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

Over the past three years, high-dose barbiturate therapy has been used in the treatment of 60 patients with head injury (N = 45), encephalitis (N = 8), acute focal cerebral ischemia (stroke, N = 4), and global anoxia secondary to drowning (N = 3). High-dose barbiturates appear to be useful adjuncts in the control of intracranial hypertension refractory to other methods of therapy. Administration of barbiturates to patients with this problem will often reduce the requirement for osmotic agents, thereby facilitating medical management by avoiding hyperosmolality and fluid and electrolyte depletion. In a carefully controlled intensive care setting the risk of barbiturate therapy is low, though the costs and demands on personnel are great. Survival appeared to be improved in aptients with ,head injury and encephalitis. Although the ultimate outcome was not altered in patients with stroke or near-drowning, intracranial hypertension did not occur until barbiturate therapy was withdrawn. This experience provides an ethical basis to justify further randomized studies for determining whether or not barbiturates materially improve the neurological outcome following cerebral ischemic and traumatic insults.
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PMID:High-dose barbiturate therapy in humans: a clinical review of 60 patients. 53 17

Ischemic brain damage can be partially ameliorated by barbiturate therapy applied postinsult. Catabolism-induced brain hyperosmolality during ischemia may contribute to the development of brain edema after restoration of circulation. To determine changes in brain osmolality during ischemia and the effect of barbiturate anesthetics in altering its course, we measured whole and regional (cerebral cortex, diencephalon-midbrain, and cerebellum) brain osmolality for up to 2 hours after decapitation ischemia in unanesthetized and pentobarbital anesthetized rats. Normal (nonischemic) brain osmolality in pentobarbital anesthetized rats was 319 +/- 2 mOsm/1 (mean +/- SEM) and higher than in unanesthetized rats (307 +/- 6 mOsm/1). The rate of increase in whole brain osmolality was 60% slower in pentobarbital anesthetized rats in the first 60 minutes of ischemia and regional brain osmolality increased by a maximum of 32 mOsm/1 compared to 45 mOsm/1 in unanesthetized rats. The potential for edema based on percent change in brain osmolality as well as the rapidity of the change was greater in unanesthetized rats. The significance of the increase in brain osmolality with barbiturate anesthesia and its attenuation of the rate and magnitude of increase during ischemia is discussed.
Stroke
PMID:Rat brain osmolality during barbiturate anesthesia and global brain ischemia. 64 23

To evaluate the influence of glucose infusate administered with insulin and potassium on left ventricular function during 4 h of ischemia, as well as mechanism of action, four groups of intact anesthetized dogs were studied. Acute regional ischemia was induced with a balloon tip catheter in the left anterior descending artery and infusates were begun after 20 min of ischemia. A threefold increase of plasma glucose concentration was associated with improved left ventricular function during ischemia, compared to animals receiving isovolumic saline. There was a significant decline of left ventricular end-diastolic pressure associated with elevation of stroke volume and ejection fraction to control levels, as determined by indicator dilution. In a separate subgroup studied by cineangiography, shortening of the ischemic anterior wall, after an initial decline, was increased in response to glucose but there was no evidence of extension of injury. Ischemic tissue exhibited a smaller gain of water as well as Na+ per gram dry weight as compared to ischemic controls. On precordial electrocardiogram mapping there was a significant decrease in the sigmaST (sum of ST elevation) as well as NST (number of ST segment elevations), but the reduction of R wave amplitude was not different from controls. To further evaluate long-term effects, eight controls and six treated animals underwent myocardial ischemia and were sacrificed after 4 mo. Calculated area and weight of scar, as well as degree of wall thinning, were similar in both groups. The glucose-treated animals had a significant decrease of plasma FFA in contrast to controls which manifested a significant rise. To examine the postulate that the decrease in FFA was important to therapeutic action, a third group was infused with Intralipid (Cutter Laboratories, Inc., Berkeley, Calif.) and heparin, simultaneously with the glucose infusate, to effect an elevation of plasma FFA during ischemia. Changes in myocardial function and electrolyte composition, as well as precordial electrocardiogram mapping, were similar to that of animals receiving glucose alone. Because serum osmolality was increased approximately 40 mosmol during the glucose infusion, the potential role of hyperosmolality was assessed by infusion of 20% mannitol during acute ischemia in a fourth group. After a transient small increase, there was a moderate decline in function by 4 h, suggesting that the response to glucose is not dependent upon extracellular osmolality. Thus, it is concluded that during the initial hours after the onset of myocardial ischemia the glucose infusate improves ventricular performance without evidence of arrhythmia induction or intensification of ischemic injury. Evolution of irreversible necrosis appears to be delayed rather than prevented under the circumstances of this study.
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PMID:Sustained effect of glucose-insulin-potassium on myocardial performance during regional ischemia. Role of free fatty acid and osmolality. 65 87

