Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To examine the interaction of epidural anesthesia, coagulation status, and outcome after lower extremity revascularization, 80 patients with atherosclerotic vascular disease were prospectively randomized to receive general anesthesia combined with postoperative epidural analgesia (GEN-EPI) or general anesthesia with on-demand narcotic analgesia (GEN). Demographics did not differ between groups except that the GEN-EPI group had a higher incidence of diabetes mellitus and of previous myocardial infarction. Coagulation status was monitored using thromboelastography. An additional 40 randomly selected patients without atherosclerotic vascular disease undergoing noncardiovascular procedures served as controls for coagulation status. Vascular surgical patients were hypercoagulable compared with control patients before operation and on the first postoperative day. Postoperatively, this hypercoagulability was attenuated in the GEN-EPI group and was associated with a lower incidence of thrombotic events (peripheral arterial graft coronary artery or deep vein thromboses). The rates of cardiovascular, infectious, and overall postoperative complications, as well as duration of intensive care unit stay, were significantly reduced in the GEN-EPI group. Stepwise logistic regression demonstrated that the only significant predictors of postoperative cardiovascular complications were preoperative congestive heart failure and general anesthesia without epidural analgesia. We conclude that in patients with atherosclerotic vascular disease undergoing arterial reconstructive surgery (a) thromboelastographic evidence of increased platelet-fibrinogen interaction is associated with early postoperative thrombotic events, and (b) epidural anesthesia and analgesia is associated with beneficial effects on coagulation status and postoperative outcome compared with intermittent on-demand opioid analgesia.
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PMID:Effects of epidural anesthesia and analgesia on coagulation and outcome after major vascular surgery. 195 66

In an effort to minimize the nutritional complications that follow resection of the pancreas for severe chronic pancreatitis, the authors have performed a duodenum-preserving total pancreatectomy in eight patients for severe unremitting pain requiring large doses of opiate analgesia. Good relief of pain was obtained in six patients (75%), in whom the quality of life was undoubtedly improved. There were no problems with the control of diabetes after this procedure in any of these patients, and no patient has suffered any hypoglycemic attacks requiring medical treatment. This improved control of the diabetic state is probably related to a more physiologic state of the upper digestive tract, enabling a normal food intake. The authors found the operation to be technically difficult, however, and although there were no post-operative deaths, major complications were encountered in four patients. These consisted of postoperative bleeding requiring reoperation (two patients), sepsis, and a duodenal fistula, which progressed to stenosis.
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PMID:Total pancreatectomy with preservation of the duodenum and pylorus for chronic pancreatitis. 195 10

The brain uptake of a number of benzodiazepines with different lipophilic and protein binding characteristics was investigated in male Sprague-Dawley rats using the rapid intracarotid artery injection technique. When the compounds were administered as a solution in Ringer's buffer, pH 7.4, the uptake was in the order of [14C]diazepam greater than [14C]L-663,581 (anxiolytic agent) greater than [3H]L-364,718 (morphine analgesia potentiator) greater than [14C]L-365,260 (anxiolytic agent) and their extraction ratio values were 71.0 +/- 6.8, 65.0 +/- 12.0, 42.0 +/- 5.0 and 6.0 +/- 2.0%, respectively. The respective permeability-surface product values were 0.755 +/- 0.152, 0.647 +/- 0.180, 0.329 +/- 0.05 and 0.035 +/- 0.011 ml/min/g. The rank order of brain extraction did not correlate well with the drugs' lipophilicity determined by octanol-buffer partition coefficient. For example, L-365,260 had the highest octanol/buffer partition coefficient, but the lowest brain extraction. Plasma protein binding significantly decreased the uptake by the brain but to a lesser extent than that predicted from the unbound drug fraction in vitro, suggesting that drug binding to plasma protein did not limit the transport of drug through the blood-brain barrier. For one compound, L-364,718, the extraction ratio and permeability-surface product values were increased markedly in CC1(4)-induced hepatic injury. Other disease states, uranyl nitrate-induced renal failure and streptozotocin-induced diabetes, had no apparent effect on the uptake of the compounds tested. The effect of disease state on the brain uptake of drug appeared to be dependent on the type of disease and the type of drug studied.
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PMID:Effects of protein binding and experimental disease states on brain uptake of benzodiazepines in rats. 197 Mar 63

