Biomedical subjects

A Sollevi

Publications and source records attributed to A Sollevi.

At least 37 records · Page 2Linked to original sources

PubMed1998

Pneumoperitoneum for laparoscopic cholecystectomy is not associated with compromised splanchnic circulation.

OBJECTIVE: To investigate the influence of increased intra-abdominal pressure during pneumoperitoneum on splanchnic circulation. DESIGN: Open study. SETTING: University hospital, Sweden. SUBJECTS: Five otherwise healthy patients (mean age of 34 years), undergoing laparoscopic cholecystectomy. INTERVENTIONS: Arterial and hepatic vein catheterization and simultaneous arterial and hepatic vein blood gas sampling in the awake state, during anaesthesia, after the establishment of pneumoperitoneum (intra-abdominal pressure level 11-13 mmHg) and after 30 and 60 minutes of pneumoperitoneum. MAIN OUTCOME MEASURES: Hepatic blood flow was estimated by the continuous infusion method and used as a measure of splanchnic blood flow. Splanchnic oxygen consumption was calculated according to the Fick principle. RESULTS AND CONCLUSION: Splanchnic blood flow and splanchnic oxygen consumption were not affected by pneumoperitoneum at this level of intra-abdominal pressure.

Abdomen↗

PubMed1998

Ventilatory responses to acute and sustained hypoxia during isoflurane anesthesia.

UNLABELLED: In the awake state, isocapnic hypoxic ventilatory responses (HVRs) are biphasic, with an acute response within 5 min of hypoxic stimulation followed by a less pronounced sustained response. In this study, we investigated the influence of isoflurane anesthesia (end-tidal concentration 1.1 kPa) on acute and sustained isocapnic HVRs in eight healthy women at pulse oximetry arterial saturations of 75%-80%. The aims were to determine whether HVR (20 min of hypoxia) during anesthesia was biphasic and to quantify ventilatory responses. Pneumotachography and in-line infrared capnometry were used. A biphasic HVR was found both in awake and anesthetized patients. Of the subjects, six had decreased and two had increased acute and sustained isocapnic HVRs in the anesthetized, compared with the awake state, which resulted in an approximately 50% reduction in both acute and sustained HVRs. In addition, the ventilatory response pattern was altered by anesthesia. Awake HVR was accomplished by increased tidal volumes while respiratory rates were unchanged. The opposite occurred during anesthesia. The underlying mechanisms for this biological action of inhaled anesthetics remains to be elucidated. In conclusion, this study clearly demonstrates the persistence of hypoxic ventilatory sensitivity during clinical anesthesia. IMPLICATIONS: We studied the ventilatory effects of 20 min of breathing air with low oxygen content (hypoxic) in eight women, before and during anesthesia with inhaled isoflurane. We demonstrated a persistent but blunted hypoxic ventilatory response during clinical anesthesia.

Adult↗

PubMed1998

Intrathecal adenosine administration: a phase 1 clinical safety study in healthy volunteers, with additional evaluation of its influence on sensory thresholds and experimental pain.

BACKGROUND: Several animal studies show antinociceptive effects of intrathecally administered adenosine and its analogs. However, there is no clinical experience regarding the effects of intrathecal adenosine in humans. METHODS: The side effects and analgesic effects of intrathecal adenosine (500-2,000 microg) on experimental pain were studied in 12 healthy volunteers. Before and after adenosine was given, the authors evaluated the cold pain rating of the foot (submersion in ice water for 1 min), the forearm ischemic pain rating during a 30-min tourniquet test, and the thermal and tactile pain thresholds on healthy and inflamed skin after application of mustard oil (4 min) to the calf. The areas of secondary allodynia surrounding the inflammation were also determined. The cerebrospinal fluid level of adenosine was determined before and after injection. RESULTS: Intrathecal adenosine caused a 1,000- to 2,000-fold elevation of the cerebrospinal fluid concentration. One volunteer experienced transient (30 min) lumbar pain after injection at a dose of 2,000 microg. There were no other complications in any other volunteers. Adenosine reduced, in a non-dose-dependent manner, the areas of secondary allodynia after skin inflammation (brush, P < 0.06; and von Frey hair, P < 0.03) and reduced the forearm tourniquet ischemic pain rating (P = 0.01). Tactile pain thresholds were significantly reduced by mustard oil inflammation during control, whereas adenosine treatment prevented this reduction. The ice water-induced cold pain rating was not influenced by adenosine. CONCLUSIONS: An intrathecal adenosine injection of 1,000 microg lacked side effects in healthy volunteers. The compound attenuated different types of experimental pain.

