Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0278134 (anesthesia)
 110,339 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human and animal studies suggest a poorer outcome in the presence of abnormal blood glucose concentration during cerebral hypoxia-ischemia. It is unknown whether this is also the case in acute severe carbon monoxide poisoning. Using Levine-prepared rats, three groups were established and exposed to CO to answer this question: (1) hyperglycemics resulting from the administration of a 50% glucose solution, (2) hypoglycemics resulting from the administration of normal saline, and (3) untreated controls. The rats inhaled 2400 ppm CO for 90 min in the absence of anesthesia. Blood glucose was raised to a mean value of 402 mg/dL just prior to CO exposure in group 1. This resulted in an increased mortality rate (i.e., 54%), and during 4 h of room air recovery an impaired ability to regain body temperature, an increased plasma lactate dehydrogenase activity, and an increased neurologic deficit as compared with group 3. Hypoglycemia, which developed during CO exposure in group 2 (mean minimum glucose after 90 min, 44 mg/dL), resulted in an increased mortality rate (i.e., 46%), and during 4 h of room air recovery an impaired ability to regain body temperature and an increased neurologic deficit as compared with group 3. Blood glucose concentration in the rats in groups 2 and 3 that died during or shortly after CO exposure was significantly depressed relative to the survivors of those groups. Plasma insulin activity was elevated during CO exposure in group 1 as compared with group 3, but fell during recovery; insulin remained low throughout CO exposure and recovery in group 2. The results demonstrate the deleterious effects of both a very high and a very low blood glucose concentration during acute CO exposure.
 ...
PMID:Acute severe carbon monoxide exposure in the rat: effects of hyperglycemia and hypoglycemia on mortality, recovery, and neurologic deficit. 178 98

The effect of postischemic halothane anesthesia on locomotor activity and delayed neuronal injury in the hippocampal CA1 sector was examined in gerbils subjected to 5-min forebrain ischemia. Locomotor activity was assessed for 48 h after ischemia using an animal activity monitor, and CA1 injury was evaluated by counting the number of surviving neurons following 7 days of recirculation. Sham-treated animals exhibited a slight decrease of motor activity for about 1 day after surgery. Gerbils subjected to ischemia without postischemic halothane anesthesia developed significant motor hyperactivity (18 times higher than control activity) between 1.7 h and 6.7 h of recirculation. Surviving CA1 neurons in this group amounted to only 17% of those in the control animals. Postischemic halothane anesthesia during the initial 1.7 h of recirculation abolished subsequent motor hyperactivity and protected 84% of all CA1 neurons. Postischemic halothane anesthesia during 1.7 h-3.3 h of recirculation and 3.3-5 h of recirculation did not abolish motor hyperactivity except during the period of anesthesia, and did not protect hippocampal CA1 neurons (only 24% and 10% neuronal survival, respectively). These results demonstrate that the therapeutic window of halothane anesthesia for protection of hippocampal injury precedes the phase of locomotor hyperactivity, and that the appearance of the latter predicts delayed neuronal death.
 ...
PMID:Therapeutic window of halothane anesthesia for reversal of delayed neuronal injury in gerbils: relationship to postischemic motor hyperactivity. 178 47

Exposure to cocaine during development has been shown to cause structural and functional alterations in the nervous system. In the current study, the mechanisms underlying these effects were examined in neonatal rats through measurement of ornithine decarboxylase activity, a key regulatory enzyme in the control of neural cell differentiation. Animals were given cocaine (30 mg/kg SC) and ornithine decarboxylase measured 1 and 4 h later in midbrain + brainstem, cerebral cortex and cerebellum. Cocaine caused inhibition of ornithine decarboxylase activity that was not secondary to local anesthesia, as lidocaine was ineffective. The effect of cocaine was independent of direct central actions, as introduction of the drug into the central compartment via intracisternal injection failed to inhibit ornithine decarboxylase. In contrast, prevention of cocaine-induced ischemia by peripheral alpha-adrenergic blockade (phenoxybenzamine) reversed the ornithine decarboxylase inhibition caused by cocaine, and actually unmasked potential stimulatory actions. These data indicate that cocaine-induced ischemia is a major contributor to the net effect of the drug on central nervous system cellular development.
 ...
PMID:Ischemia contributes to adverse effects of cocaine on brain development: suppression of ornithine decarboxylase activity in neonatal rat. 178 62

