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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

Five male subjects performed exercise at 33, 66, and 95% of their maximum power output on three occasions in random order. Each study was preceded by a 3-h period in which capsules were taken by mouth, containing either CaCO3 (control, NH4Cl (acidosis), or NaHCO3 (alkalosis) in a dose of 0.3 g/kg body wt; preexercise blood pH was 7.38 +/- 0.015, 7.21 +/- 0.033, and 7.43 +/- 0.029, respectively. Exercise was continuous and maintained for 20 min at the two lower power outputs and for as long as possible at the highest. Compared with control (270 +/- 13 s), endurance time at the highest power output was reduced in acidosis (160 +/- 22 s) and increased in alkalosis (438 +/- 120 s). No differences were observed for central cardiovascular changes in exercise (cardiac output, frequency, or stroke volume). The respiratory changes expected from changes in blood pH were observed, with a higher alveolar ventilation in acidosis. At all power outputs arterialized venous lactate was lowest in acidosis and highest in alkalosis. Plasma glycerol and free fatty acids were lowest in acidosis. Changes in blood [HCO3-] and pH were shown to have major effects on metabolism in exercise which presumably were responsible for impaired endurance.
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PMID:Effect of pH on cardiorespiratory and metabolic responses to exercise. 2 31

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

Severe heat stroke may be associated with hypophosphatemia and hypocalcemia. Hypophosphatemia is generally observed within hours after onset, but hypocalcemia usually occurs on the second or third day, and after hypophosphatemia has undergone spontaneous correction. A young man displayed respiratory alkalosis during the course of severe heat stroke. The hypophosphatemia abated spontaneously as metabolic acidosis and acute renal failure supervened. Hypocalcemia became prominent and was more severe than that ascribable to uremia. Hypocalcemia was probably the result of calcium phosphate and calcium carbonate deposition in injured skeletal muscle.
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PMID:The mechanism of hypophosphatemia in acute heat stroke. 57 61

Acute alterations in plasma bicarbonate concentration have minimal effects on intracerebral pH and cerebral blood flow, perhaps due to blood-brain barrier mechanisms. To test this hypothesis, the consequences of an acute rise in the plasma bicarbonate concentration were studied in anesthetized rats previously subjected to an acute pressure pulse in the carotid system with unilateral damage to the blood-brain barrier. In rats subjected to a "heavy" hypertensive insult, the hemisphere on the side of the lesion showed a lactic acidosis, edema, and a depression of cerebral blood flow. An increase in the plasma bicarbonate concentrations of 15--20 mEq/1 during 35 minutes provoked a marked rise in the total CO2 content of this hemisphere, and a further increase in the lactate concentration, but did not later the brain edema nor affect further the already very low cerebral blood flow. An increase in the lactate concentration and a decrease of cerebral blood flow in the "reference" hemisphere indicated that the lesion was not completely unilateral. In rats subjected to a "moderate" hypertensive insult the changes were less pronounced and statistically not significant for all the parameters. There results illustrate the importance of an intact blood-brain barrier for the maintenance of intracerebral pH in the face of acute alterations in plasma [HCO3]. The impaired cerebral blood flow after an acute hypertensive insult did not appear to be influenced by the intracerebral [HCO3].
Stroke
PMID:Effect of non-respiratory alkalosis on brain tissue and cerebral blood flow in rats with damaged blood-brain barrier. 67 46

The effects of phosphorus depletion on cardiac muscle function in six awake dogs were evaluated with surgically implanted transducers to serially measure ascending aortic root blood flow and high fidelity left ventricular pressure. After the animals recovered from surgery, phosphorus depletion was induced by feeding them a synthetic phosphorus-deficient diet plus aluminum carbonate gel for 35 days, followed by the same diet with phosphorus supplementation for 21 days. In addition to the cardiac studies, sequential measurements of phosphorus content in skeletal muscle and phosphorus in serum were obtained to ascertain the level of phosphorus depletion. Serum inorganic phosphorus concentration (mg/100 ml) decreased from 5.1 +/- 0.1 on day 0 to 0.9 +/- 0.1 on day 35 (P less than 0.01), and total muscle phosphorus (content mmul/100 g fat-free dry weight) decreased from 28.0 +/- on day 0 to 22.6 +/- 0.5 on day 35 (P less than 0.01). During the period of phosphorus depletion, there was no significant change in heart rate; however, stroke volume (milliliter) and peak blood flow velocity (centimeter per second) declined from 24 +/- 2 to 17 +/- 2 (P less than 0.01) and 121 +/- 12 to 98 +/- 7 (P less than 0.01), respectively. Maximum ascending aortic blood flow acceleration (centimeter per second square) and maximum left ventricular time rate of change of pressure (mm Hg per second) also decreased from 4,630 +/- 313 to 3,817 +/0 346 (P less than 0.01) and 2,582 +/- 347 to 2,120 +/- 297 (P less than 0.01) during phosphorus depletion. After repletion all values returned to control values. These results indicate that moderate diet-induced phosphorus depletion can depress myocardial performance. With repletion of phosphorus, myocardial performance improves.
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PMID:Reversible depression in myocardial performance in dogs with experimental phosphorus deficiency. 74 74