Adenosine↗

PubMed1998

The endothelin receptor antagonist bosentan restores gut oxygen delivery and reverses intestinal mucosal acidosis in porcine endotoxin shock.

BACKGROUND: Endothelin-1, the most potent vasoconstrictor known, is produced in septic states and may be involved in the pathophysiology of the deteriorated splanchnic circulation seen in septic shock. AIMS: To elucidate the capability of bosentan, a non-peptide mixed endothelin receptor antagonist, to attenuate splanchnic blood flow disturbances and counteract intestinal mucosal acidosis in endotoxic shock. METHODS: In 16 anaesthetised pigs, central and regional haemodynamics were monitored by thermodilution and ultrasonic flow probes, respectively. A tonometer in the ileum was used for measurement of mucosal pH. Onset of endotoxin challenge was followed by bosentan administration (to eight pigs) two hours later. RESULTS: Endotoxin infusion reduced cardiac index and systemic oxygen delivery; bosentan restored these parameters. The reduced mean arterial blood pressure and renal blood flow remained unaffected by bosentan. The profound reduction in gut oxygen delivery in response to endotoxin was completely abolished by bosentan. Bosentan significantly improved the notably deteriorated intestinal mucosal pH and mucosal-arterial PCO2 gap. The mucosal-portal vein PCO2 gap, used to monitor the mucosa in relation to the gut as a whole (including the spleen and pancreas), was also greatly increased by endotoxaemia and significantly reversed by bosentan. CONCLUSION: Bosentan completely restored the profound endotoxin induced reductions in systemic and gut oxygen delivery with a concomitant reversal of intestinal mucosal acidosis. Results suggest that endothelin is involved in the pronounced perfusion disturbances seen in the gut in endotoxic shock. Bosentan may prove useful in reducing gut ischaemia in septic shock.

Acidosis↗

PubMed1998

Reduced anti-allodynic effect of the adenosine A1-receptor agonist R-phenylisopropyladenosine on repeated intrathecal administration and lack of cross-tolerance with morphine in a rat model of central pain.

UNLABELLED: We examined the development of tolerance to the antiallodynic effect of chronic intrathecal (IT) administration of the adenosine analog R-phenylisopropyladenosine (R-PIA) in a rat model of central pain after ischemic spinal cord injury. After 10 days of IT R-PIA treatment, the effect of IT morphine was also assessed to examine whether cross-tolerance between R-PIA and morphine was present. IT R-PIA completely alleviated allodynia-like behaviors to mechanical and cold stimuli in spinally injured rats. The anti-allodynic effect of R-PIA was maintained for 6-7 days with twice-daily administration and was reduced thereafter, particularly with respect to cold allodynia. IT morphine alleviated mechanical and cold allodynia in rats rendered tolerant to R-PIA to a degree comparable to that in R-PIA-naive (control) rats, which indicates that the anti-allodynic property of R-PIA is independent of the mechanisms by which morphine acts. The possibility of using agonists of adenosine receptors in treating refractory pain in patients with spinal cord injury is discussed. IMPLICATIONS: There is often no satisfactory treatment for chronic pain after spinal cord injury. Our study suggests such pain can be treated with a spinal injection of R-phenylisopropyladenosine in rats. Reduced effect to R-phenylisopropyladenosine was noted with repeated administrations. However, there was no cross-tolerance to morphine.

Adenosine↗

PubMed1997

Adenosine receptor activation suppresses tactile hypersensitivity and potentiates spinal cord stimulation in mononeuropathic rats.

The aim of the present study was to investigate the intrathecal (i.t.) action of a selective A1-adenosine receptor agonist, R-phenylisopropyl adenosine (R-PIA), on tactile withdrawal thresholds in a rat model of mononeuropathy produced by sciatic chronic constriction injury (CCI). An additional aim was to examine whether adenosine receptor activation is involved in the effects of spinal cord stimulation (SCS), which activates low-threshold fibers and suppresses touch-evoked pain both in patients and in experimental animals with neuropathy. Animals presenting hindlimb withdrawal to von Frey filaments with a bending force of < 7.5 g on the lesioned side (compared to > or = 35 g in the normal limb), were considered as having tactile hypersensitivity ("allodynia'). R-PIA (1-10 nmol i.t.) induced a dose-dependent suppression of the tactile allodynia without producing impairment of motor function. The effect of R-PIA (3 nmol i.t.), a clearly submaximal dose, was abolished by concomitant treatment with the selective A1-adenosine receptor antagonist cyclopentylxanthine (10 nmol i.t.). In animals where SCS failed to influence tactile allodynia, concomitant i.t. administration of R-PIA (3 nmol) and SCS induced a clear-cut and long-lasting suppression of the hypersensitivity to tactile stimulation. In conclusion, adenosine receptor stimulation antagonizes tactile hypersensitivity in a CCI model of mononeuropathy and potentiates the action of spinal cord stimulation.