We hypothesized that xanthine oxidase plays a role in the postischemic reperfusion injury in the equine small intestine. Under anesthesia, four horses and two ponies underwent ischemic strangulating obstructions of segments of the proximal jejunum, mid-jejunum and ileum. Prior to vascular occlusion, and at 1 h and 2 h of ischemia, full-thickness intestinal biopsies were collected for histopathological evaluation and for determination of combined xanthine dehydrogenase (XDH) plus xanthine oxidase (XO) activity, and XO activity alone. The level of XO activity was expressed in percentage according to the ratio of XO/(XDH + XO). We found a nearly threefold increase in the combined level of XDH plus XO activity from ileum to duodenum (p less than 0.04). However, the preischemic level of % XO activity did not vary significantly (p = 0.61) between segments of jejuno-ileum. Likewise, no significant difference was noted between intestinal segments after ischemia. Therefore, the data from all intestinal segments were pooled for each time and analyzed using Wilcoxon's signed rank test (one-tailed). Compared to the pre-ischemic level of % XO activity (median 27%), the % XO activity increased after 1 h of ischemia (median 37.0%), reaching statistical significance (p = 0.016). There were no statistical differences between the preischemic % XO activity and the % XO activity in non-ischemic bowel at the end of the anesthetic period. During ischemia, % XO activity increased, which lends credence to the importance of xanthine oxidase in previously-documented reperfusion injury in the equine small intestine.
 ...
PMID:Xanthine oxidase formation during experimental ischemia of the equine small intestine. 179 Apr 84

The present study was undertaken to ascertain the role of the microcirculation in the phenomenon of hypoperfusion following complete cerebral ischemia. The experiments were performed on rats under superficial ether anesthesia. Cerebral ischemia was induced by cardiac arrest for 3.5 or 10 min, with survival periods that lasted from 3 min to 7 days. A special metal hook-like device was inserted into the chest cavity at the third intercostal spaces for occluding the cardiac vessel bundle. The effect of this procedure was total cessation of systemic circulation, i.e., clinical death. In 52% of animals with 10-min clinical death, resuscitation (external heart massage and artificial ventilation) restored heart activity. When brain circulation was restored, respiratory activity, pain reaction, corneal reflex, bioelectric activity of the cortex, and normal activities of the rats returned. Scanning electron microscopy was applied to study the effect of ischemia on the vessel wall and endothelial cells (EC). Ischemia produced a remarkable increase in the numbers of microvilli and pit-like invaginations on the luminal EC surface. The luminal wall surface of many of the microvessels (MV) formed ridges. Frequently, microthrombi of varying sizes were observed. The most prominent changes were noted from 3 min to 6 h of recirculation, and they correlated with hypoperfusion after ischemia. Seven days later, these changes completely disappeared. The data presented here indicate that progressive hypoperfusion after ischemia occurs with significant alterations in the MV walls. These studies collectively suggest that the focal responses in select MVs may be associated with receptor molecule up-regulation of some, but not all, affected ECs. Our data provide further characterization of a new and unique chronic model of brain ischemia that can be applied to relevant clinical studies.
 ...
PMID:Reassessment of a new model of complete cerebral ischemia in rats. Method of induction of clinical death, pathophysiology and cerebrovascular pathology. 179 62

The effect of KW-3635 (sodium (E)-11-[2-(5,6-dimethyl-1-benzimidazolyl) ethylidene]-6,11-dihydrodibenz[b,e] oxepine-2-carboxylate monohydrate, CAS 127166-41-0), a novel thromboxane A2 (TxA2) receptor antagonist, on collagen-induced coronary ischemia was studied in guinea-pigs. Under pentobarbital anaesthesia, intravenous injection (i.v.) of collagen (1 mg/kg) induced abnormal ECG changes such as ST-T changes, elevation of T-wave arrhythmia and cardiac arrest in severe cases. The changes of ECG (leads I, II and III) were recorded for 10 min following collagen injection. KW-3635 (25-50 mg/kg p.o.) remarkably improved the collagen-induced ischemic ECG changes. The effect of KW-3635 was more potent than those of daltroban, isbogrel and ticlopidine. Neither nifedipine nor propranolol had any effect. The plasma thromboxane B2 level in the KW-3635-treated animals was lower in comparison with those in both the control and daltroban-treated animals. These results suggest that TxA2 may play a role in this model of coronary ischemia and that KW-3635 is effective in the treatment of ischemic heart disease.
 ...
PMID:Beneficial effect of the novel thromboxane A2 receptor antagonist sodium (E)-11-[2-(5,6-dimethyl-1-benzimidazolyl)ethylidene]-6,11- dihydrodibenz[b,e]oxepine-2-carboxylate monohydrate on collagen-induced coronary ischemia in guinea-pigs. 181 24

The anesthesia for combined carotid endarterectomy (CEA) and coronary artery bypass grafting (CABG) is mentioned in this report. Although electroencephalogram was set up to detect the sign of brain ischemia during surgery, it became unreliable because of electrical noise from the medical instruments. Another monitoring method, such as trans-cranial Doppler, was thought to be needed to avoid the electrical noise. In anesthesia, a gradual measured induction with judicious fluid loading was imperative along with a protection from the reflex response to pain stimuli. Thiopental was used to protect the brain from ischemic injury during CEA. The perfusion pressure during cardiopulmonary bypass was maintained at 55-65 mmHg, and no neurological complication was seen.
 ...
PMID:[Anesthesia for combined carotid endarterectomy and coronary artery bypass grafting]. 182 6