The role of late restitution of blood volume after hemorrhage in cardiovascular stabilization was examined in awake, splenectomized dogs. Cardiovascular variables were measured: at 2 hours after hemorrhage, changes were noted in cardiac output, mean arterial pressure, heart rate, stroke volume, arterial pressure, and CVP in three hemorrhage groups (p less than 0.05), and in total peripheral resistance for 15 ml/kg and 22.5 ml/kg hemorrhage groups (p less than 0.05). At 24 hours after hemorrhage, the degree of restitution of blood volume was correlated with cardiac output (p less than 0.01), stroke volume (p less than 0.02), and total peripheral resistance (p less than 0.01). No correlation was noted with heart rate, CVP, or mean arterial pressure. Blood volume restitution was correlated with degree of hemorrhage throughout the 24-hour period of investigation. Plasma protein content restitution and blood volume restitution were correlated with changes in osmolality. The results suggest thatcardiovascular stabilization after hemorrhage is a function of the degree of restitution of blood volume mediated through a shift of fluids to the interstitutium, mediated in turn by extracellular hyperosmolality.
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PMID:Cardiovascular stabilization after hemorrhage depends upon restitution of blood volume. 73 51

The effects of moderate arterial hyperosmolality (+20 mOsm/kg H2O), produced by short term intravenous hypertonic infusion, on vascular resistance in skin, skeletal muscle, intestine, and kidney were analyzed in the anesthetized cat. Vascular resistance decreased in all four regions in response to the hypertonicity both before and after regional sympathectomy and the effects were not significantly altered by beta-adreno-ceptor blockade. Arterial blood pressure rose during the hypertonic infusion despite the decreased vascular resistance and an unchanged heart rate, indicating an increased stroke volume and cardiac output. Similar increases of arterial osmolality are known to occur in heavy exercise and in hemorrhage. The present results may therefore suggest that blood borne hyperosmolality is a factor which can contribute to the overall cardiovascular adjustments in these situations.
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PMID:Circulatory effects evoded by 'physiological' increases of arterial osmolality. 115 24

Monitoring of plasma osmolality (PO) in patients with cerebral stroke revealed the most marked changes in hemorrhagic stroke. The presence of renal failure and hyperglycemia aggravated disorders of osmotic homeostasis. The value of PO adequately reflected the severity of the state of the patients. Stable hyperosmolality and an increase in the difference between the measured and calculated PO over 30 mOsm in the acutest phase of stroke were poor prognostic signs. Determination of PO along with other traditional tests (measurement of sodium, potassium, urea and glucose) yields important information for the correct treatment of patients in the acutest phase of cerebral stroke.
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PMID:[Changes in plasma osmolality in patients in the most acute phase of a stroke]. 407 28

Starved rats sedated with a neurolept analgesic were subjected to hemorrhagic hypotension while receiving infusions of iso-osmolar and hyperosmolar solutions. The hemorrhage model used resulted in similar residual blood volumes and hematocrits in all groups. The non-metabolizable pentose, xylose, and glucose were used to induce a state of hyperosmolality, which was absent in those animals which received iso-osmolar infusions (0.29 M xylose). After 45 mins hemorrhagic hypotension and a blood loss equal to 40% of the initial blood volume, the animals receiving the hyperosmolar infusions had a better cardiovascular status compared to those which received the iso-osmolar infusions. The cardiac outputs and stroke volumes were higher and heart rate lower in the hyperosmolar groups. Evidence of better tissue perfusion was obtained in those animals with the induced state of hyperosmolality.
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PMID:Modification of cardio-vascular responses to hemorrhage by induced hyperosmolality in the rat. 688 Jul 99