Animals↗

PubMed1997

Global cerebral blood flow during infusion of adenosine in humans: assessment by magnetic resonance imaging and positron emission tomography.

Adenosine, an endogenous vasodilator, induces a cerebral vasodilation at hypotensive infusion rates in anaesthetized humans. At lower doses (< 100 micrograms kg-1 min-1), adenosine has shown to have an analgesic effect. This study was undertaken to investigate whether a low dose, causing tolerable symptoms of peripheral vasodilation affects the global cerebral blood flow (CBF). In nine healthy volunteers CBF measurements were made using axial magnetic resonance (MR) phase images of the internal carotid and vertebral arteries at the level of C2-3. Quantitative assessment of CBF was also obtained with positron emission tomography (PET) technique, using intravenous bolus [15O]butanol as tracer in four of the subject at another occasion. During normoventilation (5.4 +/- 0.2 kPa, mean +/- s.e.m.), the cerebral blood flow measured by magnetic resonance imaging technique, as the sum of the flows in both carotid and vertebral arteries, was 863 +/- 66 mL min-1, equivalent to about 64 +/- 5 mL 100 g-1 min-1. The cerebral blood flow measured by positron emission tomography technique, was 59 +/- 4 mL 100 g-1 min-1. All subjects had a normal CO2 reactivity. When adenosine was infused (84 +/- 7 micrograms kg-1 min-1.) the cerebral blood flow, measured by magnetic resonance imaging was 60 +/- 5 mL 100 g-1 min-1. The end tidal CO2 level was slightly lower (0.2 +/- 0.1 kPa) during adenosine infusion than during normoventilation. In the subgroup there was no difference in cerebral blood flow as measured by magnetic resonance imaging or positron emission tomography. In conclusion, adenosine infusion at tolerable doses in healthy volunteers does not affect global cerebral blood flow in unanaesthetized humans.

Adenosine↗

PubMed1997

Cerebral blood flow of the exposed brain surface measured by laser Doppler perfusion imaging.

A novel application of laser Doppler flowmetry (LDF) laser Doppler perfusion imaging (LDPI), was used to study cerebral cortical blood flow (CBFcortex). In contrast to the conventional laser Doppler perfusion monitor, LDPI creates two dimensional maps of the tissue perfusion in a well defined area of up to 120 x 120 mm comprising 4096 measurements points. Measurements of CBFcortex were made through an optically transparent polyester film applied to a cranial window preparation in ventilated anaesthetized pigs. Temporal and spatial heterogeneity in CBFcortex were visualized by LDPI during provocations which are known to alter CBF (varying arterial PCO2 or MABP, or infusion of adenosine at constant MABP (concomitant angiotensin administration) or by hyperoxemia). During hypercapnia the recorded CBFcortex increased homogeneously. The adenosine-mediated increase in recorded CBFcortex was concentrated on the lower flow interval, as was the hyperoxemia-caused decline. At decreasing MABP the autoregulatory threshold was found to vary locally within the cortex. The results suggest that LDPI, apart from detecting localized changes in CBFcortex' also visualizes flow changes within different vascular segments. Together with the practical advantages of the system, i.e. not necessitating direct contact with the tissues, this feature makes the technique suitable for studies of CBFcortex distributions.

Animals↗

PubMed1997

Intrathecal adenosine analog administration reduces substance P in cerebrospinal fluid along with behavioral effects that suggest antinociception in rats.

