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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of ischemia, reperfusion and hypoxia on the cardiac acetylcholine, choline, norepinephrine and cyclic AMP contents were investigated in isolated, spontaneously beating rat hearts perfused under constant pressure (100 cm H2O) with Krebs-Henseleit solution gassed with 95% O2-5% CO2. Acetylcholine, choline and norepinephrine were determined by high performance liquid chromatography with electrochemical detection. Cyclic AMP was determined by radioimmunoassay. One min reperfusion following 15 min ischemia (termination of perfusion) caused a significant decrease in both cardiac acetylcholine (P less than 0.05) and norepinephrine (P less than 0.01) contents, but had no significant effect on the cardiac norepinephrine/acetylcholine content ratio, or choline or cyclic AMP content. By contrast, 16 min ischemia did not significantly affect the cardiac acetylcholine, norepinephrine, choline or cyclic AMP content. Also, 16 min hypoxia (perfusion with Krebs Henseleit solution gassed with 95% N2 5% CO2) decreased the cardiac norepinephrine content significantly (P less than 0.01) and norepinephrine/acetylcholine content ratio slightly but not significantly. However, hypoxia had no significant effect on the cardiac acetylcholine, choline or cyclic AMP content. Pre-treatment with 10 microns atropine sulfate prevented the decrease in the cardiac acetylcholine content caused by reperfusion but caused a significant depletion in the cardiac norepinephrine content in the control (P less than 0.01) and ischemia (P less than 0.05) groups and a significant decrease in the norepinephrine/acetylcholine content ratio in all three groups (all, P less than 0.05). Extending the reperfusion period to 5 and 10 min following 15 min ischemia also caused a significant decrease in both cardiac acetylcholine and norepinephrine contents compared with the control groups. However, no significant difference in these contents was found between 1 min reperfusion group and 5 or 10 min reperfusion group. Twenty or 25 min ischemia alone did not significantly affect these contents. These findings suggest that reperfusion disturbs both the sympathetic and parasympathetic nervous systems in the heart and that pre-treatment with atropine adversely affects the balance of the autonomic nervous system.
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PMID:Effect of reperfusion on the cardiac acetylcholine and norepinephrine contents in rat hearts. 254 84

Small mesenteric arteries supplying partially isolated jejunal segments were totally occluded for 5 minutes and then released. With video microscopy, blood flow was calculated from measurements of submucosal arteriolar diameter and red blood cell velocity. For the first 30 minutes of reperfusion, the serosa was superfused with a Ringer's vehicle containing either adenosine (ADO; 10(-4) M), acetylcholine (ACh; 10(-5) M), or prostacyclin (PGI2; 3 x 10(-7) M). Thereafter, the substances were removed from the suffusate, and superfusion continued with vehicle alone for an additional 10-30 minutes. These concentrations were equieffective for causing vasodilation. During the first minute of reperfusion, blood flow increased more than 300% of baseline in all groups. Within the subsequent 30 minutes, blood flow fell to 45 +/- 3% of baseline with vehicle alone, which demonstrates the no-reflow phenomenon. While either ADO, ACh, or PGI2 was in the suffusate, vasodilation was persistent. After washout of these substances, the postocclusion blood flows were significantly higher with each treatment than with vehicle alone, which shows that each substance had a positive action. However, with ADO, blood flow was 121 +/- 7% of baseline after washout, whereas with ACh or PGI2, it was 64 +/- 10% or 69 +/- 5% of baseline after washout. This property of ADO was observed if the mucosa was superfused with a Ringer's solution or with a bile salt solution, which suggests that ADO might have similar properties in situ. After 60 minutes of reperfusion, the intestinal villi were short, thick, and edematous with epithelial necrosis and crypt degeneration. ADO attenuated most of these histological changes to a greater extent than either PGI2 or ACh. Furthermore, ADO reduced a biochemical index of neutrophil infiltration; tissue myeloperoxidase concentration was increased to 169 +/- 14% of baseline with vehicle but was increased to 120 +/- 8% with ADO. Overall, these observations suggest that ADO protects the intestine from ischemia-reperfusion injury by causing vasodilation and by inhibiting neutrophil function. The vasodilatory effect probably is a minor component because other vasodilators (ACh and PGI2) had minimal protective effects in these conditions.
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PMID:Attenuation of no-reflow phenomenon, neutrophil activation, and reperfusion injury in intestinal microcirculation by topical adenosine. 266 71

