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

Together with embolic risk, hemodynamic risk tends to play an important role in cerebrovascular pathology. Studies of cerebral reserve have resulted from the difficulty of accurately estimating the repercussions of arterial lesions. The vascular reserve of a given region is the ratio between maximum and baseline flow. Maximum cerebral flow is obtained by inhalation of a gaseous mixture containing CO2 5%. An excellent correlation was found between lesion size and a decrease in the reserve. Three stages could be defined by positron emission transaxial tomography: a zone of hemodynamic reserve without modification of oxygen extraction; a zone of extraction reserve in which inflow insufficiency is compensated by increased oxygen extraction (this is the critical zone requiring action); and a zone of actual ischemia in which the extraction reserve is not exhausted. However, this technique is cumbersome and difficult to apply. Protocols are now being developed using the transcranial Doppler examination to define "a limit of autoregulation reserve", in which case it will be possible to assess the effects of arterial lesions. In fact, it would appear that cerebral irrigation depends on a very large number of factors, many of which are variable, whereas only a "snapshot" of the vascular situation can be obtained. Nevertheless, hemodynamic risk can be better assessed through an association of different explorations.
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PMID:[Cerebral reserve. A method for evaluating cerebro-vascular hemodynamic risk]. 228 23

Experiments were designed and performed to determine whether endothelial function remained chronically impaired after coronary artery reperfusion. Canine left anterior descending coronary arteries were exposed to ischemia (60 minutes) followed by reperfusion (12 weeks). Rings (3-4 mm wide) of the reperfused artery and of normal left circumflex (control) coronary artery segments were suspended in organ chambers containing physiological saline solution (37 degrees C, gassed with 95% O2-5% CO2) for isometric force measurement. Endothelium-independent contractions to KCl or prostaglandin F2 alpha and endothelium-independent relaxations to nitric oxide or isoproterenol were comparable in control and chronically reperfused arteries. However, chronically reperfused coronary arteries exhibited impaired endothelium-dependent relaxations to aggregating platelets. In addition, the reperfused coronary arteries exhibited impaired endothelium-dependent relaxations to the platelet-derived compounds adenosine diphosphate, serotonin, and thrombin. However, the endothelium-dependent relaxations to acetylcholine were comparable between control and reperfused arteries. Thus, after 12 weeks of reperfusion, previously occluded coronary arteries exhibited a selective impairment of endothelium-dependent relaxation evoked by aggregating platelets. In vivo, this phenomenon could favor platelet adhesion, aggregation, and platelet-induced contraction of coronary smooth muscle and thus facilitate ischemic events such as vasospasm and coronary thrombosis.
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PMID:Long-term impairment of endothelium-dependent relaxations to aggregating platelets after reperfusion injury in canine coronary arteries. 234 84

Innate biochemical responses of rabbit renal proximal convoluted (PCT) and straight (PST) segments following in vitro exposure to anoxia or hypoxia were investigated to delineate the mechanisms responsible for segment-selective injury in vivo. After bulk isolation, suspensions (1 mg/ml) enriched in either PCT or PST were preincubated in Dulbecco's modified Eagle's-Ham's F-12 medium for 1 h before being exposed to either 40 min of anoxia (N2) or 120 min of hypoxia (1% O2) and 1 h of recovery under air-CO2 conditions. After recovery from anoxia, the percent of control values for each viability indicator in PCT and PST, respectively, were as follows: O2 consumption (QO2), 30/50; ATP content, 22/49; K+ content, 60/70; and percent lactate dehydrogenase (LDH) release, 66/45. Likewise, following recovery from hypoxia, the percent of control values for PCT and PST, respectively, were as follows: QO2, 50/90; ATP, 16/57; K+, 52/79; LDH, 45/17. These differential responses indicate that PCT segments were innately more susceptible to anoxic and hypoxic injury than PST segments. Because ATP content was significantly higher in PST segments immediately after anoxia and hypoxia, we investigated glucose-dependent responses during anoxia by exposing these segments to 30 min of anoxia in nutrient buffer with or without glucose. Results from these experiments demonstrate that the PST protection from anoxia was glucose dependent because removal of glucose from the nutrient buffers during anoxia abolishes the differential responses between PCT and PST. The in vitro PCT sensitivity observed here contrasts with the PST sensitivity observed following in vivo ischemia, suggesting that hemodynamic factors present in vivo may ultimately determine the overall susceptibility of PST segments in situ.
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PMID:Bulk isolation of renal PCT and PST. II. Differential responses to anoxia or hypoxia. 237 90