UNLABELLED: Adenosine and adenosine analogs induce analgesia in humans and presumed antinociception in animal models when administered both systemically and intrathecally. In the present investigation in rats, we studied the effects of intrathecally administered adenosine analogs, with or without systemic coadministration of an adenosine antagonist (theophylline), on substance P (SP) and calcitonin gene-related peptide (CGRP) concentrations in cerebrospinal fluid (CSF). In parallel, nociceptive reflex testing (tail immersion latency) and motor function were evaluated. The potent unselective adenosine receptor agonist N-ethylcarboxamide-adenosine (NECA) and the relatively adenosine A1 receptor selective agonist R-phenyl-isopropyl-adenosine (R-PIA) both reduced SP-like immunoreactivity (-LI) by 50%, whereas CGRP-LI remained unchanged. There was a dose-dependent increase in tail immersion latency. This effect was present without motor impairment when R-PIA was administered in doses up to 5 nmol. R-PIA (10-100 nmol), as well as 1-100 nmol of the unselective agonist NECA, produced dose-dependent motor impairment. The reduction of SP-LI as well as the behavioral effects were reversed by theophylline. We conclude that SP reduction in CSF, which possibly reflects reduced SP turnover after adenosine receptor stimulation, provides an additional possible mechanism of action for the analgesic effects of adenosine. IMPLICATIONS: We studied the interactions between the known pain mediator substance P and substances with effects similar to the endogenous pain modulator adenosine in rats. The results suggest that the pain-reducing effect of adenosine is, at least partly, due to a reduction of substance P in cerebrospinal fluid.

Adenosine↗

PubMed1997

Effects of propofol on cerebral blood flow, metabolism, and cerebral autoregulation in the anesthetized pig.

We studied the effects of propofol on the cerebral circulation and flow/pressure autoregulation in eight anesthetized pigs. Regional cerebral blood flow (rCBF) was measured with a cerebral venous outflow technique. Autoregulation was tested with angiotensin infusions and gradual blocks of the caval vein for hyper- and hypotensive challenges, respectively. Propofol was given in a bolus of 2.5 mg.kg-1 followed by an infusion starting at 12 mg.kg-1.h-1 and gradually reduced to 8 mg.kg-1.h-1. As expected, propofol caused a substantial reduction in cerebral metabolic rate of oxygen, which was accompanied by an increase in cerebrovascular resistance and a decrease in CBF. In the control situation, i.e., during background anesthesia (low-dose isoflurane+nitrous oxide) only, the autoregulation was well preserved, and its lower limit was found at a mean arterial blood pressure (MABP) of 48 mm Hg. Propofol did not affect autoregulation in the group as a whole: the slope of the regression line of regional cerebrovascular resistance (rCVR) versus MABP during blood pressure reduction (caval test) was not significantly changed during propofol when compared to the control, neither was the lower limit of autoregulation (MABP, 54 mm Hg). All pigs but one followed this response pattern. The nonautoregulating pig had a completely pressure-dependent rCBF during propofol anesthesia, despite a perfectly intact auto-regulation in the control situation. It is concluded that propofol in clinical dosage does not affect autoregulation in this pig model, although individual animals may display a different response pattern.

Anesthetics, Intravenous↗

PubMed1997

Cardiopulmonary dysfunction during porcine endotoxin shock is effectively counteracted by the endothelin receptor antagonist bosentan.

In a porcine endotoxin shock model, the mixed nonpeptide endothelin receptor antagonist bosentan was administered 2 h after onset of endotoxemia (n = 8). Cardiopulmonary vascular changes, oxygen-related variables, and plasma levels of endothelin-1-like immunoreactivity were compared with a control group that received only endotoxin (n = 8). Bosentan abolished the progressive increase in mean pulmonary artery pressure and pulmonary vascular resistance seen in controls. Possible mechanisms include blockade of vasoconstrictive endothelin receptors, and a lesser degree of edema and inflammation indicated by less alveolar protein and a lower inflammatory cell count observed in bronchoalveolar lavage. Further, bosentan restored cardiac index to the pre-endotoxin level by an increase in stroke volume index, improved systemic oxygen delivery, and acid base balance. Because mean arterial blood pressure was unaffected, bosentan reduced systemic vascular resistance. Endotoxemia resulted in an increase in tumor necrosis factor-alpha and endothelin-1-like immunoreactivity plasma levels, the latter being further increased by bosentan. In conclusion, in porcine endotoxemia, treatment with the endothelin receptor antagonist bosentan, administered during fulminate shock, abolished pulmonary hypertension and restored cardiac index. These findings suggest that bosentan could be an effective treatment for reversing a deteriorated cardiopulmonary state during septic shock.

Acid-Base Imbalance↗

PubMed1997

Antinociceptive effect of perioperative adenosine infusion in abdominal hysterectomy.

