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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

51 patients who were selected for aorto-bifemoral bypass operation (infrarenal aortic aneurysm, iliac or iliofemoral occlusive disease) were randomized into two groups. 26 patients were operated on under neuroleptanaesthesia and 25 patients had a continuous thoracic epidural, which was supplemented with a light general anaesthesia during the operation. All patients were optimally volume loaded prior to surgery. The most marked haemodynamic alterations (tachycardia, arterial hypertension, increase of cardiac index, left ventricular stroke work index and cardiac minute work) were provoked by eventration of the gut. In the epidural group, these changes were attenuated and in contrast to the neuroleptanaesthesia group, there were a few patients who had a serious fall in blood pressure. These reactions were regularly accompanied by a generalized flush which led to the hypothesis that they were caused by the release of intestinal hormones, reactive peptides and neurotransmitters, from the mechanically irritated gut. Clamping of the aorta was relatively uneventful. Heart rate and cardiac index decreased in both groups but mean arterial pressure and pulmonary capillary wedge pressure remained stable. Systemic vascular resistance increased slightly in the neuroleptanaesthesia, but not in the epidural group. Declamping was followed by significant but transient falls in systemic vascular resistance and arterial pressure in both groups, despite sufficient volume loading before opening the clamp. In the neuroleptanaesthesia group these changes spontaneously returned to normal; in the epidural group 6 patients received vasopressors or positive inotropic drugs. These results indicate the following: Epidural anaesthesia prevents hypertension and tachycardia and lowers cardiac minute work. Eventration of the gut, acute blood losses and declamping of the aorta may be critical situations, which can lead to profound hypotension. Under neuroleptanaesthesia eventration of the gut is followed by tachycardia and hypertension whereas blood losses and declamping are not as critical as when an epidural is used. Only experienced anaesthetists should use epidural anaesthesia for aortic surgery. An intensive monitoring of haemodynamic function during this form of anaesthesia is mandatory.
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PMID:[Aortofemoral bifurcation bypass--effect of the anesthesia procedure (NLA, thoracic continuous catheter peridural anesthesia) on circulation, respiration and metabolism. Intraoperative circulatory reactions]. 390 40

The effects of intravenous infusion of diltiazem on regional blood flow (radioactive microspheres), hemodynamics, and maximum rate of oxygen consumption were evaluated in conscious rats with congestive heart failure caused by large myocardial infarction (n = 10, infarct size 41.8% of left ventricle) and compared with data obtained from rats subjected to sham surgical procedures (n = 9). In both groups data were obtained at rest and during submaximal treadmill exercise during alternate infusion of diltiazem and saline. In the group with heart failure, diltiazem increased stroke volume at rest and during exercise (p less than .05), reduced heart rate (p less than .05), and improved cardiac output during exercise (p less than .05) without increasing left ventricular end-diastolic pressure in any of the animals. Blood flow to renal and splanchnic circulations was reduced in the group with heart failure but was increased by diltiazem to values similar to those observed in sham-operated animals. Although skeletal muscle flow during exercise was significantly increased by the drug, maximal rate of oxygen consumption was not, indicating unchanged oxygen availability within working muscle. Thus diltiazem caused redistribution of blood flow to kidney and gut in animals with myocardial infarction and failure, thereby restoring blood flow to circulatory beds known to be impaired in this setting.
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PMID:Effects of diltiazem on cardiac function and regional blood flow at rest and during exercise in a conscious rat preparation of chronic heart failure (myocardial infarction). 399 15

