Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirteen patients undergoing lower abdominal gynaecological surgery were allocated to general anaesthesia (halothane and nitrous oxide) or general anaesthesia plus extradural analgesia (T8-S5). I.v. glucose tolerance tests were performed on the day before surgery and 8 h after skin incision. All patients having extradural analgesia (T8) were pain-free following surgery. Extradural analgesia blocked the hyperglycaemic response to surgery but not the late postoperative cortisol response, although values were significantly less than in the group receiving general anaesthesia alone. Impairment of glucose tolerance and of insulin response to the glucose load in the period after operation were not influenced by extradural analgesia and this may have resulted from insufficient inhibition of the stress-induced release of catecholamines or cortisol, or both, or from blockade of stimulatory efferent sympathetic pathways to pancreatic islets.
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PMID:Postoperative glucose tolerance during extradural analgesia. 703 45

Glucose loading caused a significant increase in insulin response (IRI) in patients undergoing caesarean section both under general anaesthesia and under epidural analgesia. After a fast intravenous glucose loading given just before the administration of epidural bupivacaine, similar but more variable serum immunoreactive insulin levels were found as compared with those determined after a slower intravenous glucose infusion in patients under general anaesthesia. Plasma renin activity values did not change significantly in either group, but, differing from general anaesthesia, antidiuretic hormone levels (ADH) increased significantly in patients under epidural analgesia. The changes in IRI and ADH response may be caused by a higher psychic stress reaction of the conscious patients during caesarean section under epidural analgesia.
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PMID:Blood glucose, insulin, antidiuretic hormone and renin activity response during caesarean section performed under general anaesthesia or epidural analgesia. 704 9

A diabetic patient who was taking an intermediate-acting insulin preparation developed sudden hypoglycaemic coma after epidural analgesia between T5 and L1. Several diagnostic possibilities are discussed. It is concluded that prophylactic intravenous infusion of glucose and small doses of local anaesthetic are always advisable in diabetic patients having epidural analgesia.
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PMID:Hypoglycaemic coma following epidural analgesia. 744 12

Pharmacological studies suggest that diabetes produces changes in the brain opioid system, affecting several behavioral functions including analgesia, feeding and self-stimulation. Previous investigations of opioid receptor binding have failed to explain the unusual opioid pharmacology of the diabetic animal. In the present study, the effects of streptozotocin-induced diabetes on levels of three immunoreactive (ir)-prodynorphin-derived peptides, ir-dynorphin A1-17 (A1-17), ir-dynorphin A1-8 (A1-8) and ir-dynorphin B1-13 (B1-13), were determined in eleven brain regions known to be involved in appetite, taste and reward. Diabetes was found to increase levels of A1-17 in the ventromedial and dorsomedial hypothalamic nuclei (+60% and +25%, respectively) and levels of A1-8 in the dorsomedial and lateral hypothalamus (+45% and +35%, respectively). The possible significance of these results is discussed in relation to (i) diabetic hyperphagia, (ii) medial hypothalamic transduction of circulating insulin levels, and (iii) the potentiation of reward by metabolic need states.
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PMID:Effects of streptozotocin-induced diabetes on prodynorphin-derived peptides in rat brain regions. 758 38

Primary treatment of patients suffering from acute pancreatitis is conservative, irrespective of its etiology and initial severity. There is no effective specific therapy for treating the underlying disease process. As a result, the current therapeutic approach involves the provision of supportive care, the elimination of causal (biliary tract) disease, and the treatment of complications. Since complications may develop at any time, patients with moderate or severe disease should be admitted to an intensive care unit for interdisciplinary assessment and constant observation of their clinical status and computed tomography findings. Basic therapy should include total fasting, replacement of deficits in volume, electrolyte and albumin, as well as adequate analgesia. Depending on the patient's specific clinical condition, nasogastric suction, respiratory support, antibiotics, insulin and heparin may become necessary. The use of enzyme inhibitors and drugs capable of inhibiting pancreatic exocrine secretion has not proved effective in clinical trials. The value of prostaglandins, non-steroidal anti-inflammatory drugs and cholecystokinin receptor antagonists remains to be established. Early endoscopic retrograde cholangiopancreatography should be performed in patients with suspected underlying biliary disease. Papillotomy should be carried out only when calculi are present in the common bile duct. Local complications, such as pseudocysts and abscesses can often be treated by ultrasound- or CT-guided aspiration and drainage. However, when bacterial infection of pancreatic necrosis becomes evident, surgical intervention should be considered. Future evaluation of new therapeutic approaches by controlled studies needs to include a sufficient number of patients with severe acute pancreatitis.
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PMID:Current conservative treatment of acute pancreatitis: evidence from animal and human studies. 811 38