A case of a 76-year-old man with the syndrome of inappropriate secretion of antidiuretic hormone (ADH) is discussed. The patient was initially treated with fluid restriction followed by the administration of hypertonic saline. After failure to achieve rapid correction of the condition and continued lethargy and muscle weakness in the patient, a trial with lithium carbonate 300 mg three times daily via nasogastric tube was initiated. This resulted in a prompt reversal of the hyperosmolar state and improvement in electrolyte balance. However, despite the apparent success in treating his inappropriate ADH, the patient expired as a result of a massive cerebral vascular accident. The potential benefit of using lithium in the treatment of the syndrome of inappropriate secretion of ADH, and possible mechanisms of action, are reviewed.
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PMID:Lithium carbonate treatment in the syndrome of inappropriate secretion of antidiuretic hormone. 92 Jul 46

Gasometric determinations of pCO2, pO2, HCO3 and SO2 were performed in arterial blood in 100 patients with brain stroke. The following conclusions have been drawn. 1. In 2/3 of cases of brain stroke decreased partial oxygen pressure and in 1/3 of cases acid-base equilibrium disturbances are observed. 2. Hypoxia occurs in brain stroke mainly in patients with consciousness disturbances, which suggests that impaired airways patency plays a role in the pathomechanism of this disturbance. 3. Acid-base equilibrium disturbances in cases of brain stroke have in most patients the character of respiratory alkalosis which seems to be due to hyperventilation determined by central nervous mechanisms as well as to hypoxia caused by insufficient patency of airways. 4. Gasometric investigations of arterial blood in brain stroke are important for establishing the degree of homeostasis disturbances and for choice of methods of therapeutic management.
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PMID:[Gasometric studies of arterial blood in patients with stroke]. 95 71

A 57-year-old man with no personal or family history of manic-depressive disease developed symptoms of hypomania after a cerebrovascular accident and surgical trauma to the brain. The patient responded well to lithium carbonate treatment over a 2-year period. Although this therapy is contraindicated in cases of organic brain syndrome, the authors suggest that it should be considered in the management of hypomanic behavior following organic brain dysfunction.
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PMID:Positive therapeutic response to lithium in hypomania secondary to organic brain syndrome. 116 80

The effects of brain trauma on cardiovascular and endocrine responses to hemorrhage were investigated. Forty anesthetized rats were randomly assigned to one of four groups of 10 rats each: a control group (Group C): a group with induction of hemorrhage at 16.2 ml/kg/10 min (Group H); a group with fluid-percussion brain injury at a peak pressure of 1.7 atm and an impulse duration of 25 msec (Group T); and a group receiving hemorrhagic shock following brain trauma (Group TH). Group C and T rats showed no significant alterations in cardiovascular function. At the end of hemorrhage there were no significant differences between Groups TH and H in the nadirs of mean arterial blood pressure (MABP) (mean values +/- standard error of the mean: 42 +/- 2 vs. 40 +/- 4 mm Hg) and stroke volume index (SVI) (0.61 +/- 0.11 vs. 0.66 +/- 0.10 ml/bt/kg); however, 1 hour post-hemorrhage recovery was blunted in Group TH compared to Group H (MABP 56 +/- 4 vs. 65 +/- 3 mm Hg; cardiac index 182 +/- 15 vs. 220 +/- 15 ml/min/kg; and SVI 0.71 +/- 0.06 vs. 0.81 +/- 0.06 ml/bt/kg). Since the two groups showed no significant differences in heart rate, preload (central venous pressure), and afterload (systemic vascular resistance), the reduced cardiac index recovery in Group TH is believed due to the attenuation of cardiac contractile performance. The Group TH preparation potentiated hormonal responses to hemorrhage with significantly higher epinephrine and aldosterone levels than in Group H. Brain trauma enhanced the norepinephrine response to hemorrhage, even at an injury level that by itself did not result in an increase in this hormone. Group TH rats also had significantly lower blood pH and HCO3 levels. The data suggest that brain trauma suppresses MABP and cardiac index recovery after hemorrhage mainly by inhibiting cardiac contractile performance, probably due to high catecholamine levels and severe metabolic acidosis.
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PMID:Suppression by traumatic brain injury of spontaneous hemodynamic recovery from hemorrhagic shock in rats. 165 79


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