A single dose of acrylonitrile can produce fatal adrenal apoplexy within approximately 2 h. Our previous studies also indicate that multiple injections of the chemical cause acute hemorrhagic and occasional nonperforating duodenal ulcers. Other authors have reported increase in gut and lung neoplasia after chronic exposure. The present study was designed to elucidate the subacute and chronic actions of acrylonitrile on the adrenals, stomach and duodenum by correlating biochemical, functional and morphologic investigations, as well as to gain insight into the mechanisms of action of acrylonitrile. Rats were exposed to 0, 0.0001% (1 ppm), 0.002%, 0.01%, 0.05% or 0.2% acrylonitrile in drinking water, or to the same amount of the chemical given through daily gavage, for 7, 21 or 60 days. Acrylonitrile caused a time- and dose-dependent decrease in plasma corticosterone levels; aldosterone was affected only by the 'high' dose and prolonged time of exposure. Young rats were more susceptible than adults to this action of acrylonitrile. The adrenal cortex, especially the zona fasciculata, was atrophic in rats that had ingested the nitrile through drinking water. At 0.05% and 0.2%, it also caused decreased food intake and body weight gain. The adrenals were enlarged with a hyperplastic zona fasciculata after daily doses of a bolus of acrylonitrile. Ingestion of the chemical did not interfere with compensatory enlargement of the adrenal gland following unilateral adrenalectomy. On the other hand, the ACTH-induced elevation of corticosterone plasma concentration was significantly attenuated by acrylonitrile in drinking water. Electron microscopy of the adrenal glands revealed no consistent changes in the steroid-producing cells. We thus postulate that accelerated turnover of circulating corticoids and/or interference with the secretion or action of ACTH may primarily be responsible for the decreased plasma levels of corticosterone and aldosterone in rats that ingest acrylonitrile. The mucosa in the stomach at the junction of the forestomach and glandular region of animals that had ingested acrylonitrile was hyperplastic. The corpus also showed regional mucosal hyperplasia with the appearance of 'cobble-stoning'. These changes were preceded and associated with an elevated concentration of non-protein sulfhydryls mostly in the mucosa of the glandular stomach. A similar, less prominent elevation also occurred in the proximal duodenum. These alterations may resemble the preneoplastic combination of elevated glutathione and focal hyperplasia described in the liver with hepatocarcinogens.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Subacute and chronic action of acrylonitrile on adrenals and gastrointestinal tract: biochemical, functional and ultrastructural studies in the rat. 674 95

Endothelin is a novel, potent, endogenous vasoconstrictor derived predominantly from endothelium and macrophages. Release of endothelin-1 (ET-1) into biological fluids was determined by radioimmunoassay in pigs undergoing either a hemorrhagic (3 h) or superior mesenteric artery (SMA) occlusion (5 h) shock followed by reperfusion (90 min) or a control group which was observed for 8 h. After surgery, there was a significant increase in ET-1 in jugular and carotid plasma, lymph, and ascitic fluid in all three models. The portal plasma ET-1 level was significantly increased (p < .05, assessed by the Spearman rank coefficient rho) in both shock models, but no significant increase was noted in the control group. In the SMA occlusion shock model, four pigs died within 30 min of reperfusion, and these animals had a much higher level of portal ET-1 (22.3 +/- 5.5 fmol/mL) than the two pigs that were alive by the end of the observation period (11.5 +/- 1.3 fmol/mL). Reperfusion in the SMA occlusion shock model induced a critical form of circulatory shock characterized by hypotension, decreased cardiac output, and decreased left and right ventricular stroke work index, and death occurred usually within 90 min. Reperfusion of the shed blood in the hemorrhagic shock model almost normalized the hemodynamic derangements caused by the hypovolemia (with the exception of RVSWI), and the portal plasma and ascitic ET-1 levels decreased. These results indicate that ET-1 is released from the gut in response to both general hypoperfusion and selective intestinal ischemia and reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Endothelin and hemodynamic responses to superior mesenteric artery occlusion shock and hemorrhagic shock in pigs. 774 37

During a period of 3 years in a University Hospital in Israel, 339 episodes of bacteraemia were observed in patients 80 years of age or older, and 658 episodes in patients 60-79 years of age. Patients older than 80 were more often residents of nursing homes, frequently had a history of a cerebrovascular accident, but were less often neutropenic. Twenty-four per cent of bacteraemia episodes in the very old were hospital acquired compared with 40% in the old patients. The most common source of bacteraemia was the urinary tract, 50% of episodes in the very old, and 34% of episodes in the old. The percentage of episodes in which anaerobic bacteria were isolated was 5% in the very old and 1% in the old, and the difference was significant when corrected for the sources of bacteraemia. All cases of community-acquired bacterial endocarditis in patients of 80 or over were caused by pathogens originating from the gut. Thirty-five per cent of patients of 80 and over and 30% of patients aged 60-79 years died during hospitalization. Fatality was not associated with advanced age in the very old. Factors significantly and independently associated with fatality in both groups were a hospital-acquired infection, shock, low serum albumin, renal dysfunction and inappropriate antibiotic treatment.
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PMID:Bloodstream infections in patients older than eighty years. 831 Aug 89