The effects of neuroleptanaesthesia on endocrine-metabolic changes during elective gastrectomy was investigated, comparing with those of epidural anaesthesia. Nine patients were given neuroleptanaesthesia and fifteen patients given thoracic epidural analgesia combined with general anaesthesia. We evaluated the levels of stress hormones, insulin and blood glucose. Epidural anaesthesia suppressed the increase of catecholamine, but neuroleptanaesthesia did not inhibit the elevation of the catecholamines. In neuroleptanaesthesia group, glucagon and growth hormone increased during surgery, and the levels of these hormones were significantly higher than those of epidural analgesia group. Blood glucose increased during operation in both groups. In epidural anaesthesia, the levels of insulin and insulin/glucose ratio were kept higher than those of neuroleptanaesthesia group, but this was not statistically significant. Lactate/pyruvate ratio and free fatty acid did not show any significant change during the study in both groups. These results suggest that neuroleptanaesthesia is not a suitable method for upper abdominal surgery.
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PMID:[Effect of neuroleptanaesthesia on endocrine-metabolic response during upper abdominal surgery]. 816 18

In situ saphenous vein arterial bypass flow was studied in 16 patients with respect to level of epidural anaesthesia. Arterial pressure and electromagnetic flow were used to evaluate arterial tone by intra-arterial (i.a.) papaverine. Eight patients had a low epidural block (< or = Th. 10) and eight patients were operated during high epidural anaesthesia (> Th. 10). Flow increased and arterial pressure decreased after i.a. papaverine in all patients. When compared with patients operated during high epidural anaesthesia, flow increase and decrease in vascular resistance took place in patients operated during low epidural anaesthesia (P < 0.02). Increase in arterial flow after i.a. papaverine was not significantly different in patients operated in low epidural and general anaesthesia (n = 8). In eight patients with insulin-dependent diabetes mellitus who had low epidural anaesthesia, the increase in flow after i.a. papaverine was not significantly different to that noted during high epidural anaesthesia. The results indicate that the level of analgesia influences graft flow after i.a. papaverine, probably reflecting differences in the effect of epidural anaesthesia on sympathetic tone to the leg.
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PMID:Intra-arterial papaverine and leg vascular resistance during in situ bypass surgery with high or low epidural anaesthesia. 842 5

The objective demonstration of improved postoperative recovery suggests that the surgical injury response induced by the laparoscopic approach is less intensive than that after open surgery. Twenty-five patients diagnosed as having noncomplicated gallstones were studied prospectively. They were operated by laparoscopy (group I, n = 12) or open surgery (group II, n = 13). Analgesia requirements (p < 0.026) and postoperative stay (p < 0.001) were significantly less in group 1. Cholecystectomy performed by either technical options induced a significant increase over basal values of glucose, lactate, white blood cell count, prolactin, ACTH, cortisol, interleukin 6, C-reactive protein, and PCO2. Both surgical procedures induced a significant reduction of total proteins, albumin, prealbumin, free fatty acids hemoglobin, hematocrit, and pH. There were no differences between the levels of growth hormone, insulin, glucagon, or PO2 during any of the periods studied. Comparison of the results of the two cholecystectomy techniques showed that laparoscopic cholecystectomy induced a significantly less intensive acute-phase response (area under the curve) of interleukin 6 (17 +/- 17 versus 47 +/- 26 pg/ml x hr x 10(2); p < 0.003), C-reactive protein (16 +/- 12 versus 35 +/-16 mg/dl x hr x 10; p < 0.004), and prealbumin (16 +/- 2.7 versus 13.8 +/- 2.3 mg/dl x hr x 10(2); p < 0.05). The surgical injury response after laparoscopic cholecystectomy is similar to that after open cholecystectomy, but the aeute-phase response component is less intense. This finding may be a consequence of the reduced size of the operative wound with laparoscopic cholecystectomy.
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PMID:Acute phase is the only significantly reduced component of the injury response after laparoscopic cholecystectomy. 866 26

