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

Cardiac output and stroke volume were measured in two environments and at metabolic rates ranging from rest to the maximum rate that could be sustained for 25 minutes. One environment was indoors at about 23 degrees C, the other outdoors in desert sunshine and low water vapor pressure. The age range of the one female and four of the male subjects was from 19 to 40; the fifth male subject was 85 years old. Cardiac output was the same in the two environments; stroke volume was less at higher metabolic rates in the heat. The cardiac output for the old man was about one-tenth less and stroke volume about 20 ml less than that observed for the same work 50 years earlier.
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PMID:Cardiac output during rest and exercise in desert heat. 52 32

The efficacy of pentobarbital in the treatment of ischemic cerebral edema was evaluated in 160 gerbils. Animals underwent carotid ligation under ether or pentobarbital (50 mg/kg) anesthesia. The pentobarbital anesthetized group received an additional dose of 30 mg/kg 4 h after ligation. Animals were evaluated for neurologic deficit at 4 and 8 h post-ligation, then sacrificed. Water content of each hemisphere and swelling percentage were calculated from the wet and dry weights of the hemispheres. Swelling percentage in animals anesthetized with ether was 6.374 +/- 0.89 SE, whereas gerbils who underwent sham carotid ligation showed a negligible (0.491 +/- 0.15) swelling percentage (p less than 0.01). Pentobarbital animals had a swelling percentage of 3.359 +/- 0.68. This represents a significant edema reduction compared to ether-anesthetized animals (p less than 0.01). Neurologic deficit was decreased by 56.7% (17/60 vs 30/60) in pentobarbital animals compared with ether animals (p less than 0.025). Mortality at 8 hours was reduced by 75% (2/60 vs 8/60) in pentobarbital animals (p less than 0.05).
Stroke
PMID:Attenuation of ischemic brain edema by pentobarbital after carotid ligation in the gerbil. 52 3

Brain edema was induced in rats by injecting 50 mu microspheres, labelled with 85Sr, into the internal carotid artery. The use of radioactive microspheres as embolic agents enabled the number of microspheres to be determined in each cerebral hemisphere. Edema was assessed 12 or 24 h after embolization by measuring brain water content and, in some experiments, sodium and potassium. Pretreatments with dexamethasone, parachlorophenylalanine (an inhibitor of 5-hydroxytryptamine synthesis), mepyramine and metiamide (H1 and H2 histamine receptor antagonists) or aminophylline did not influence significantly the development of brain edema evaluated 24 h after embolization. Aminophylline treatment (100 mg/kg) markedly increased mortality following embolization. Gamma-butyrolactone (300 mg/kg, every 2 h) inhibited significantly the development of brain edema evaluated 12 hours after embolization. Increases in water and sodium in the embolized cerebral hemisphere were reduced by about 50%. This protective effect may be related to the known depressant action on brain metabolism.
Stroke
PMID:Influence of various agents on the development of brain edema in the rat following microembolism. Protective effect of gamma-butyrolactone. 52 4

Two aspects of the recovery period after endurance exercise were investigated: a) the fluid distribution between the intra- and extravascular parts of the extracellular fluid volume (ECFV) induced by exercise dehydration, b) the cardiovascular response pattern [blood pressure (BP), heart rate (HR), cardiac output (CO), total peripheral resistance (TPR), and central venous pressure (CVP)] to the heat load which results from the preceding exercise. Seven conscious dogs performed endurance exercise in a cool environment (16 degrees C) on a horizontal treadmill till 4% of the body weight was lost. It was found that about 70% of the total fluid loss of the body came from intracellular water. During exercise sodium and chloride concentrations rose by 6 mMol and 7 mMol respectively (P less than 0.005) and remained elevated throughout the early recovery period indicating a fluid loss of about 100-200 ml out of the ECFV. Direct measurements of the ECFV as sulfate space confirmed these values. Since the plasma volume remained unchanged, this fluid loss was carried totally by the interstitial fluid volume. Immediately after exercise body temperature was elevated by 1.5 degrees C and returned towards control within 90 min. Cardiac output was above control level for 2 h after the end of exercise, at first due to an increased HR and thereafter to an elevated stroke volume (SV) (P less than 0.02). CVP and TPR were below control levels for at least 2 h (P less than 0.01). A linear correlation was found between CVP and TPR. A close correlation existed between the body temperature and the cardiovascular parameters. It can be concluded that even long after exercise the cardiovascular system has to serve thermoregulatory needs.
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PMID:Extracellular fluid volume and central circulation after long lasting exercise and dehydration in conscious dogs. 55 92

Rapid administration of intravascular volume expanders is often necessary during anesthesia. Significant controversy still exists on the relative values of different volume expanders. Fifteen hypoxemic patients (Pao2 less than 70 torr on room air) were studied preoperatively. They were randomized into three groups. One group received 1.5 ml/kg of 25% salt-poor human albumin, a second group, 7 ml/kg of fresh frozen plasma; a third group, 7 ml/kg of 0.9% NaCl in water (normal saline). The infusions were given intravenously and completed in 20 minutes. Changes in hemodynamic pressures and flows, blood chemistries, and oxygen uptake and transport variables were studied. It was concluded that fresh frozen plasma afforded the greatest increase in cardiac output and oxygen availability with the least increase in left ventricular stroke work. Colloid osmotic pressure was more significantly increased by fresh frozen plasma than by salt-poor human albumin. Normal saline caused both a decrease in oxygen availability and colloid osmotic pressure. Pulmonary venous admixture increased to some extent in all patients receiving fresh frozen plasma or normal saline. In three patients, this increase was very marked and accompanied by severe arterial hypoxemia.
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PMID:Rapid volume expansion in patients with interstitial lung diseases. 57 Dec 16