Serum levels of cortisol, T3, T4 and blood levels of glucose, lactate and pyruvate were measured 15 min before anaesthesia, 15 and 60 min after skin incision and at 2 h after surgery, in 16 patients undergoing elective surgery on lower extremities either under epidural analgesia (group I) or general anaesthesia (group II). The results showed that as long as the effect of epidural analgesia persisted, it could inhibit the increases in cortisol and blood glucose and the decreases in T3 levels, observed under general anaesthesia. This is probably because of the blocking effect of epidural analgesia on the afferent neurogenic impulses from the area of surgery. T4, lactate and pyruvate levels were not affected to any significant extent. These observations could be of value in the operative management of patients with diabetes mellitus and others with a high surgical morbidity.
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PMID:Role of epidural analgesia on endocrine & metabolic responses to surgery. 234 6

Spontaneous or induced diabetes, as well as glucose loading, reduce opiate antinociception, presumably through induction of hyperglycemia. While peripheral administration of alloxan is a potent pancreatic beta-cell toxin, intracerebroventricular (ICV) alloxan reduces glucoprivic feeding in the absence of hyperglycemia, presumably through interactions with specific brain glucoreceptors. Our laboratory demonstrated that opioid-mediated 2-deoxy-D-glucose (2DG) antinociception is significantly reduced by central pretreatment with alloxan, and that this deficit is reversed by coadministration with 3M-D-glucose. The present study compared ICV and intravenous (IV) routes of alloxan (200 micrograms) upon morphine (1-10 mg/kg, SC) analgesia on the tail-flick and jump tests in rats, and evaluated these effects in terms of concomitant changes induced by ICV alloxan upon nonopioid-mediated continuous cold-water swim (CCWS: 2 degrees C for 3.5 min) antinociception. Two weeks following central, but not peripheral pretreatment with alloxan, morphine (2.5 and 5.0 mg/kg, SC) antinociception was markedly (30-56%) reduced on both nociceptive tests. In contrast, central pretreatment with alloxan respectively reduced (30 min) and subsequently potentiated (60 and 90 min) CCWS antinociception on the jump test. Alterations in antinociception by central alloxan occurred in the absence of changes in basal nociceptive thresholds, hypothermia or hyperglycemia. These data suggest that central alloxan may be acting upon either specific, but unidentified brain glucoreceptors and/or a glucoprivic control mechanism.
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PMID:Differential actions of central alloxan upon opioid and nonopioid antinociception in rats. 262 9

The metabolic-endocrine state of diabetes mellitus affects the brain and behavior of diabetic animals. Feeding, paradoxical sleep, analgesia, submissive behavior, and avoidance behavior, are generally increased in diabetic compared with nondiabetic rodents. In contrast, sexual behavior, aggressive behavior and sensitivity to the behavioral effects of amphetamine are decreased in diabetic rodents. This review examines behavioral changes in diabetes mellitus within the context of known disease-linked alterations in hypothalamo-pituitary relationships and brain monoamine metabolism.
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PMID:The psychoneuroendocrinology of diabetes mellitus in rodents. 268 24