We previously reported in working swine hearts a preferred use of fatty acids during early myocardial reperfusion. The purpose of these studies was to test whether this pattern of substrate oxidation was the result of excess energy demands during mechanical recovery. Two groups of pig hearts (n = 15) were compared. Both received Intralipid with heparin (serum fatty acids, 1.02 +/- 0.05 mumol/ml) to ensure preferred substrate availability and both received [2-14C]pyruvate to monitor myocardial use of a carbohydrate substrate. In one group (n = 8) oxfenicine was administered to suppress fatty acid utilization. Left anterior descending (LAD) coronary flow was maintained at aerobic levels for 30 min, reduced by 60% for 45 min, and restored to aerobic levels for a final 50 min. Ischemia caused the expected decreased in global and regional mechanical performance. Recovery in motion during reflow was less in oxfenicine-treated hearts (73 vs. 32% decrease in systolic shortening from aerobic values in treated and control hearts, P less than or equal to 0.01 and P less than or equal to 0.05, respectively). Pyruvate oxidation declined dramatically in both groups during ischemia but recovered disparately. In control hearts CO2 production remained depressed during reperfusion (NS from ischemic values), whereas in treated hearts it increased 5.5-fold (but did not exceed aerobic values). Tissue levels of acetyl CoA and acetylcarnitine were not statistically different between perfusion beds (aerobic vs. reperfusion) within groups. Oxfenicine reduced levels of acetyl carnitine in both perfusion beds.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanisms of substrate preference for oxidative metabolism during early myocardial reperfusion. 238 16

This study was designed to investigate the hemodynamic characteristics of cavernous angiomas of the brain. Five adult patients with a cavernous angioma underwent local cortical blood flow studies and vascular pressure measurements during surgery for the excision of the cavernous angioma. Clinical presentation included headache in four patients, seizures in four patients, and recurring diplopia in one patient. Magnetic resonance imaging demonstrated the cavernous angiomas in all patients and revealed an associated small hematoma in two. Four patients with a cerebral cavernous angioma were operated on in the supine position and the remaining patient, whose lesion involved the brain stem, was operated on in the sitting position. Mean local cortical blood flow (+/- standard error of the mean) in the cerebral cortex adjacent to the lesion was 60.5 +/- 8.3 ml/100 gm/min at a mean PaCO2 of 35.0 +/- 0.6 torr. Mean CO2 reactivity was 1.1 +/- 0.2 ml/100 gm/min/torr. The local cortical blood flow results were similar to established normal control findings. Mean pressure within the lesion in the patients undergoing surgery while supine was 38.2 +/- 0.5 mm Hg; a slight decline in cavernous angioma pressure occurred with a drop in mean systemic arterial blood pressure and PaCO2. Mean pressure in the cavernous angioma in the patient operated on in the sitting position was 7 mm Hg. Jugular compression resulted in a 9-mm Hg rise in cavernous angioma pressure in one supine patient but no change in the patient in the sitting position. Direct microscopic observation revealed slow circulation within the lesions. The hemodynamic features demonstrated in this study indicate that cavernous angiomas are relatively passive vascular anomalies that are unlikely to produce ischemia in adjacent brain. Frank hemorrhage would be expected to be self-limiting because of relatively low driving pressures.
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PMID:Vascular pressures and cortical blood flow in cavernous angioma of the brain. 239 87