BACKGROUND: Adenosine (ADO), and stable analogs thereof, have been shown to exert antinociceptive action in cutaneous and deep somatic pain under experimental and clinical conditions in animals and in humans. The aims of this randomized double-blind placebo-controlled study were to evaluate if a low dose of intravenous (i.v.) ADO could reduce the requirements of volatile anesthetic and postoperative opioid in connection to hysterectomy, where visceral nociception significantly contributes to pain. METHODS: Forty-three women, age 32-65 years, ASA I and II, scheduled for abdominal hysterectomy, were assigned to receive an i.v. infusion of either adenosine, 80 micrograms.kg-1.min-1, or placebo during surgery. Anesthesia was maintained with isoflurane (ISO)/N2O/ O2 inhalation. Postoperatively, a reduced dose of 40 micrograms.kg-1.min-1 was continued for 3 h. RESULTS: The end-tidal (ET-) ISO was equal between groups before surgery. During surgery, the ISO requirement was increased, compared to the preoperative level, in the placebo group, while the requirement declined in the ADO group. The overall ISO requirement in the ADO group was reduced by 36% (P < 0.002). The first 24 h postoperative opioid requirement, with equal resting pain in both groups, was 18% (P < 0.05) lower in the ADO group. CONCLUSION: A low dose of perioperative adenosine infusion in abdominal hysterectomy reduces the requirements of volatile anesthetic and postoperative opioid analgesic.

Adenosine↗

PubMed1997

Vectorcardiographic changes during laparoscopic cholecystectomy may mimic signs of myocardial ischaemia.

BACKGROUND: Laparoscopic surgery involves the use of intra-abdominal carbon dioxide insufflation (pneumoperitoneum). The increased intra-abdominal pressure causes marked haemodynamic changes, which may influence electrocardiographic monitoring. The aim of the present study was to elucidate the influence of pneumoperitoneum on vectorcardiographic recordings. METHODS: Vectorcardiographic changes (QRS vector difference = QRS-VD, QRS loop area, QRS magnitude, ST vector magnitude, spatial ST vector change) were recorded continuously applying computerized vectorcardiography in 12 anaesthetised cardiovascularly healthy patients, scheduled for laparoscopic cholecystectomy. Measurements were made before and during pneumoperitoneum in three different body positions (supine, Trendelenburg and reversed Trendelenburg), also employing transesophageal echocardiography and invasive blood pressure monitoring. RESULTS: Pneumoperitoneum significantly increased QRS-VD, in parallel with an enlargement in loop area and magnitude. The magnitude was significantly increased in the transversal and frontal planes and there was a tendency to increase the magnitude in the sagittal plane. The increase in QRS-VD reached levels previously associated with the development of myocardial ischaemia in patients with coronary artery disease. The ST-variables were not changed by the pneumoperitoneum. The positional changes also influenced QRS-VD significantly. CONCLUSIONS: When computerized vectorcardiography is used for ischaemia monitoring during pneumoperitoneum, the ST-variables seem reliable. However, vectorcardiographic QRS-changes should be interpreted with caution, as the QRS alterations found during pneumoperitoneum mimic the changes seen during myocardial ischaemia.

Adult↗

PubMed1997

Adenosine for pain control.

The antinociceptive actions of adenosine and adenosine analogs in animal models has been known for more than 10 years. The recent development with regard to the pain modulatory effects of adenosine, primarily in clinical studies, has generated a renewed interest in this principle for pain control. This review summarizes the current knowledge in adenosine mediated pain modulation in acute and chronic conditions, with focus on studies in man. The endogenous compound adenosine has various modulatory effects in the peripheral and central nervous system, mediated through specific cell-surface associated receptors. The current view is that adenosine receptors of the A1-subtype are associated with a modulatory effect on pain transmission at spinal cord level. Animal studies have repeatedly demonstrated adenosine- and adenosine analog mediated inhibitory influences on presumed nociceptive reflex responses (1,2). These examinations in rodents have tested acute pain models involving tactile, pressure and heat stimulations. More recently, animal lesion models presumably reflecting chronic pain, has shown that adenosine analogs can suppress nociceptive behaviour both by systemic and intrathecal (i.t.) administration (3,4). Consequently, there is substantial evidence that adenosine can modulate nociceptive input. Further, it has been proposed that endogenous adenosine formation is involved in physiological pain control at the spinal cord level and that its release is involved in the action of opioid antinociception (1). Clinical studies have revealed that adenosine administration by bolus injection or by infusion at doses above 70 micrograms x kg-1 x min-1 is associated with pain symptoms from different parts of the body. This algogenic effect of higher doses of adenosine is probably related to sensitization/activation of peripheral nociceptive afferents (5).

