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

Myocardial cell pH was measured with 5, 5 dimethyl-2, 4-oxazolidinedione (DMO) in intact anesthetized dogs by a transient indicator dilution technique. Bolus injections of labeled DMO, vascular, extracellular and water indicators were made into the left anterior descending coronary artery, and blood samples were collected from the great cardiac vein. The steady state distribution of DMO between cells and plasma was calculated from the mean transit times of the indicator. Normal myocardial cell pH averaged 6.94 and changed by 58% of the concomitant alterations in plasma pH after infusions of acid or alkali. Myocardial ischemia induced by inflation of a balloon tip catheter in the left anterior descending coronary artery resulted in progressive decreases in cell pH to 6.59 by 1 hour. Infusions of sodium carbonate diminished intracellular acidosis. Hemodynamic studies during 4 hours of ischemia with blood pH at 7.55 to 7.60 indicated a significantly reduced left ventricular end-diastolic pressure and increased stroke volume by comparison with findings in animals given infusions of saline solution. Ventriculograms revealed improved wall motion in the ischemic segment after infusion of alkali. Precordial mapping showed a significant reduction in the number of leads with S-T segment elevation as well as in the sum of S-T segment elevations, but R wave amplitudes did not differ from those in control studies. Calculations of extracellular space, tissue water and cation content revealed a reduced gain of cell sodium ion and loss of cell potassium ion during ischemia after alkali treatment. The latter may account for the S-T segment responses, whereas enhanced ventricular performance may be related to reduced competition of hydrogen ion with calcium ion for binding sites on contractile protein.
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PMID:Myocardial ischemia and cell acidosis: Modification by alkali and the effects on ventricular function and cation composition. 0 59

Cardiac performance was assessed in 33 lambs less than 1 to 5 days of age by means of left ventricular function curves. Performance was quantified by determining stroke volume ejected at end diastolic pressure 10 cm H2O (SV10) with constant afterload. Coronary flow, myocardial O2 consumption (MVO2), blood gas tensions and pH were determined. Measurements were obtained before and at 30 min intervals following hemorrhage to 30 mm Hg arterial pressure, and in controls (arterial pressure 75 mm Hg). Effects of metabolic acidosis, hypercapnia and beta-blockade were determined. In control lambs acidosis and hypercapnia failed to reduce SV10 after two hours. In hemorrhaged animals both factors sharply reduced SV10 and lambs with prior beta-blockade showed no greater reduction. MVO2 fell following hemorrhage but did not differ with metabolic conditions and did not relate to SV10. It is concluded that beta-adrenergic function is critically important in preserving left ventricular performance in newborn exposed to acidosis or hypercapnia. With sustained hemorrhage this mechanism fails leading to a significant depression of ventricular function. MVO2 was not a determining factor in these studies.
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PMID:Cardiac function and metabolism following hemorrhage in the newborn lamb. 1 55

In experiments in dogs the ventilatory and circulatory conditions prevailing with the ventilatory pattern in high-frequency positive-pressure ventilation (HFPPV) were investigated with use of a pneumatic valve principle and a ventilator system of an "open" character. Keeping the gas input constant the importance of insufflation frequency and insufflation time and the reactions to various levels of positive end-expiratory pressure (PEEP) were investigated in terms of changes in arterial pH, Pco2 and Po2. With the volumes of delivered gas kept constant, an increasing insufflation frequency from 60 to 100 per min gave a parallel decrease in tidal volume accompanied by lower maximum intratracheal pressures and a significant decrease in alveolar ventilation. Also taking into account the possibilities of inducing a suppression of the spontaneous respiration, higher ventilatory frequencies than 60 per min do now seem to introduce any further advantages. Including the associated effects on cardiac output and venous admixture, the cardio-pulmonary and circulatory parameters studied did not show any substantial changes with PEEP levels below 7.5--10 cm H2O. Thus the level of PEEP, which often is part of the ventilatory pattern in HFPPV, does not seem to have any untoward influence on the circulation (stroke volume, cardiac output, total peripheral vascular resistance) and oxygen transport (arterial oxygen content and oxygen flux) in normovolaemic dogs.
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PMID:Physiologic evaluation of the HFPPV pneumatic valve principle and PEEP. An experimental study. 2 76

