesic effects have been presented following exogenous adenosine administration. A recent study on anaesthetized patients, however, suggested an anti-nociceptive effect during i.v. adenosine. We have studied the pain-reducing effect in healthy volunteers using adenosine 50-80 micrograms.kg-1.min-1 (n = 10), morphine 0.1 mg.kg-1 (n = 5), adenosine 50 micrograms.kg-1.min-1 + morphine 0.1 mg.kg-1 (n = 6), and ketamine 0.1 mg.kg-1 (n = 5); all drugs given i.v., single-blind. Quantitative sensory tests (QST) revealed a significantly increased cutaneous heat pain threshold following adenosine. No effect was seen following ketamine or morphine. Suprathreshold heat pain perception was unchanged in all subjects. Furthermore, warm and cold perception thresholds were not influenced significantly by any drug. Adenosine, morphine and ketamine produced well-known side-effects but of a mild intensity not necessitating any treatment. The present results show that i.v. adenosine can provide a modest but selective increase of cutaneous heat pain thresholds, suggesting a pain-reducing capacity of adenosine in humans.

Adenosine↗
PubMed1995

Hypoxic and hypercapnic ventilatory responses during isoflurane sedation and anaesthesia in women.

This study primarily examined the effect of three endtidal isoflurane concentrations (0.2, 1.0 and 1.4%) on the isocapnic hypoxic ventilatory response (HVR), as well as the hypercapnic ventilatory response (HCVR), in 18 women (ASA I) who were all in the follicular phase of their menstrual cycle. Capnography was used, together with pulseoximetry to indicate desired levels of hypoxia (SpO2 75-80%). This hypoxic challenge resulted, after 3-4 min, in a stable ventilation, and ventilation measurements were then taken during a 90 s period. The HCVR provocation (inhalation of 4.5% CO2 in air) and measurements were conducted using a similar time frame as for HVR. Isoflurane 0.2% did not affect any ventilatory parameter. Isoflurane 1.0 and 1.4% dose-dependently increased endtidal CO2 and respiratory rate, while tidal volumes decreased. Minute ventilation was not reduced. HVR, as well as HCVR, were both uninfluenced by isoflurane 0.2%. HVR was reduced by 60-70% at isoflurane 1.4% (P < 0.01), and was parallelled by a similar depression of HCVR (P < 0.01). The HVR during anaesthesia was accomplished by a respiratory rate response, while the increase in tidal volume, seen in the awake state, was abolished. The HCVR during anaesthesia was, on the other hand, the result of a dose-dependently depressed tidal volume response, without any increase in respiratory rate. In conclusion, isoflurane 0.2% did not affect the ventilatory response to mild isocapnic hypoxia, nor to mild hypercapnic challenge. During anaesthesia with isoflurane (1.0 and 1.4%), there was a parallel reduction of HVR and HCVR.

Adult↗
PubMed1995

Isoflurane anaesthesia (0.6 MAC) and hypoxic ventilatory responses in humans.

In order to evaluate the difference between poikilo-capnic (no CO2 added to inspired gas) and iso-capnic (CO2 added to keep end-tidal CO2 constant) hypoxic ventilatory responses (HVR) awake and during 0.6 MAC isoflurane anaesthesia, seven cardio-pulmonary healthy patients were investigated. Pneumotachography and capnography were used before and during hypoxia (end-tidal O2 tension approx. 7 kPa). In the awake state, poikilo-capnic hypoxic challenges resulted in an increased HVR as indicated by a VE that on average increased by 1.4 +/- 1.0 (mean +/- s.d.) l.min-1, whereas the iso-capnic hypoxic challenges resulted in a VE increase that was 4.7 +/- 2.3 l.min-1 on average. In the anaesthetized state, the corresponding value during poikilocapnia was 1.3 +/- 0.8 l.min-1 (88% of the awake responses, n.s.) and during iso-capnia 2.3 +/- 1.4 l.min-1 (49% of the awake, P < 0.02). Awake HVR was achieved by greater tidal volumes during poikilocapnia as well as during isocapnic challenges, while respiratory rates were unchanged. In the anaesthetized state, during poikilocapnia, however, HVR was mediated by an increased respiratory rate, (from 17.5 +/- 1.7 breath.min-1 to 20.2 +/- 2.2) and during isocapnia by a combination of increased rate (from 17.1 +/- 1.9 breath.min-1 to 19.1 +/- 1.8) and tidal volume (from 496 +/- 80 to 560 +/- 83 ml). It is concluded that poikilocapnic HVR is maintained at 0.6 MAC isoflurane whereas iso-capnic HVR is depressed by 50%.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

A role for adenosine in coronary vasoregulation in man. Effects of theophylline and enprofylline.