Acute Disease↗

PubMed1997

Modulation of spinal pain mechanisms by spinal cord stimulation and the potential role of adjuvant pharmacotherapy.

Experimental studies indicate that the effects of spinal cord stimulation (SCS) on 'hypersymptoms' in neuropathic pain conditions may at least partly be mediated via GABAergic and adenosine-dependent mechanisms. Concomitant intrathecal administration of receptor-active drugs modulating the function of the GABA and adenosine systems may both depress and enhance the effects of SCS. The first few patients with simultaneous intrathecal administration of the GABAB agonist baclofen and/or adenosine together with SCS, when the stimulation alone proved insufficient, are reported.

Adenosine↗

PubMed1996

Intrathecal and systemic R-phenylisopropyl-adenosine reduces scratching behaviour in a rat mononeuropathy model.

The aim of the present study was to investigate the effect of intravenous or intrathecal (i.t.) administration of R-phenylisopropyladenosine (R-PIA), a selective A1 adenosine receptor agonist, on spontaneous scratching behaviour, a phenomenon presumably related to pain in a mononeuropathy model (sciatic nerve ligation) in rats. The acute effect of daily i.t. R-PIA injections was studied up to 21 days following nerve ligation. The results demonstrate that both i.v. (30 nmol) and i.t. (3 nmol) R-PIA, in doses not producing any motor impairment, significantly reduces scratching behaviour in this animal model. The mechanism of action for this presumed antinociceptive effect is suggested to occur at the spinal cord level.

Adenosine↗

PubMed1996

Effects of posture and pneumoperitoneum during anaesthesia on the indices of left ventricular filling.

BACKGROUND: Laparoscopic surgery requires the use of pneumoperitoneum (PP). When combined with positional changes, pneumoperitoneum may cause marked circulatory alterations. METHODS: Eight anaesthetized cardiovascularly healthy patients, scheduled for laparoscopic cholecystectomy, were studied before and during pneumoperitoneum in three different postures (supine, Trendelenburg and reversed Trendelenburg), employing transesophageal echocardiography and pulmonary artery pressure monitoring. RESULTS: PP significantly increased end-diastolic area (EDA) and pulmonary capillary wedge pressure (PCWP) irrespective of posture. PCWP was significantly influenced by postural changes, whereas EDA was not. Further, changes in EDA and PCWP covaried during the investigation, but showed no linear correlation. Systolic function, measured as end-systolic area (ESA) and fractional area shortening (FAS), was not altered. Diastolic function, as assessed by the velocity rate of the transmitral flow during the early filling phase (E) and the atrial contraction (A), showed no change of the E/A ratio, whereas after the induction of PP there was a significant reduction of the E component. CONCLUSIONS: In cardiovascularly healthy patients, the left ventricular volume is increased during pneumoperitoneum. Further, changes in invasive pressure determinations (PCWP) do not correlate linearly with changes in volume indices of left ventricular filling (EDA).

Adult↗

PubMed1996

Peroperative adenosine infusion reduces isoflurane concentrations during general anesthesia for shoulder surgery.

BACKGROUND: Adenosine (ADO), and stable analogs thereof, have been shown to exert antinociceptive action under experimental conditions in animals and in humans. The aim of this randomized double-blind placebo-controlled study was to evaluate if a low dose of intravenous (i.v.) ADO could reduce isoflurane requirements during joint-associated surgery, as an indication of antinociception in deep somatic pain. METHODS: Thirty-two patients, age 19-62 years, ASA I and II, scheduled for shoulder joint surgery, were assigned to receive an i.v. infusion of either adenosine, 80 micrograms.kg-1.min-1, or placebo, during the surgical procedure. Anesthesia was maintained with isoflurane/N2O/O2 inhalation. RESULTS: The peroperative isoflurane concentration was significantly reduced at 50 minutes of surgery in the group receiving adenosine infusion. Also, the systolic blood pressure level was peroperatively more stable during adenosine infusion than during placebo. Other clinical parameters, such as pain, postoperative analgesic requirements and nausea, were not different between groups. CONCLUSION: A peroperative infusion of a low dose of adenosine during shoulder joint surgery may reduce the peroperative isoflurane requirement.

Adenosine↗