Body fluid gas pressure and electrolytes of patients with ruptured aneurysm were continuously analyzed. Intracranial pressure (ICP) was regulated at the level of 120-100 mm H2O by cerebral ventricular drainage. There was no significant change in the pH, PCO2, HCO3-, Na+, K+, Ca++ in the cerebrospinal fluid (CSF) of patients with slight or moderate disturbance of consciousness (lethargic-drowsy state). The PcsfO2 of the patients with marked disturbances of consciousness (semicoma-coma) was significantly low. PcsfO2 of the patients with cerebral vasospasm was significantly lower than for those without vasospasms. PcsfO2/PaO2 was 0.27 +/- 0.01 in the patients with vasospasm and 0.50 +/- 0.01 in those with vasospasm. PcsfO2 tended to decrease in patients with markedly bloody CSF. When the bloody CSF was cleared by ventricular drainage, PcsfO2 increased. PcsfO2 did not return to a normal value in the patients with marked disturbances of consciousness despite sufficient arterial oxygen tension. This suggests that PcsfO2 and PcsfO2/PaO2 should provide a convenient index for the prognosis of patients with ruptured aneurysm.
Stroke
PMID:Body fluid oxygen tension and prognosis in patients with ruptured aneurysm. 4 45

In cats air embolism of the brain was produced by injecting 0.6 ml blood foam into the innominate artery proximal to the origin of both common carotid arteries. Air embolism caused transient ischemia of the brain, reaching a maximum within 1 min after injection. Resolution of the air embolism began a few minutes later and was completed within 15 min in the center and within 30 min in the border zone of the main supplying arteries. During this phase tissue perfusion was inhomogenous with reduced flow rates in some areas and reactive hyperemia up to 300% in others. This resulted in venous hyperoxia and a decrease of arteriovenous oxygen difference to as low as 2 ml/100 ml blood. Reactive hyperemia was accompanied by brain swelling and an increase in intracranial pressure from 3.6 +/- 1.2 to 12.3 +/- 2.0 mm Hg. The reason for hyperemia was a decrease of cortical pH which fell from 7.33 +/- 0.03 to 7.03 +/- 0.05, and which caused a dilation of pial arteries up to 260%. Immediately after embolism, the EEG flattened and oxygen consumption decreased. After normalization of flow, oxygen consumption returned to normal, but EEG only partially recovered. Air embolism had little effect on the water and electrolyte content of the brain, and produced very little damage to the blood-brain barrier.
Stroke
PMID:Arterial air embolism in the cat brain. 4 47

Twenty-four h after permanent occlusion of the middle cerebral artery (MCA) in the cat, the hemispheric swelling due to edema is markedly reduced under treatment with large doses of dexamethasone than is the case with the untreated group. The increase of regional water and sodium content in the MCA territory is less in the dexamethasone treated group, whereas the potassium changes in the ischemic tissue showed only small differences between the two groups. The potassium content of the non-ischemic tissue is slightly increased in the dexamethasone treated animals when comparing with the untreated group. RISA activity in the tissue is increased in the grey and the white matter of both groups. The less marked RISA-131 activity in the cortical grey matter of the treated animals indicates blood-brain barrier damage of a smaller degree due to dexamethasone. These findings indicate a beneficial effect of dexamethasone on local ischemic edema. Regarding our results and the pharmacokinetics of this steroid the dexamethasone loading of a patient has to be in the range of about 100 mg per day for the adult, and has to be started immediately after the onset of a stroke.
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PMID:The response of focal ischemic cerebral edema to dexamethasone. 8 11

Experimental regional cerebral ischemia was produced in the middle cerebral artery (MCA) territory in primates (M. mulatta) by macrosphere embolization. Determinations of percentage tissue dry weight and tissue sodium and potassium concentrations were obtained in samples from the ischemic and non-ischemic hemispheres at various time from 12 to 48 hours after the onset of cerebral ischemia. Samples from the cortex normally supplied by the occluded MCA showed maximal accumulation of edema fluid with fluxes in sodium and potassium in reciprocal directions at 12 hours and similar edematous changes in putamen at 24 hours after embolization By 48 hours after MCA occlusion and despite the presence of infarction, partial reversal was observed in the redistribution of water and electrolytes in these gray matter structures. In contrast to cerebral cortex and putamen, the adjacent subcortical white matter showed progressive increases in water content from 12 to 48 hours and definite increases in tissue sodium with decreases in potassium were not observed until 48 hours after MCA occlusion. This late severe white matter edema associated with cerebral infarction appears to be a major factor responsible for the hemispheric swelling observed at this state.
Stroke
PMID:Experimental regional cerebral ischemia in the middle cerebral artery territory in primates. Part 3: effects on brain water and electrolytes in the late phase of acute MCA stroke. 9 10