Adenosine has been suggested to have a role in regulation of the tone of the cardiac resistance vessels. To elucidate the coronary vasoregulatory role of endogenous adenosine in man, we studied the effects of adenosine receptor antagonism by theophylline on coronary blood flow at rest and during light exercise. However, theophylline may also exert pharmacological effects not related to adenosine antagonism. To clarify the contribution of endogenous adenosine in coronary hyperaemia, the effect of theophylline was compared to that of enprofylline, a xanthine which exerts similar pharmacological effects as theophylline while lacking antagonistic action at adenosine receptors. Twenty healthy subjects (10 males) aged 22-39 years were examined. Coronary sinus (CS) blood flow and blood oxygen content were determined at rest and during supine bicycle exercise, at a load of 50 watts, for 10 min. Thereafter, stepwise infusion of adenosine (30 to 60 micrograms/kg/min into the subclavian vein) was performed. Theophylline or enprofylline treatment was instituted randomly and double-blind (10 in each group), and the procedures (i.e. determinations at rest, during exercise and during infusion of adenosine) were repeated. In all 20 subjects, basal CS flow was 70 +/- 6 ml/min and the cardiac oxygen extraction ((A-CS)O2D) was 123 +/- 3 ml/l. During exercise, CS flow and (A-CS)O2D increased to 135 +/- 17 ml/min and 132 +/- 3 ml/l, respectively. Adenosine increased CS flow dose dependently to 161 +/- 27 ml/min, while (A-CS)O2D decreased to 66 +/- 7 ml/l. The vasodilatory effect of adenosine was readily counteracted by theophylline, the increase in CS flow being 33% vs. 133% in the control situation. Enprofylline, on the other hand, enhanced the response to exogenous adenosine. Theophylline, at a dose lacking effect on heart rate and blood pressure, decreased CS flow at rest by 14% (P < 0.05) and during exercise by 18% (P < 0.05). ((A-CS)O2D increased by 14% at rest and during exercise (P < 0.001). Enprofylline, on the other hand, was without effect. The differences in responses between theophylline and enprofylline with respect to coronary flow and oxygen extraction were significant both at rest and during exercise. It is concluded that theophylline increases coronary vascular resistance, while enprofylline, lacking adenosine antagonistic properties, was without such effect. This indicates a physiological role of adenosine in regulation of coronary flow.

Adenosine↗
PubMed1995

Theophylline increases coronary vascular tone in humans: evidence for a role of endogenous adenosine in flow regulation.

To elucidate the role of adenosine in coronary vasoregulation, we studied the effects of adenosine antagonism (by theophylline) on coronary blood flow at different levels of adenosine formation (stimulated by hypoxia and exercise). Six healthy subjects were studied. Coronary sinus (CS) blood flow (thermodilution) and cardiac oxygen extraction [(A-CS)O2D] were determined while breathing room air at rest, and 12% oxygen, both at rest and during light exercise, on two occasions. One of the experiments was performed during infusion of theophylline. The basal CS flow was 118 (67-168) mL min-1 (mean and 95% confidence interval), and the (A-CS)O2D was 125 (111-142) mL L-1. Inhalation of 12% O2 decreased the arterial haemoglobin oxygen saturation to 83 (80-86)% at rest and to 77 (73-81)% during exercise. CS flow increased to 167 (93-214) and 261 (179-343) mL min-1, respectively, and (A-CS)O2D decreased to 102 (85-119) and 94 (77-111) mL L-1, respectively. Theophylline, at a dose lacking effects on myocardial work, markedly attenuated the coronary flow response to exogenous adenosine, and decreased CS flow to 89 (58-119), 120 (79-161) and 190 (162-218) mL min-1 at normoxic rest, hypoxic rest and hypoxic exercise, respectively. The overall decrease amounted to 23% (P < 0.05). The calculated coronary vascular conductance also decreased by 23% (P < 0.05) and (A-CS)O2D increased by 15% (P < 0.001). In conclusion, the data support the hypothesis that endogenous adenosine is involved in regulation of human coronary tone.

Adenosine↗
PubMed1995

Pneumoperitoneum for laparoscopic surgery does not increase venous admixture.

Venous admixture as a measure of pulmonary gas exchange was studied before and during laparascopic cholecystectomy in 12 patients with normal healthy cardio-pulmonary function. After induction of anaesthesia the patients were studied by radial and pulmonary arterial catheterization and simultaneous arterial and mixed venous blood gas sampling in the horizontal, 15-20 degrees head-down and 15-20 degrees head-up tilt positions. After establishing the pneumoperitoneum (PP) by insufflation of carbon dioxide to an intraabdominal pressure level of 11-12 mmHg, the measurements were repeated in the same positions. The laparoscopic cholecystectomy then started and measurements were repeated every 30 min during surgery. The venous admixture was 4 +/- 0.6% (range 2-6%) in the horizontal position and was not influenced by altered body position. Immediately after establishment of PP, there was a 31 +/- 5% (P < 0.05) reduction of venous admixture and a 15 +/- 3% (P < 0.01) elevation of PaO2 compared with the control situation without PP. These changes were maintained during pneumoperitoneum and were not influenced by posture. It is suggested that alterations in the distribution of ventilation and/or lung perfusion results in a reduced venous admixture during PP without surgery. In addition, there was no indication that venous admixture is elevated as a result of laparoscopic surgery in the reversed Trendelenburg position.

