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Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The possible reversal of nitrous oxide analgesia by naloxone was investigated. Two studies were conducted in 21 healthy male subjects, who responded to ischemic pain produced by tourniquet applied to the upper arm for 15 min, while breathing air or nitrous oxide, 33 per cent. Using a double-blind procedure, the subjects received intravenous injections of naloxone and saline solution on different days. In eight subjects, naloxone, 8 mg, administered without nitrous oxide, had no effect on pain report. However, unlike saline solution, naloxone, 8 mg, decreased significantly the analgesia induced by nitrous oxide. In 13 subjects, naloxone, 4 mg, also decreased significantly the effect of nitrous oxide analgesia in comparison with saline solution. Naloxone showed its reversal effect mainly on sensory response rating obtained during the painful stages of ischemia, between 11 and 15 min. The results suggest that analgesia induced by nitrous oxide may be partly related to the opiate receptor--endorphin system in man.
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PMID:Antagonism of nitrous oxide analgesia by naloxone in man. 737 74

Results of 52 consecutive below-knee amputations for lower extremity ischemia were evaluated to determine whether use of immediate fit prostheses (IPOP) instead of soft stump dressings had any bearing postoperative hospitalization time, functional recovery, postoperative pain, morbidity, and mortality in amputees. Of 34 patients receiving IPOP, 21 per cent developed stump necrosis, 21 per cent had wound infection, 26 per cent required major reamputation, and 12 per cent died within 30 days of operation. Of 18 patients treated with soft stump dressings, 17 per cent developed necrosis, 33 per cent infection, 44 per cent required reamputation, and 11 per cent died postoperatively. None of these differences was statistically significant. Mean hospitalization time and average narcotic requirements for analgesia were also similar in both groups. Fifty-six per cent of patients with IPOP and 22 per cent of those with soft dressings ultimately ambulated with prostheses (P less than 0.05). Whether or not IPOP was used had little if any effect on the early evolution of vascular amputees in this series.
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PMID:The rigid versus soft postoperative dressing controversy: a controlled study in vascular below-knee amputees. 738 90

The course of ischemic increase of extracellular potassium concentration ([K+]e) was studied in rat cerebral cortex with potassium selective microelectrodes and correlated to the preischemic functional and metabolic state. Complete cerebral ischemia was induced in artificially ventilated rats by cardiac arrest. Seven different functional states including conditions with cerebral hypermetabolism (seizures, amphetamine intoxication, hyperthermia) and hypometabolism (barbiturate anesthesia, hypothermia) were chosen in order to cover a wide range of cerebral metabolic rates (CMRO2 : 28.7--2.4 ml O2/(100 g)/min). The ischemic increase of [K+]e was delayed in conditions with low CMRO2 and accelerated in conditions with high CMRO2; the time interval to the terminal steep rise in extracellular potassium concentration varied within the extremes of 35 +/- 5 and 365 +/- 12 sec (means +/- S.E.M.), the control state (N2O-analgesia) being 116 +/- 5 sec. In groups with high CMRO2 electrocortical activity ceased within 15 sec and in groups with low CMRO2 within 22 sec. The rates of the ischemic [K+]e increase, measured as rate of change in the potassium electrode potential (mV/sec), remained high in conditions with high preischemic CMRO2 and low in conditions with low CMRO2, indicating a remaining influence of the preischemic metabolism on membrane ion permeability. These results support previous metabolic data indicating that the rate of consumption of high energy phosphates during ischemia mirrors the preischemic cerebral metabolic rate. Phenobarbital anesthesia did not change the initial rate of [K+]e increase but reduced the rate of [K+]e increase later during ischemia, suggesting a special effect of barbiturates on partly depolarized membranes.
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PMID:The increase in extracellular potassium concentration in the ischemic brain in relation to the preischemic functional activity and cerebral metabolic rate. 740 19