1. In the present three-part study electrophysiological techniques were used to characterize responses of afferent fibers in the rat hypogastric nerve to mechanical or chemical stimulation of the uterus, and anatomical techniques were used to identify the spinal segments through which uterine afferent fibers enter the spinal cord. 2. In an in vivo barbiturate-anesthetized preparation, hypogastric afferent fibers responded in a time-locked manner to mechanical stimulation confined to restricted regions of the uterus and adjacent ligament. Receptive fields were most often located on the uterine body, particularly over the cervix. The few located on the uterine horn were usually near regions irritated during preparative surgery. Effective mechanical stimuli (pressure, stretching, squeezing, probing, rarely contractions) were typically greater than 5 g and simultaneously accompanied by transient ischemia around the probe or contracted area. Distension, unless extreme, was not an effective stimulus. Retrospective analysis of the data indicated that fibers may be more sensitive to uterine stimulation when rats are in vaginal estrus/proestrus than in diestrus/metestrus. 3. In an in vitro preparation, hypogastric afferent fibers responded in a dose-dependent fashion to injections into the uterine artery of the algesic chemicals bradykinin, 5-hydroxytryptamine, and KCl. They also responded to high doses of CO2 (in saline) and NaCN, but rarely to lower doses. Nearly all fibers responded to more than one chemical with response characteristics unique to each chemical (e.g., latency, duration, peak rate). 4. Injections of horseradish peroxidase into the uterine body and small portions of the adjacent horns in rats in vaginal estrus consistently labeled a small number of cells in the L1-S1 dorsal root ganglia, with peaks at L2 and L6. Virtually no cells were labeled in rats whose estrous cycle had been disrupted (by inadvertently keeping them in constant light conditions for several weeks). 5. These results indicate that uterine afferent fibers travel to the central nervous system through both the hypogastric (e.g., L1-L4 ganglia) and pelvic (e.g., L5-S1 ganglia) nerves in the rat, and that hypogastric fibers are capable of conveying fairly precise information about temporal and spatial aspects of uterine mechanical and chemical stimulation. The results also encourage future research into the possibility that the responses of these fibers vary as a function of estrous stage or other aspects of the condition of the uterus (e.g., its irritation).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Afferent fibers supplying the uterus in the rat. 244 20

We studied the in vivo effects of Daflon 500 mg on transvascular movement of macromolecules induced by bradykinin (BK) and ischemia. The experimental preparation involved the rat cremaster muscle. The muscle was fashioned as a single bag (new procedure), placed in a transparent chamber and superfused with a bicarbonate buffer solution equilibrated with a 5% CO2 95% N2 gas mixture in order to obtain pH 7.40, PCO2 = 40 mmHg, PO2 = 20-40 mmHg and thermostated at 35 degrees C. FITC-Dextran 150 (MW 150,000) was injected i.v. as a macromolecular tracer. BK was added to the buffer solution at the concentration of 2 micrograms/ml five minutes after a control period of 60 minutes. Ischemia was performed during 60 min by a clamp positioned on the main artery of the cremaster muscle. Animals treated with Daflon 500 mg (100 mg/kg) 18 and 2 hours before experiments showed a significant reduction in FITC-Dextran 150 leakage in both BK and ischemia protocols. Leakage of FITC-Dextran 150 started 2-3 min after application of BK in the two animal groups but the response was less important (+ 270%) and the preparation returned to control appearance after 40 min in the treated rats in contrast with control rats (+ 450% and 70 min). The amplitude of FITC-Dextran 150 leakage was identical just one hour after ischemia in the two animal groups, but microvascular permeability returned to basal state in treated animals (30 min), a fact non observed in non treated animals. These data demonstrate the protective effect of Daflon 500 mg on the microvascular muscle network in vivo.
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PMID:Daflon 500 mg depresses bradykinin-ischemia-induced microvascular leakage of FITC dextran in rat cremaster muscle. 248 28