To examine the relationship between myocardial ischemia in patients with steal-prone coronary anatomy and the administration of isoflurane anesthesia, we reviewed coronary angiograms of 955 patients who had participated in a randomized trial of the use of one of four primary anesthetics for coronary artery bypass operations. Steal-prone anatomy was found in 31.8% of patients who had received enflurane; 40.0%, halothane; 32.6%, isoflurane; and 31.7%, sufentanil. Detected by greater than or equal to 0.1 mV ST segment displacement, ischemia during anesthesia occurred in 290 (30.4%) of all patients with no difference in the incidence among the four primary anesthetics (27.5%-32.9%). Patients with steal-prone anatomy did not suffer more ischemia than patients who needed coronary artery bypass surgery but with other varieties of coronary anatomy. In patients with steal-prone coronary anatomy, the incidence of myocardial ischemia by primary anesthetic was 24.0% with enflurane, 34.4% with halothane, 32.1% with isoflurane, and 38.2% with sufentanil. Systolic blood pressure less than 90 mm Hg during anesthesia occurred in 416 (45.6%) patients and was twice as common during administration of volatile anesthetics than during that of sufentanil. Hypotension did not increase ischemia frequency in patients with steal-prone anatomy with use of any of the four primary anesthetics including isoflurane. Ischemia was temporally related to hypotension in only 9 patients (0.9%). In none of the 42 patients who had steal-prone anatomy and hypotension during isoflurane anesthesia was ischemia temporally related to hypotension.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Steal-prone coronary anatomy and myocardial ischemia associated with four primary anesthetic agents in humans. 182 84

Whether isoflurane has the potential to produce coronary artery steal and associated myocardial ischemia is still controversial. Previous studies addressing this issue in humans did not purposefully control hemodynamics or use continuous measures of myocardial ischemia. The authors used transesophageal echocardiography (TEE) and continuous Holter electrocardiography (ECG) to study the relative risk of myocardial ischemia during isoflurane or sufentanil anesthesia under strict control of hemodynamics in 186 high-risk patients undergoing elective coronary artery bypass graft (CABG) surgery. Overall, hemodynamics were well controlled (increased heart rate = 9.8%; increased systolic blood pressure = 7.1%; decreased systolic blood pressure = 10.8% of total prebypass time compared with preoperative baseline values), with no difference between the two anesthetics. In the 162 patients with interpretable TEE recordings, moderate to severe TEE ischemic episodes (grade change greater than or equal to 2) developed in 33 (21%) during the prebypass period, with no difference between isoflurane (12 of 56 = 21%) and sufentanil (21 of 106 = 20%) (P = 0.97). The duration and severity of TEE episodes were not significantly different between the two groups. No correlation was observed between TEE ischemic episodes and isoflurane concentrations (range 0.47-1.75%). In the 181 patients with interpretable ECG recordings, ECG evidence of ischemia developed in 34 (19%) during the prebypass period, with no difference between isoflurane (12 of 59 = 20%) and sufentanil (22 of 122 = 18%) (P = 0.87). The duration and severity of electrocardiographic ischemic episodes were also similar in patients receiving either isoflurane or sufentanil. Four of the 62 patients (6%) who received isoflurane had an adverse cardiac outcome versus 15 of 124 patients (12%) who received sufentanil (P = 0.34). The authors' findings demonstrate that, when hemodynamics are controlled, the incidence of myocardial ischemia (TEE or ECG) during isoflurane and sufentanil anesthesia is similar.
 ...
PMID:Isoflurane anesthesia and myocardial ischemia: comparative risk versus sufentanil anesthesia in patients undergoing coronary artery bypass graft surgery. The SPI (Study of Perioperative Ischemia) Research Group. 182 89

Treatment of severe hand ischemia a associated to progressive systemic sclerosis and other disorders is controversial. We studied prospectively 45 patients, 41 female and 4 males, over an 11 year period. Age ranged from 16 to 73 years, mean 46. Underlying disease was systemic sclerosis in 30, CREST in 8, overlapping syndrome in 4, systemic lupus in 1 and non rheumatic vasculitis in 2 patients. Treatment consisted of intravenous injection of reserpine, 1 mg, at a superficial arm vein after controlled local circulatory block for 15 min. Regional anesthesia was required in 38 patients. Adequate follow up was obtained in 32 females and 2 males, receiving a mean of 3.1 therapy sessions (range 1 to 13). Morphologic improvement from 3.09 +/- 0.16 to 1.57 +/- 0.13 and functional improvement from 3.6 +/- 0.12 to 1.75 +/- 0.14 (5 grade scoring system), was observed (p < 0.001). These results correlate with adequate rehabilitation confirmed clinically.
 ...
PMID:[Severe ischemia of the hand. Treatment with regional intravenous sympathicolysis with reserpine]. 184 85


<< Previous 1 2 3 4 5 6 7 8 9 10