Epidural infiltration easily causes without surgical intervention, paralysis of the sympathetic nervous system and analgesia. In this way, spasm and vasoconstriction are inhibited and the use of collateral vessels which are still permeable is facilitated. The antalgesic position of the dropped foot, which is a cause of oedema and hemodynamic disconfort, is eliminated. Out of 17 patients showing an acute ischemia of the lower limbs treated by this method, seven were cured, 3 of whom already having trophic disorders, 7 underwent local amputations and 3 had leg and thigh level amputations. Six months later 10 of these patients were doing well. The best therapeutic conditions of this treatment are non-atheromatous arteritis: angiospasm, toxic or inflammatory acute ischemia and Buerger's disease. On the other hand, the results are mediocre with atheromatous arteritis.
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PMID:[Contribution of epidural infiltration in the treatment of acute ischemia in the lower inoperable limbs (author's transl)]. 742 23

In 21 patients with critical ischemia and/or inflammation of the leg facing possible amputation, retrograde intravenous perfusion (RVP) was used to administer fibrinolytics, vasodilators and antibiotics. Amputation was avoided in 15 patients. In 4 patients, RVP was interrupted due to unsuitable veins for putting in cannulas. After introducing a 3-in-1-Block (Winnie) for analgesia, 7 courses of treatment at least were reached before unbearable pain became a reason for stopping therapy. RVP should, therefore, be considered as the last resort in the treatment of critical ischemia and/or inflammation of the leg of patients facing possible amputation.
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PMID:[Retrograde intravenous perfusion as ultima ratio in potential amputation patients with peripheral arterial occlusive disease]. 767 39

Transient forebrain ischemia induced in rats by the four-vessel occlusion method produced analgesic effects in the hotplate test that persisted for 2 weeks. Ischemia-induced analgesia was attenuated by low doses of alpha 2-agonist clonidine (0.01-0.10 mg/kg, IP) and enhanced by low doses of alpha 2-antagonists yohimbine (1-2 mg/kg, IP) and idazoxan (0.25-1.00 mg/kg, IP) administration 7 days after ischemia. Ischemia-induced analgesia was not affected by methysergide, naloxone, propranolol, or phenoxybenzamine administered 7 days after ischemia, when motor control and arousal level of rats recovered to normal conditions. The enhanced response to yohimbine was antagonized by pretreatment with clonidine (0.75 mg/kg, IP) and naloxone (10 mg/kg, IP), suggesting the involvement of endogenous opioid peptides. The enhanced response to yohimbine was still present 2 months after ischemia, when preischemic hotplate threshold was restored. As alpha 2-agonists reduce and alpha 2-antagonists increase the outflow of central noradrenaline, it is suggested that activation of central noradrenergic systems is involved in the mediation of ischemia-induced analgesia.
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PMID:Involvement of alpha 2-receptors in the analgesia induced by transient forebrain ischemia in rats. 810 77

The development of tolerance to morphine analgesia in amnesic model mice and the role of arginine vasopressin (AVP) in the underlying mechanism was examined. Hypoxia, brain ischemia, scopolamine and electroconvulsive shock (ECS) manipulation caused amnesia in the step-through type passive avoidance learning test performed at 24 h after the training trial. The amnesic state lasted for at least 3 days and recovered to naive control level on the 20th day after each manipulation. In all amnesic groups, radioimmunoassayable AVP content in hypothalamus was decreased, in particular, the reduction was significant in hypoxia and ischemic induced amnesic animals, then recovered to the control level by 20 days after each treatment. Daily morphine, 10 mg/kg, s.c. easily resulted in the development of tolerance to the analgesic effect in control animals; however, such treatment failed to develop tolerance in amnesic model animals, leaving the analgesic effect unchanged to the control levels. Daily pretreatment with i.c.v. AVP, dose-dependently reinstated the development of tolerance in amnesic model mice. When morphine injection was started from 20 days after the amnesia inducing treatment, tolerance developed as in a similar pattern as in control animals. Thus, amnesic model mice are deficient in brain AVP levels, and consequently, a certain level of AVP in the hypothalamus is required for maintaining the normal function such as the development of tolerance to morphine and the recovery from amnesia.
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PMID:Lack of the development of morphine tolerance in experimental amnesia: role of arginine vasopressin. 850 24