Adolescent↗
PubMed1994

Renal effects of local infusion of adenosine in man.

1. The effects of local intra-arterial infusion of adenosine on renal blood flow, glomerular filtration and renin release in eight healthy awake subjects have been examined. 2. Renal blood flow and glomerular filtration rate were measured as the clearances of p-aminohippurate and inulin, respectively. After basal samplings, adenosine was infused intra-arterially at successive rates of 2 and 10 micrograms min-1 kg-1 for 40 min at each rate. 3. Apart from a small increase in heart rate (65 +/- 4 to 71 +/- 4 beats/min), there were no signs of sympathetic activation (unchanged blood pressure and catecholamine levels) during the infusion. Clearance of p-aminohippurate tended to increase, but not significantly, during adenosine infusion (518 +/- 48 ml/min basal, 563 +/- 52 ml/min during the highest dose of adenosine). The arterial plasma concentration of p-aminohippurate decreased by 9 +/- 3% (P < 0.05), consistent with a small increase in renal blood flow in the infused kidney. Inulin clearance was reduced from 115 +/- 3 to 97 +/- 2 ml/min (P < 0.001). The extraction of inulin, reflecting the filtration fraction, was 18% in both kidneys in the basal state. During infusion of adenosine the extraction in the infused kidney decreased to 12 +/- 3% (P < 0.01 compared with the control kidney, 23 +/- 3%). 4. The total excretion of Na+ was unchanged, but there was a minor decrease in K+ clearance. Thus, the K+/Na+ excretion ratio decreased from a basal value of 13 +/- 2 to 10 +/- 2 (P < 0.01) at the highest dose of adenosine.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1994

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

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

Anesthesia↗
PubMed1994

Poikilocapnic hypoxic ventilatory response in humans during 0.85 MAC isoflurane anesthesia.

Ventilatory responses to hypoxia (HVR) were investigated using poikilocapnic conditions (i.e. end-tidal CO2's allowed to seek it's own level) in 15 cardio-pulmonary healthy patients who were first studied awake and then at 0.85 MAC isoflurane. The influence of hypercapnia (HyperCapnic Ventilatory Response, HCVR) was also elucidated. Pneumotachography, capnography and airway occlusion pressures at 0.1 s (P degree 0.1) were used before and during both mild hypoxia (end-tidal O2 tension 8.7 kPa) and hypercapnia achieved by an inspired CO2 concentration of 5%. HCVR was attenuated by 60% during anesthesia (P < 0.01). In the awake state, five of the 15 patients decreased HVR during hypoxia as compared with during normoxia. This resulted in a VE that on average increased by 0.6 l.min-1 (P < 0.05) whereas P degree 0.1 was unchanged. In the anesthetized state, no case of decreased HVR was seen and hypoxia induced a mean VE increase (+/- s.d.) by 1.0 +/- 0.2 l.min-1 (P < 0.001) and a P degree 0.1 that on average was improved by 0.63 +/- 0.27 cm H2O (P < 0.01). It is suggested that when the aim is to evaluate the influence of volatile anesthetic agents on HVR and to quantitate its clinical relevance during and immediately after anesthesia, a poikilocapnic technique should be used. It is concluded that the poikilocapnic HVR to PEO2's of 8.7 kPa was maintained during 0.85 MAC isoflurane.

Adult↗
PubMed1994

Haemodynamic effects of pneumoperitoneum and the influence of posture during anaesthesia for laparoscopic surgery.

The laparoscopic operating technique is being applied increasingly to a variety of intra-abdominal operations. Intra-abdominal gas insufflation, i.e. pneumoperitoneum (PP), is then used to allow surgical access. The haemodynamic effects of PP in combination with different body positions have not been fully examined. Eleven patients without signs of cardiopulmonary disease were studied before and during laparoscopic cholecystectomy under propofol-fentanyl anaesthesia with controlled ventilation. Swan-Ganz and radial arterial catheterization were used to determine haemodynamic data in the horizontal position, with a 15-20 degree head-down tilt and a 15-20 degree head-up tilt. The measurements were repeated after insufflation of carbon dioxide to an intraabdominal pressure of 11-13 mmHg, as well as during surgery. The ventricular filling pressures of the heart were strictly dependent on body position. PP in the horizontal position increased pulmonary capillary wedge pressure by 32% (P < 0.01), central venous pressure by 58% (P < 0.01), and mean arterial pressure by 39% (P < 0.01). When PP was combined with a head-down tilt, there was a further increase in filling pressures by approximately 40% (P < 0.01), while the reduction in filling pressures during the head-up tilt was counteracted by PP. During PP with a head-up tilt, the filling pressures did not differ from those in the horizontal position without PP. CI showed a certain dependency on filling pressures. It is concluded that PP causes signs of elevated preload and afterload. The combination of PP and a head-up tilt is associated only with signs of an elevated afterload.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
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↗