Improvement in tissue perfusion following surgically induced ischemia in limbs of dogs was experimentally evaluated to clarify the improvement of hemodynamics following walking exercise in chronic, peripheral arterial occlusive diseases. With the use of a computer system in conjunction with medical mass spectrometry, the local tissue perfusion rate was calculated on the basis of the clearance curve of tissue partial pressure of CO2 following electrical stimulation of the ischemic leg to simulate exercise. Ischemia was created in the leg by ligation of the proximal and peripheral arteries. In one month, intermittent claudication improved in accordance with improvement in muscle tissue perfusion. Angiographic evidence of distal runoff became visible six months after surgery, indicating that tissue perfusion played an important role in peripheral hemodynamics. The local tissue perfusion rate improved from 9.51 +/- 2.62 ml/100 g/min to 12.41 +/- 2.42 in one month, to 14.59 +/- 3.19 in three months, to 15.11 +/- 3.24 in six months and to 17.19 +/- 2.63 in twelve months. The improvement of ischemic symptoms following long-term exercise is attributed to improvements in tissue perfusion or collateral circulation.
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PMID:Evaluation of tissue perfusion in ischemic legs of dogs by CO2 clearance rate. 249 22

Previous studies from our institution demonstrated significant hypercarbic acidosis in the mixed venous (pulmonary artery) blood in animals and human patients during cardiac arrest and cardiopulmonary resuscitation (CPR). In the present study, the acid-base state of the myocardium during cardiac arrest was investigated. Cardiac arrest was electrically induced in 11 pentobarbital-anesthetized and mechanically ventilated domestic pigs. Precordial compression was begun 3 minutes after onset of ventricular fibrillation and continued for 8 minutes. During CPR, there was rapid onset of profound myocardial acidosis with an increase in intramyocardial [H+] from 54 +/- 5 to 146 +/- 20 nmol/l (7.27 +/- 0.04 to 6.88 +/- 0.20 pH units). Great cardiac vein PCO2 increased from 57 +/- 2 to 158 +/- 12 mm Hg. Profound hypercarbic acidosis in great cardiac vein blood was associated with myocardial lactate production to levels of 8.1 +/- 0.7 mmol/l. Only moderate decreases in cardiac vein bicarbonate concentrations from 31 +/- 1 to 23 +/- 1 mmol/l were observed. These acid-base changes were almost completely reversed over an interval of 60 minutes after the animals were successfully resuscitated by DC countershock. The PCO2 in cardiac vein blood was significantly greater than that of mixed venous blood, demonstrating disproportionate myocardial production of CO2 during CPR. Accordingly, it is CO2 production during ischemia that is implicated as the predominant mechanism accounting for myocardial [H+] increases during cardiac arrest. Important clinical implications for buffer therapy during CPR and, in particular, treatment with bicarbonate emerge from these observations.
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PMID:Myocardial acidosis associated with CO2 production during cardiac arrest and resuscitation. 250 12

The effect of chronic ischemia on glucose metabolism of the rabbit urinary bladder was studied. Unilateral ischemia was produced by ligation of one of the two vesical arteries which supply the rabbit bladder. Two weeks after the operation, the in vitro glucose metabolism of normal bladder tissue was compared to the glucose metabolism of tissue isolated from both the ischemic side and contralateral (non-ischemic) side of the ischemic bladder. The results can be summarized as follows: 1) ischemic and contralateral side bladder tissues contained less glycogen than normal; 2) glucose utilization was higher in the ischemic and contralateral side tissues; 3) ischemic and contralateral side tissues incorporated more glucose into lactate and produced more total lactate than normal tissues; 4) whereas contralateral side tissue produced more 14CO2 than ischemic side tissue, the ability of normal bladder tissue to form 14CO2 is significantly higher than both ischemic and contralateral side tissues; 5) the degree of reduced CO2 production correlated well with previous studies on the contractile response of smooth muscle strips isolated from the ischemic and contralateral sides, and the reduced functional ability of the in vitro whole bladder to empty; 6) histologically, smooth muscle degeneration and necrosis is only present on the ischemic side of the bladder although the contralateral side shows signs of generalized degeneration and edema. In general, we conclude that although only the ischemic tissue demonstrated major smooth muscle degeneration and necrosis, unilateral ischemia resulted in marked alterations in glucose metabolism on both the ischemic and contralateral sides.
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PMID:Effect of chronic ischemia on glucose metabolism of rabbit urinary bladder. 250 96


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