Ergot's derivatives are widely used in the treatment of migraine and in the prophylaxy of deep venous thrombosis in association with heparin. Clinical ergotism is rarely observed and can affect all the arteries, especially of the inferior limbs. Vasospasm of the peripheral arteries and collateral formation are specific findings on angiography. We report the illustrative case of a 38 years old woman hospitalized for a small bowel occlusion. She suffers from chronic migraine treated by ergotamine tartrate. During her hospitalization, she develops an acute ischemia of the lower limbs. An ergotism was clinically suspected and confirmed by Duplex sonography which demonstrate multiple vasospasm. Under iv sodium nitroprusside and peridural analgesia the spasm resolved in 24 hours. The control Duplex sonography confirm the normality of the lower limb arteries. This examination modality allow a non-invasive diagnosis and evolution control of arteriospasm.
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PMID:[Value of duplex ultrasound in diagnosis of ergotism of the legs]. 858 19

The anticardiolipin or antiphospholipid antibody syndrome is characterized by an increased incidence of venous and arterial thromboses. This syndrome may occur in association with systemic lupus erythematosus or independently. Gastroenterological manifestations have included Budd-Chiari syndrome, hepatic infarction, esophageal necrosis with perforation, intestinal ischemia and infarction, pancreatitis, and colonic ulceration. We report a 39-yr-old man with antiphospholipid antibody syndrome complicated by adrenal insufficiency secondary to bilateral adrenal infarction who presented with severe epigastric pain. Endoscopic evaluation disclosed progressive gastric ulceration with necrosis in the distal body. Angiography revealed no vasculitis. Because of intractable pain despite intravenous anticoagulation and narcotic analgesia, the patient was taken to surgery, and an antrectomy with Billroth II gastrojejunostomy was performed. Histological examination revealed widespread vascular occlusive disease involving veins, small arteries, and arterioles present in all layers of the stomach and the perigastric fat consistent with the vasculopathy of the antiphospholipid antibody syndrome. Treatment with high intensity oral anticoagulation and corticosteroids resulted in clinical and endoscopic improvement. This case report extends the gastroenterological manifestations of the antiphospholipid antibody syndrome to include giant gastric ulceration and emphasizes the importance of anticoagulation in treatment.
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PMID:Giant gastric ulceration associated with antiphospholipid antibody syndrome. 912 46

Gastrointestinal problems, with an incidence of about 1%, may complicate the postoperative period after cardiovascular surgery, increasing morbidity, length of stay, and mortality. Several risk factors for the development of these complications, including preexisting conditions; advancing age; surgical procedure, especially valve, combined bypass/valve, emergency, reoperative, and aortic dissection repair; iatrogenic conditions; stress; ischemia; and postpump complications, have been identified in multiple research studies. Ischemia is the most significant of these risk factors after cardiovascular surgery. Mechanisms that have been implicated include longer cardiopulmonary bypass and aortic cross-clamp times and hypoperfusion states, especially if inotropic or intra-aortic balloon pump support is required. These risk factors have been linked to upper and lower gastrointestinal bleeding, paralytic ileus, intestinal ischemia, acute diverticulitis, acute cholecystitis, hepatic dysfunction, hyperamylasemia, and acute pancreatitis. Gastrointestinal bleeding accounts for almost half of all complications, followed by hepatic dysfunction, intestinal ischemia, and acute cholecystitis. Identification of these gastrointestinal complications may be difficult because manifestations may be masked by postoperative analgesia or not reported by patients because they are sedated or require prolonged mechanical ventilation. Furthermore, clinical manifestations may be nonspecific and not follow the "classic" clinical picture. Therefore, astute assessment skills are needed to recognize these problems in high-risk patients early in their clinical course. Such early recognition will prompt aggressive medical and/or surgical management and therefore improve patient outcomes for the cardiovascular surgical population.
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PMID:Acute gastrointestinal complications after cardiac surgery. 865 62


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