Cardiorespiratory, thermal, and renal responses to a 30-min head-out immersion in 15 degree C water were studied at 1-ATA air and 11-ATA helium-oxygne environments in four male subjects wearing dry suits. Cardiorespiratory responses to immersion (reductions in heart rate, expiratory reserve volume, vital capacity, and thoracic impedance; and increases in stroke volume, cardiac output, and inspiratory capacity) were comparable at both pressures. However, thermal responses to immersion (a reduction in mean skin temperature and increases in skin heat flux and suit conductance) were significantly greater at 11 ATA compared to those at 1 ATA. The rate of urinary excretion of norepinephrine increased significantly during and after immersion at 11 ATA but not at 1 ATA. In contrast, the urinary excretion of epinephrine was not altered by pressure or immersion. The immersion diuresis was greater and lasted longer at 11 ATA than at 1 ATA although there was no difference in the endogenous creatinine excretion . This diuresis was accompanied by a significant natriuresis which was more marked at 1 ATA than at 11 ATA. At 1 ATA, the urinary excretion of both aldosterone and antidiuretic hormone (ADH) decreased during immersion. At 11 ATA, the rate of excretion of these hormones before immersion was lower compared to that at 1 ATA and did not change significantly during immersion. These results indicate that immersion in a hyperbaric helium-oxygen environment presents a greater cold stress than at 1-ATA air, and also that immersion diuresis and natriuresis at high pressure may be induced by a factor other than inhibition of aldosterone and ADH.
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PMID:Physiological responses to head-out immersion in water at 11 ATA. 63 73

Seven chronically prepared dogs (electromagnetic flow transducers around the pulmonary and left renal artery, left atrial catheter) maintained on a controlled sodium and water intake were studied. About 20 h after the last intake of food and water, the effects of i.v. methohexitone (initial dose: 6.10 +/- 0.84 mg/kg bw; sustaining infusion: 0.34 +/- 0.10 mg/min.kg bw) on renal excretion of sodium, potassium, urea and water as well as on several haemodynamic values were investigated over a period of 60 min (MP) after a control period (CP) of 60 min in the unanaesthetized state. In 18 of 19 experiments water diuresis (U/Posm less than 1) was observed between 20 and 40 min after starting the administration of methohexitone. Urine volume increased from 44 +/- 21 microliter/min.kg bw (CP) to 104 +/- 62 microliter/min.kg bw (MP).I.v. administration of arginine-vasopressin (ADH) completely abolished water diuresis. During MP, there was a decrease in cardiac output (-11%), stroke volume (-36%) and left atrial pressure (-27%), heart rate increased (+ 43%). Mean arterial blood pressure and renal blood flow did not change. It is assumed-as plasma osmolality did not change-that the central release of antidiuretic hormone is suppressed by methohexitone.
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PMID:[Water diuresis during methohexitone anaesthesia. Studies in chronically instrumented dogs (author's transl)]. 65 67

We evaluated the effects of methylprednisolone sodium succinate (MPSS) on 60 minutes of myocardial ischemia during profound (5 degrees C) topical cardiac hypothermia (ice chips) in a canine right heart bypass preparation. The ventricular function curve shifted to the right and downward, but not significantly, after ischemia, and stroke work declined significantly for both control and treated dogs. Contractility (rate of rise of left ventricular pressure and maximum velocity of the contractile element) declined for both groups but not significantly. Total coronary flow, oxygen consumption, and metabolism of lactate and pyruvate were not different for control and treated dogs. Ultrastructure of the outer and inner myocardium did not demonstrate benefit from MPSS. Intracellular and extracellular edema of moderate severity was slightly worse in the subendocardium, and reversible mitochondrial injury of a mild to moderate degreee was symmetrically present. Ice-related injury was not noted. We were unable to deomonstrate that pretreatment with MPSS favorably alters cardiodynamics or ultrastructure after 60 minutes of profound topical cardiac hypothermia.
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PMID:Topical cardiac hypothermia: the effect of methylprednisolone sodium succinate. 65 47

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

Total hemodynamic values and left ventricular blood flow were studied using Sapirstein's method of 86Rb uptake in female rats 24 h after a last exposure to high altitude. A stimulated altitude of 1350 m was used, initial exposure being for 30 min, gradually increased by 30 min daily up to 330 min daily for 5 days a week; the total number of exposures was 32. In another animal group the hypobaric exposure was combined with swimming in water at 37 degrees C. In both experimental groups the cardiac output and stroke volume increased, and in rats undergoing swimming the total peripheral resistance decreased as well. In the rats exposed to intermittent hypoxia only, left ventricular blood flow increased by about the same proportion as the cardiac output. The ratio of left ventricular work to coronary blood flow was significantly increased. In rats exposed to the combined influence of hypoxia and swimming, the increase in left ventricular blood flow did not match either the increase in cardiac output, or the weight gain of the left ventricle. The ventricular work to coronary blood flow ratio was the same as in controls.
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PMID:Resting values of left ventricular work to coronary blood flow ratio in rats exposed to intermittent high altitude hypoxia and swimming. 68 17


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