Non-starved (fed) and starved rats, sedated with a neurolept analgesic, were subjected to 45 min of hemorrhagic hypotension. The hemorrhage inflicted did not cause hypoxic changes, and left fed and starved animals with the same residual blood volume. Fed animals developed a state of hyperglycemic hyperosmolality and their free fatty acids tended to rise, while these observations were modified among starved animals. After 15 min of hemorrhage the cardiovascular parameters were the same in fed and starved animals, but at 45 min striking differences were observed. In fed animals, cardiac output, stroke volume, skin and muscle flows were substantially higher than starved animal values, while the latter animals had a higher heart rate and peripheral resistance. These effects are attributed to the state of hyperosmolality developed by the fed animals, and can explain the association between nutritional status and survival in hemorrhage.
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PMID:Cardio-vascular and metabolic alterations caused by hemorrhage in fed and starved rats. 688 Aug

Glycerol is a potent osmotic dehydrating agent with additional effects on brain metabolism. In doses of 0.25-2.0 g/kg glycerol decreases intracranial pressure in numerous disease states, including Reye's syndrome, stroke, encephalitis, meningitis, pseudotumor cerebri, central nervous system tumor, and space occupying lesions. It is also effective in lowering intraocular pressure in glaucoma and shrinking the brain during neurosurgical procedures. Hyperosmolality with rebound cerebral overhydration is of concern, especially in patients with altered blood brain barriers. They may be avoided if glycerol is administered on an intermittent rather than a continuous basis. Intravascular hemolysis does not occur with oral use. When administered intravenously, hemolysis can be minimized by using glycerol 10% in dextrose 5% with normal saline at rates of 6 mg/kg/min or less. However, intravenous doses of 1-2 g/kg every 2 hr can be administered safely in severe cases of elevated ICP. In such patients, glycerol serum concentration, serum osmolality and ICP monitoring are required to optimize glycerol therapy.
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PMID:Glycerol: a review of its pharmacology, pharmacokinetics, adverse reactions, and clinical use. 692 4

The aim of this study was to elucidate the interactive effect of central hypovolemia and plasma hyperosmolality on regulation of peripheral vascular response and AVP secretion during heat stress. Seven male subjects were infused with either isotonic (0.9%; NOSM) or hypertonic (3.0%; HOSM) NaCl solution and then heated by perfusing 42 degrees C (heat stress; HT) or 34.5 degrees C water (normothermia; NT) through water perfusion suits. Sixty minutes later, subjects were exposed to progressive lower body negative pressure (LBNP) to -40 mmHg. Plasma osmolality (P(osmol)) increased by approximately 11 mosmol/kgH(2)O in HOSM conditions. The increase in esophageal temperature before LBNP was much larger in HT-HOSM (0.90 +/- 0.09 degrees C) than in HT-NOSM (0.30 +/- 0.07 degrees C) (P < 0.01) because of osmotic inhibition of thermoregulation. During LBNP, mean arterial pressure was well maintained, and changes in thoracic impedance and stroke volume were similar in all conditions. Forearm vascular conductance (FVC) before application of LBNP was higher in HT than in NT conditions (P < 0.001) and was not influenced by P(osmol) within the thermal conditions. The reduction in FVC at -40 mmHg in HT-HOSM (-9.99 +/- 0.96 units; 58.8 +/- 4.1%) was significantly larger than in HT-NOSM (-6.02 +/- 1.23 units; 44.7 +/- 8.1%) (P < 0.05), whereas the FVC response was not different between NT-NOSM and NT-HOSM. Plasma AVP response to LBNP did not interact with P(osmol) in either NT or HT conditions. These data indicate that there apparently exists an interactive effect of P(osmol) and central hypovolemia on the peripheral vascular response during heat stress, or peripheral vasodilated conditions, but not in normothermia.
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PMID:Plasma hyperosmolality augments peripheral vascular response to baroreceptor unloading during heat stress. 1584 84


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