Thrombin inhibitors have been thought to play a pivotal role in myocardial infarct and stroke incidences and their aftermath. Quite some time ago potent synthetic thrombin inhibitors became known based on peptide derivatives D-Phe-Pro-Arg and benzamidine. One of them, fairly well characterised was beta-naphthylsulphonylglycyl-D,L-4-amidino-phenylalanylpiperidi de (NAPAP). NAPAP was prone to being administered intravenously due to its short plasma half life. Drawbacks to this compound such as effects on histamine release and blood pressure may have obstructed its clinical use. Long half life and oral bioavailability would be desirable for prophylactic treatment of thrombotic disorders. We have used NAPAP as a template for new synthetic compounds to improve some characteristics of its profile. For screening purposes we have investigated fairly simple surrogate parameters, aspects that were considered to contribute to pharmacological effects. Potency was correlated to thrombin inhibition, side effects were addressed by specificity toward thrombin as well as reduction in basicity, and plasma half life was considered to be modulated by plasma stability of the compound. Oral bioavailability would be affected by instability during the passage through the gut wall. Chemical introduction of a carboxylic group and exchange of the naphthyl group for 4-methoxy-2,3,6-trimethylphenyl led to a compound that when compared to NAPAP, exhibited a 4-fold increase in thrombin inhibitory activity and a 3-fold increase in trypsin specificity. Plasma stability decreased to 22 h, however, sufficient enough not to play a major role in plasma half life. Gut homogenate stability of the compound has not changed. The potency increase did not translate into a reduction in IC50-values for the coagulation assay aPTT and TT, in contrast to the IC50-values for thrombin-induced platelet aggregation.
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PMID:Synthesis and characterisation of novel thrombin inhibitors based on 4-amidinophenylalanine. 856 67

Less well established alternative neuromodulatory pathways are neuropeptide-mediated axon reflexes of sensory neurons, gut immunotrafficing, gut transmucosal transport of endogenous bacterial toxin, and the direct secretion of immunoregulatory cytokines by the brain. TNF-alpha and IL-1ra enter peripheral blood after their intracerebroventricular (i.c.v.) injection. Closed head injury or stroke increases blood IL-6 and the acute phase response; neuroblastomas immunosuppress by secreting TGF-beta. The IL-6 that appears in the blood after i.c.v. IL-1 in the rat is partly derived by secretion from the brain into the superior sagital sinus (Romero et al.; 1996. Am. J. Physiol. 270: R518) and is not dependent on peripheral sympathetic activation. Central endothelium and choroid plexus are potential sources of sagital sinus IL-6. TNF-alpha, which appears in blood after i.c.v. LPS, but not IL-1 beta, is due largely to toxin leaving the brain compartment and activating peripheral immunoreactive tissues. Antigens and cytokine immunoregulators drain into cervical lymph. Changes in glial milieu induced by intrinsic neuronal activity could by secretion from brain to blood modulate peripheral immunoreactivity.
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PMID:Alternative pathways of neural control of the immune process. 962 58

Heat stroke is a syndrome which reduces systemic vascular resistance and cardiac collapse. The gut plays an important role in shock. In hyperthermia, many of the same symptoms as heat stroke may be present, including inhibition of splanchnic vasoconstriction and endotoxemia. Furthermore, both conditions result in shock, in which the gut plays an important role. Detection of insufficient oxygenation of gut tissue, which sustains an earlier and more severe hypoxia, can warn of impending shock and can be performed by monitoring intramucosal pH (pHim). This index is very sensitive to tissue hypoxia and ischemia. In the present study both pHim, using tonometry, and gut blood flow during whole body heating (WBH) in pigs were measured. WBH was achieved by circulating warm water through a vinyl sheet covering the animal. Central venous pressure was maintained by fluid infusion. Body temperature was measured using a thermometer probe inserted into the right jugular vein. Mean arterial pressure, cardiac output and gut blood flow were also measured. pHim was evaluated using a tonometer placed into the midileum lumen. During WBH, cardiac index and mean arterial pressure increased, however systemic vascular resistance decreased. Gut blood flow was either maintained at the normal rate or increased. Intraarterial pH did not change significantly, however pHim significantly decreased from 7.30 at the beginning of WBH to approximately 7.05 after the body temperature reached 42.5 degrees C. These findings suggest that there was reduced oxygen delivery to the tips of the small intestinal villi during regional ischemia following WBH. In conclusion, insufficient tissue oxygen delivery as detected by a reduction in inramucosal pH is an important index in whole body heating.
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PMID:Changes in intramucosal pH and gut blood flow during whole body heating in a porcine model. 967 8