The role of opioid receptors in diabetes and hyperglycemia-induced analgesia was studied in male Sprague-Dawley rats. Animals maintained under controlled environmental conditions were used in all studies. Pain latency was determined by the hot plate test (55 degrees C) and analgesy-meter force method. The results of these studies indicate that streptozotocin-induced diabetic animals have a significantly higher pain threshold (P less than 0.01) than the control groups. The pain threshold was found to be diurnally controlled with a peak at the beginning of the light phase (1000 hours) and a trough at the end of the dark phase (0800 hours). Diabetes-induced analgesia was found to be reversed by both acute or chronic insulin administration. In another study, glucose-induced hyperglycemic rats were found to have a significantly higher pain threshold (P less than 0.01) than control animals, with a peak occurring at the beginning of the dark phase (2000 hours), and a trough at the beginning of the light phase (0800 hours). The administration of the opioid antagonist naloxone (2 mg/kg) reversed the hyperglycemia and diabetic-induced analgesia. The results of these studies might indicate that analgesia found in diabetic or hyperglycemic animals may be related to the endogenous opioid system.
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PMID:The role of opioid receptors in diabetes and hyperglycemia-induced changes in pain threshold in the rat. 282 14

Possible changes in blood-brain barrier (BBB) function as a result of diabetes were investigated by assessing antagonism of morphine analgesia in diabetic mice by methylnaltrexone (MeNTX), an opioid receptor blocker that does not cross the BBB when administered subcutaneously (SC). In streptozotocin (STZ)-treated diabetic mice--but not vehicle-treated, non-diabetic mice--treatment with SC MeNTX significantly reduced morphine analgesia. In vehicle-treated, non-diabetic mice, morphine analgesia was antagonized by MeNTX administered intracerebroventricularly and by SC naltrexone, which crosses the BBB. Reduction of STZ-induced hyperglycemia by insulin reversed the effectiveness of SC MeNTX in antagonizing morphine analgesia. We hypothesize that in STZ diabetic mice, MeNTX was able to cross the BBB and block brain opioid receptors.
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PMID:Central pharmacological activity of a quaternary ammonium compound in streptozotocin diabetic mice. 284 78

Carotid endarterectomy in 39 elderly patients was carried out under local anesthesia and neuroleptic analgesia. There were no deaths within 30 days. Two patients required an intraoperative shunt because of signs of ischemic changes (aphasia, motor changes) during two-minute test cross-clamping. In two patients, transient vocal cord paresis was observed, and seven patients (18%) experienced immediate postoperative hypertension. Our results support the contention that in awake elderly patients the need for an intraoperative shunt can be accurately assessed by simple neurological monitoring. Carotid surgery under local anesthesia and neuroleptic analgesia appears to be a safe procedure, and is especially recommended for elderly patients with hypertension, diabetes mellitus or ischemic heart disease.
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PMID:Carotid surgery under local anesthesia in the elderly. 337 34

2-Deoxy-D-glucose (2DG) analgesia, mediated in part by endogenous opiate and hypothalamo-hypophysial systems is presumably activated by its stress-related properties. Recently 2DG hyperphagia, but not 2DG hyperglycemia was reduced by central pretreatment with the pancreatic beta-cell toxin, alloxan; this deficit was eliminated by co-administration of 3M D-glucose. The present experiment examined whether intracerebroventricular pretreatment with alloxan (40 or 200 micrograms) altered 2DG analgesia (400 or 700 mg/kg, IP) on the tail-flick and jump tests, and whether 3M D-glucose co-administration ameliorated any deficits. Both alloxan doses significantly reduced 2DG analgesia (400 mg/kg) on both tests. 2DG analgesia (700 mg/kg) was significantly reduced by both alloxan doses on the jump test, but only by the higher alloxan pretreatment on the tail-flick test. 3M D-glucose co-administration ameliorated alloxan-induced analgesic deficits more effectively at the lower 2DG dose. Neither alloxan nor alloxan/3M D-glucose treatments altered basal thresholds. These data pertain both to alloxan's effects upon coding of 2DG effects as stressful, and to the role of diabetes and/or central glucoreceptors in analgesic processes.
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PMID:Intracerebroventricular alloxan reduces 2-deoxy-D-glucose analgesia. 339 8


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