Epilepsy is a clinical paroxysmal disorder of recurring seizures, excluding alcohol or drug withdrawal seizures or such recurring exogenous events as repeated insulin-induced hypoglycemia. Epilepsy has a profound impact on each individual diagnosed with this disease. Seizures have been and are thought to arise as a result of abnormalities in (a) neural circuits, (b) excitation/inhibition balance, (c) potassium, and (d) genetic abnormalities. Therapy for epilepsy is either medical, entailing the use of a variety of antiepileptic drugs, or surgical. An urgent approach to seizure control is indicated when status epilepticus occurs. When all standard therapy fails, general anesthesia can be used to control status epilepticus. Surgery is an option in the treatment of epilepsy and requires extensive preoperative evaluation. The primary concerns for the neuroanesthesiologist anesthetizing the patient with epilepsy are the capacity of anesthetics to modulate or potentiate seizure activity and the interaction of anesthetic drugs with antiepileptic drugs. Proconvulsant and anticonvulsant properties have been reported for nearly every anesthetic. If seizure spikes are to be evoked during seizure surgery, then light anesthesia with a proconvulsant anesthetic is used. Conscious analgesia can be used for awake seizure surgery. However, if electrocorticography is not planned, then a general anticonvulsant anesthetic maintenance regimen is used. The latter technique also may be useful in patients whose anesthetic management is complicated by an incidental history of epilepsy.
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PMID:Anesthetic implications of epilepsy, status epilepticus, and epilepsy surgery. 933 9

Coronary artery disease (CAD), arterial hypertension, chronic bronchitis and diabetes mellitus are the most frequently encountered diseases complicating the clinical course of the vascular patient. Clinical signs of cardiac or pulmonary disease are often absent in patients with decreased functional capacity due to claudication. For instance, clinical evidence of coronary artery disease was found in 36% of patients scheduled for different vascular surgical procedures, whereas coronary angiography revealed significant stenoses in as many as 53-68%. Patients with chronic hypertensive disease, coronary artery disease and increased impedance to left ventricular ejection due to atherosclerosis frequently develop impairment of left ventricular (LV) function. Even without clinical or radiological evidence, approximately 20-35% of vascular patients have a LV ejection fraction below 50% indicating impaired systolic LV function. The incidence of diabetes mellitus in vascular surgical patients is around 18%. When requiring insulin treatment, diabetes is an independent risk factor for postoperative ischemic events and congestive heart failure. Those with autonomic neuropathy are often asymptomatic as regards coronary artery disease. Coronary artery disease is responsible for over 50% of the immediate, medium- and long-term mortality and morbidity. Unstable myocardial ischemia, acute myocardial infarction which is detected by troponin I and ischemic pulmonary edema are the most common immediate postoperative cardiac complications. A large number of recent studies, using long-term ECG recording techniques, have allowed more accurate estimation of the incidence and time course of perioperative myocardial ischemia in vascular surgical patients. The highest incidence of ischemia when compared to daily life activities has been noted during the first two days after surgery but has been reported to remain elevated even 3-5 days after surgery. Interestingly, the incidence of intraoperative ischemia is lower than that observed during daily life. Knowledge of the etiology of perioperative myocardial infarction is essential if one is to improve cardiac outcome after vascular surgery. Many studies have addressed this important field in patients undergoing vascular surgery. They have documented a relationship between perioperative myocardial ischemia and postoperative myocardial infarction. Although postoperative myocardial infarctions are in most cases limited to endocardium (non Q wave infarction) they significantly reduce life expectancy of the vascular surgical patients. The reduction of cardiac risk following general surgery should focus on methods by which the incidence of myocardial ischemia, particularly during the postoperative period, could be reduced. These methods include intensive intraoperative analgesia or preventive administration of cardiovascular treatment which limit postoperative stress: alpha-2 agonists or betablocking agents. There are, at present, no studies which convincingly confirm an overall decreased mortality if coronary bypass surgery is performed prior to peripheral vascular surgery. Although it has been demonstrated that the mortality of the peripheral procedure is reduced to approximately one half, the mortality of a coronary bypass procedure in vascular surgical patients is five to eight times that recorded in a coronary artery bypass population without peripheral vascular disease. It remains to be shown if the use of coronary angioplasty prior to peripheral vascular surgery can provide a more satisfactory overall outcome. Several non-invasive techniques have been suggested to improve the identification of high-risk patients undergoing vascular surgery. These tests include exercise ECG, ambulatory ECG, dipyridamolethallium scintigraphy and determination of left ventricular ejection fraction by gated radionuclide imaging. (ABSTRACT TRUNCATED)
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PMID:[Physiopathologic introduction to anesthesia and resuscitation of the vascular patient]. 955 51


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