Acetylcholine (ACh) is the neurotransmitter related to learning and memory. The activity of its metabolic enzyme - choline acetyltransferase (CAT) is found to be remarkably decreased at autopsy. We consider that there is some relationship between ACh and cerebrovascular dementia such as dementia in ischemia and forgetfulness after ischemia. So we studied the relationship between ischemia and cholinergic neuron. We examined changes of muscarinic cholinergic receptor (m-ChR) in experimental ischemia by binding assay and autoradiography, and performed immunohistochemical study of CAT that is, acetylcholine synthetase, by PAP method. We also studied delayed neuronal death from the aspect of cholinergic system because the hippocampus receives ACh pathway arising from the basal nucleus. Materials used include: Pulsinelli's 4 vessel occluded rats, Tamura's MCA occluded rats and forebrain ischemia mongolian gerbils. In ischemia, the number of m-ChR decreased and binding affinity of m-ChR increased, and recirculation caused increased the number of m-ChR. While m-ChR changed immediately after ischemia, it was not until the fourth day that CAT positive cells decreased in hippocampus. In other words, at first m-ChR in postsynaptic membrane changed in ischemia, and with the progress of neuronal damage, CAT also changed. After m-ChR decreased in the thalamus, stria terminalis and Meynert nucleus 1 day following ischemia, it decreased in hippocampus after 7 days. We can consider receptor changed corresponding to the pathway of cholinergic neuron. Our study suggested that the receptor change in cholinergic system plays some role in the delayed neuronal death in the hippocampus.
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PMID:[Changes in muscarinic cholinergic receptor and choline acetyltransferase in experimental ischemic brain]. 267 78

We measured regional cerebral blood flow and acetylcholine and choline concentrations in tissue fragments of normally perfused and ischemic cortical regions from 10 rats. Tissue uptake of [14C]iodoantipyrine was used to indicate regional cerebral blood flow, and gas chromatography-mass spectrometry was used to measure acetylcholine and choline concentrations. Cerebral cortical ischemia was induced by permanent occlusion of the middle cerebral artery, and variables were measured 2.5 or 24 hours later. A close correlation was found between tissue choline concentration and the reciprocal of regional cerebral blood flow. A large increase in tissue choline concentration was observed in the ischemic cortex. Choline production rate was estimated by plotting choline concentration against the reciprocal of regional cerebral blood flow. This rate was independent of choline concentration. Acetylcholine concentration, on the other hand, was constant in ischemic and normally perfused regions, except in the center of the ischemic region 2.5 hours after middle cerebral artery occlusion, where a significant decrease was observed.
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PMID:Effects of middle cerebral artery occlusion on cerebral cortex choline and acetylcholine in rats. 281 87

Effects of ischemia (20 min) on cerebral cortical prostanoid synthesis and microvascular responses to hypercapnia and topical acetylcholine were examined in anesthetized newborn pigs. Pial arteriolar dilation in response to hypercapnia (10% CO2 ventilation, 10 min) was absent 2 h after ischemia and reversed toward constriction by 24 h postischemia. In sham control piglets, hypercapnia increased cortical periarachnoid fluid prostanoid concentrations. After ischemia, hypercapnia did not affect prostanoid concentrations on the brain surface. Acetylcholine (10(-3) M)-induced pial arteriolar constriction was reversed toward dilation 24 h after cerebral ischemia. Further, acetylcholine-induced prostanoid synthesis was markedly attenuated after ischemia. We conclude that cerebral ischemia-reperfusion alters cerebral prostanoid synthesis and microvascular control in newborn pigs. These abnormalities persist for at least 24 h.
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PMID:Ischemia alters cerebral vascular responses to hypercapnia and acetylcholine in piglets. 291 33

Abnormal renovascular reactivity, characterized by paradoxical vasoconstriction to a reduction in renal perfusion pressure (RPP) in the autoregulatory range, increased sensitivity to renal nerve stimulation (RNS), and loss of vasodilatation to acetylcholine have all been demonstrated in ischemic acute renal failure (ARF). To determine if ischemic injury alters vascular contractility by increasing smooth muscle cell calcium or calcium influx, the renal blood flow (RBF) response to reductions in RPP within the autoregulatory range and to RNS were tested before and after a 90-min intrarenal infusion of verapamil or diltiazem in 7-d ischemic ARF rats. Both calcium entry blockers, verapamil and diltiazem, blocked the aberrant vasoconstrictor response to a reduction in RPP and RNS (both P less than 0.001). In a second series of experiments the potential role of an ischemia-induced endothelial injury and of the absence of endothelium-derived relaxing factor (EDRF) production were examined to explain the lack of vasodilatation to acetylcholine. Acetylcholine, bradykinin (a second EDRF-dependent vasodilator), or prostacyclin, an EDRF-independent vasodilator, was infused intrarenally for 90 min, and RBF responses to a reduction in RPP and RNS were tested in 7-d ischemic ARF rats. Neither acetylcholine nor bradykinin caused vasodilatation or altered the slope of the relationship between RBF and RPP. By contrast, prostacyclin increased RBF (P less than 0.001), but did not change the vascular response to changes in RPP. It was concluded that the abnormal pressor sensitivity to a reduction in RPP and RNS was due to changes in renovascular smooth muscle cell calcium activity that could be blocked by calcium entry blockers. A lack of response to EDRF-dependent vasodilators, as a result of ischemic endothelial injury, may contribute to the increased pressor sensitivity of the renal vessels.
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PMID:Smooth muscle calcium and endothelium-derived relaxing factor in the abnormal vascular responses of acute renal failure. 326 1