Both achalasia and Hirchsprung's disease arise from defects of innervation of the oesophagus and distal large bowel respectively. Their consequences are confined to disorders of motility in the relevant part of the gastrointestinal tract. Many neurogenic and primary muscle disorders are associated with abnormalities of gut motility. Stroke, even when unilateral, is commonly associated with dysphagia. Transcranial magnetoelectric stimulation has established that the pharyngeal phase of swallowing tends to receive its innervation principally from one hemisphere. In many neurological disorders, dysphagia is only one part of the clinical picture but in some--for example, the Chiari malformation--dysphagia may be the sole or major feature. Disturbances of small and large bowel motility, when seen in neurogenic disorders, are associated with autonomic neuropathy and are particularly common in diabetes mellitus. Primary muscle disorders can lead to dysphagia (for example, with polymyositis or oculopharyngeal dystrophy) or defects of large bowel motility (for example, with Duchenne's muscular dystrophy). Primary gut disorders particularly associated with neurological disease include pernicious anaemia, nicotinamide and thiamine deficiencies, selective vitamin E deficiency, and coeliac disease. Inflammatory bowel disease is associated with thromboembolic complications which may include the CNS, inflammatory muscle disease, and abnormalities on MRI of the brain of uncertain relevance. Whipple's disease is a rare condition which sometimes is largely or entirely confined to the CNS. In such cases, a particular neurological presentation can indicate the diagnosis.
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PMID:Neurology and the gastrointestinal system. 1040 May 14

The renin angiotensin system is highly activated in shock states and has been suggested to be involved in the pathophysiology of the markedly deteriorated splanchnic circulation seen in septic shock. The purpose of the present study was to elucidate the capability of losartan, a nonpeptide angiotensin II type 1 (AT1) receptor antagonist, to attenuate splanchnic blood flow disturbances and counteract intestinal mucosal acidosis in endotoxin shock. A total of 20 pigs were anesthetized and catheterized. Central and regional hemodynamics were monitored. A tonometer in the ileum was used for measurement of mucosal pH. Onset of endotoxin challenge was followed by losartan administration (n = 10) 2 h later. Ten animals receiving endotoxin only served as controls. The experiments were terminated 5 h after onset of endotoxin challenge. Endotoxin infusion induced an hypodynamic shock with a reduction in cardiac index and systemic oxygen delivery. Losartan reduced both systemic vascular resistance and pulmonary capillary wedge pressure while stroke volume was improved. Pulmonary hypertension induced by endotoxin was significantly reduced by losartan without further changes in gas exchange. The profound reduction in gut oxygen delivery in response to endotoxin was counteracted by losartan administration. However, losartan failed to improve the markedly deteriorated intestinal mucosal pH and mucosal-arterial PCO2gap (i.e., difference in intestinal mucosal PCO2 and arterial PCO2). Also the mucosal-portal venous PCO2gap, used as a monitor of the mucosa in relation to the gut as a whole (including the spleen and pancreas), was greatly increased by endotoxemia but unaffected by losartan administration. In summary, although the angiotensin II type 1 receptor antagonist losartan improved gut oxygen delivery and reduced pulmonary hypertension during established endotoxin shock, it had no effect on intestinal mucosal acidosis. These findings suggest contribution of the angiotensin II type 1 receptor to perfusion disturbances, but not to deterioration of intestinal mucosal homeostasis seen during endotoxemia.
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PMID:Angiotensin II receptor antagonism increases gut oxygen delivery but fails to improve intestinal mucosal acidosis in porcine endotoxin shock. 1003 Aug


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