The relationship between increase in water content in ischemic brain and levels of regional blood flow has been studied in 11 primates. Flows were recorded using the method of hydrogen (2-minute) clearance, from a total of 128 electrodes in cortex and white matter, and a gradation of ischemia was produced by middle cerebral occlusion transorbitally. The flows were reduced in the area of densest ischemia from control levels of 12.0 +/- 12.0 ml/100g/min to 7.0 +/- 5.4 ml/100g/min, with lesser decreases over the remainder of the ischemic hemisphere. Water content was measured in cortex and white matter, in regions topographically related to those of flow measurements, by densitometric assessment using precalibrated kerosene/bromobenzine columns. The average water content of cortex in regions remote from ischemia was 797.4 +/- 5.8 mg/gm and in white matter 708.5 +/- 8.2 mg/gm. Significant increases in water content (comparing corresponding regions of the two hemispheres) of up to 11.4 +/- 7.5 mg/gm were demonstrated in the most ischemic cortical areas. A gradient of water increase was evident in the ischemic hemisphere, increases water content being greatest in the opercular zone and least in the parasagittal area. Significant differences in white matter water content between the 2 hemispheres were demonstrated only in the most densely ischemic areas in the current experiments where ischemia was limited to 93 +/- 20 mins in the 11 animals without reperfusion. The relationship between ischemic density and water content increase showed that significant increases in water content occurred in regions where terminal flows had been below 20 ml/100g/min, indicating that accumulation of water in ischemic brain begins at flow values comparable to those associated with the failure of synaptic transmission, higher than those associated with failure of the ionic pump of the cell. Possible pathophysiological mechanisms are discussed.
Stroke
PMID:Ischemic brain edema following middle cerebral artery occlusion in baboons: relationship between regional cerebral water content and blood flow at 1 to 2 hours. 10 19

The Frank-Starling relationship of hearts from adult spontaneously hypertensive rats (SHR, Okamoto 1969), representing the established phase of hypertension, and of young SHR, representing the initial phase of hypertension, was investigated by using the isolated working heart preparation. In the "normal" diastolic pressure range (5 to 10 cm H2O), the left ventricle of both SHR groups displayed significantly reduced stroke volumes compared with hearts of normotensive controls (NCR); the degree of reduction being proportional to the left ventricular hypertrophy. This is suggested to be due to a reduced left ventricular diastolic compliance in SHR, as indicated by direct measurements of ventricular wall thickness and end-diastolic volumes in arrested hearts exposed to different end-diastolic filling pressures. Such a progressive shift of the Frank-Starling relationship to the right with duration of hypertension could, in combination with the gradual development of "structural autoregulation" of the precapillary resistance vessels, constitute dominating factors in shifting the hemodynamic situation in labile hypertension into that characterizing the established, or "fixed", state of hypertension.
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PMID:Consequences of myocardial structural adaptation on left ventricular compliance and the Frank-Starling relationship in spontaneously hypertensive rats. 12 25

We studied the performance of ventricular muscle and cardiac function of hearts from rats conditioned by swimming (CH) and from sedentary rats (SH) in an isolated working heart apparatus modified to measure end-diastolic volume by dye dilution. Instantaneous aortic flow, left ventricular (LV) pressure and oxygen consumption were measured. Heart rate and mean aortic pressure were kept constant, and atrial filling pressure was varied from 5 to 20 cm H2O. Heart weights of SH and CH were equal and end-diastolic pressures and volumes were similar at all atrial pressures. However, ejection fraction, calculated circumferential fiber velocity, peak systolic pressure, peak aortic flow, cardiac output, and stroke work were all greater in CH than in SH, and the differences increased as atrial pressure was increased. Maximal negative dP/dt was greater in CH than SH at all preloads (P less than 0.001). Oxygen consumption of CH was increased in proportion to the increase in work. These results indicate that the improved pumping performance of CH is due to a change in ventricular muscle function. Faster relaxation is a prominent effect of physical training on the rat heart and may foster more complete filling at high heart rates.
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PMID:Effects of physical training on end-diastolic volume and myocardial performance of isolated rat hearts. 14 27


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