Simultaneous recordings of focal slow potentials (sVs) and chemosensory discharges were made from cat carotid body-nerve preparations in situ. Chemoreceptor stimulants (100% N2, asphyxia, NaCN, ACh and nicotine), and depressants (100% O2, spontaneous gasps and dopamine) changed receptor polarization. sVs evoked by stimulants had a negative polarity whereas depressants elicited positive deflections. There was a direct correlation between maximal frequency of chemosensory discharges and peak sV amplitude when NaCN injections or N2 inhalation were used. However, cholinergic agents, dopamine and substance P evoked sVs which lacked correlation in time-course, amplitude or polarity with changes in sensory frequency. After a 6-day carotid nerve crush, different stimuli still evoked sVs even in the absence of sensory discharges. Both sVs and chemosensory discharges were abolished after 1 h ischemia produced by ligature of carotid body blood vessels. Thus, sVs from carotid body chemoreceptors probably include a neuronal component (the generator potential) directly responsible for the origin of chemosensory discharges, and a non-neuronal component (receptor or secretory potentials) probably originating in glomus and/or sustentacular cells.
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PMID:Bioelectric potentials in the carotid body. 392 Nov 96

Interrupting the blood supply to the carotid body by ligating arteries of its vascular peduncle altered the chemoreceptive properties of the carotid nerve and produced structural changes in parenchymal (glomus and sustentacular) cells. The onset of ischemia was marked by an increase in the discharge of both A (myelinated) and C (unmyelinated) sensory fibers followed by depression and finally by receptor silence. The discharge of A-fibers disappeared after 30-50 min and that of C-fibers after 60-90 min. During ischemia of 15-60 min duration the threshold to pharmacological (NaCN, ACh) and 'natural' (hypoxic) stimuli progressively increased and was accompanied by reversible changes in the structure of parenchymal cells and nerve endings. Ischemia for 2 h or longer produced irreversible functional damage and disappearance of glomus and sustentacular cells from the carotid body. Following ischemic injury, nerve fibers regenerated and all responded to mechanical stimuli but only a few were stimulated by natural or pharmacological agents. Thus, parenchymal cells of the carotid body appear to be most important in transduction by allowing sensory fibers to respond to chemical stimuli.
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PMID:Effects of ischemia on the function and structure of the cat carotid body. 687 17

Acetylcholine neurons in the striatum are believed to be primarily intrinsic. In cats a cylinder of caudate tissue was isolated unilaterally from all afferent and efferent connections while preserving the blood supply through the base of the cylinder. Cats were decapitated two and four weeks after operation. Dorsal, intermediate and ventral portions of the viable isolated cylinder, and corresponding tissue from the contralateral hemisphere serving as control, were removed, weighed and frozen. Deuterated internal standards at concentrations approximating those of acetylcholine and choline in the tissue were added and acetylcholine and choline extracted, reacted with propionyl chloride and demethylated with sodium benzenethiolate. The derivatives were separated by gas chromatography, and the acetylcholine and choline concentrations in the tissue evaluated using selected ion monitoring of m/z 58, 60 and 64. The observed decrease in the acetylcholine concentration in the dorsal portion could be due either to the interruption of the cholinergic thalamic input or to the more severe ischemia in this portion. The increase in the acetylcholine concentration in the ventral portion, where blood circulation is normal, may reflect accumulation of acetylcholine in inactive intrinsic neurons after severance of their input, or indicate sprouting of intrinsic acetylcholine neurons.
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PMID:Changes in acetylcholine in caudate nucleus tissue isolated in situ detected by gas chromatography mass spectrometry selected ion monitoring. 722 34

Effects of short-term ischemia on chemoreceptor responses to various stimuli and ultrastructural features of the carotid body of the cat were examined. Total occlusion of the arteries supplying the carotid body induced an increase in chemoreceptor discharges. After 1-hr ischemia, chemoreceptor responses to NaCN and asphyxia were markedly depressed to 10-40% of the control, while those to ACh and HCl were not greatly affected. Prolonged ischemia (2-3 hr) produced a marked decrease in responsiveness to all stimuli. One-hr ischemia induced changes in the ultrastructural appearance of the glomus cell, including a decrease in the number of dense-cored vesicles, the appearance of swollen or vacuolated mitochondria and amorphous substances, while the nerve ending showed a relatively well-preserved appearance. Prolonged ischemia (2-3 hr) produced degenerative changes both in the glomus cell and nerve ending; vacuolation, a marked decrease in electron density of cytoplasmic matrix of the glomus cell and nerve ending, and marginal shrinkage of the nuclei. The results indicate that the markedly depressed responses to NaCN and asphyxia after 1-hr ischemia are due to dysfunction of the glomus cell, while ACh and HCl, acting directly on the nerve ending which was not greatly affected by ischemia, evoked well-preserved responses in the chemoreceptors.
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PMID:Alteration of chemoreceptor responses and ultrastructural features of ischemic carotid body of the cat. 732 17


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