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

The hemodynamic effects of dihydralazine and prazosin (0.1 and 1.0 mg/kg i.v.) on the circulatory system and left ventricular dynamics and contractility has been performed in 10 purebred beagle dogs (15.5 +- 1.4 kg) under pentobarbital sodium (35-40 mg/kg i.p.) anaesthesia by means of thermodilution and catheter technics. The changes of cardiovascular values were: 1. Either dihydralazine and prazosin decreased mean arterial blood pressure in the dose of 0.1 mg/kg i.v. Following application of 1.0 mg/kg intravenously, the arterial pressure abruptly decreased after prazosin. 2. Both pharmaca caused tachycardia. Being slowly introduced but continued by dihydralazine, the increase of pulse rate after prazosin was only initial. 3. The cardiac dynamics were differently influenced by dihydralazine and prazosin. In the estimated dose range prazosin led to an increase of cardiac output directly after application while dihydralazine induced a gradual enhancing of cardiac output. 4. The stroke volume was decreased by prazosin and slightly increased by dihydralazine. 5. While distinctly decreasing initially after prazosin, peripheral total resistance was slowly reduced by dihydralazine. 6. The contractility of the left ventricle, estimated as dp/dtmax and VCE, showed a distinct increase of the myocardial inotropy after both compounds. The maximal effect after prazosin, however, was to be seen immediately post applicationem. Dihydralazine led to a deferred enhancing of the measured contractility parameter.
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PMID:[Dihydralazin versus prazosin. The hemodynamic effect of the modul substances (author's transl)]. 60 53

The haemodynamic shifts during head up and head down tilt were investigated in adult spontaneously hypertensive rats (SHR) and matched normotensive control rats (NCR) under nembutal anaesthesia and autonomic blockage. During head up tilt a greater fall in blood pressure and stroke volume was observed in SHR than in NCR, while the reverse was true when tilted in the opposite direction. This altered cardiac response to venous filling, also observed in patients with essential hypertension, is suggested to be caused by an altered Frank-Starling relationship of the hypertrophied heart in hypertensive individuals.
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PMID:Haemodynamic changes during tilt after autonomic blockade in spontaneously hypertensive rats. 60 71

The value of esophageal phonocardiography as a noninvasive monitor during anesthesia was studied in dogs. Esophageal phonocardiograms were analyzed using fast Fourier transform and least squares linear regression technics. This method has demonstrated that it is feasible to estimate two parameters of cardiac contractility--1/(PEP)2 and stroke power--and one parameter that demonstrates the state of the vasculature--total peripheral resistance. A continuous time (analog) processor that will accomplish this task is described.
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PMID:Intraoperative patient monitoring: a method of analyzing esophageal phonocardiograms. 62 25

The effects of halothane anesthesia on coronary circulation and cardiac work were studied in normovolemic and hypovolemic dogs, with aid of the radioactive microsphere technique. During normovolemia, halothane depressed the heart rate, cardiac output, arterial mean blood pressure and left ventricular work, with a simultaneous decrease in the coronary blood flow. During moderate hypovolemia, the arterial blood pressure was reduced as well as the coronary blood flow; whereas during hemorrhagic hypotension (severe hypovolemia), the arterial blood pressure was slightly increased and the coronary blood flow was unchanged with a reduced heart rate and increased stroke volume.
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PMID:The effect of halothane anesthesia on heart function during normovolemia and hypovolemia in the dog. 63 11

The effects of enflurane-pancuronium anaesthesia on cardiovascular haemodynamics were studied before operation in six patients with valvular heart disease. A ten per cent decline in cardiac index and a 20 per cent decline in stroke volume were the only changes observed. Mean arterial, pulmonary arterial, contral venous, and pulmonary capillary wedge pressures were unaffected, as were systemic vascular resistance and pulmonary vascular resistance. The authors therefore conclude that enflurane-pancuronium anaesthesia causes only minimal cardiovascular depression in patients with valvular heart disease.
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PMID:Cardiovascular haemodynamics during enflurane-pancuronium anaesthesia in patients with valvular heart disease. 63 21

The relationships between right atrial mean, pulmonary artery diastolic, mean, and wedge pressures, and stroke index were studied in 100 patients. The various pressures correlated fairly well with one another, but poorly with stroke index. However, this correlation improved when the values of individual patients were analyzed. Infusion of calcium chloride modified the correlation of the various pressures with the stroke index over a short period of time. During anesthesia, when pulmonary vascular resistances, systemic resistances and myocardial contractility were stable, both pulmonary artery mean and wedge pressure correlated significantly with the stroke index.
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PMID:Hemodynamic pressure variables and stroke index. 63 27

The effect of racemic mephobarbital and its optical isomers on survival time of mice exposed to 5% O2 was studied. There was an increase in survival time from 4.2 minutes to 12.6 minutes for 100 mg/kg of the anesthetically active (-) isomer and the racemic form, but no increase for 100 mg/kg of the inactive (+) isomer. Since it has been shown that there is no difference in brain concentrations between the isomers, we conclude that the barbiturate protective effect is bound to the anesthetic effect. All mice convulsed, and since the non-anesthetized animals convulsed earlier and stronger than the anesthetized, it was possible that barbiturate protection was accounted for by its anticonvulsant effects. Diazepam 7.5 mg/kg, while reducing convulsions to the same degree as barbiturates without producing anesthesia, only increased survival time to 6.2 minutes. Thus, the barbiturate protective effect is distinct from the anticonvulsant effect. It seems to be bound to a stereospecific receptor for both protection and anesthesia.
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PMID:Cerebral protection with barbiturates: relation to anesthetic effect. 64 7

Cerebral cortical blood flow was measured in rabbits with the hydrogen clearance technique. The reactivity to CO2, tested by changing the end tidal CO2 (ETCO2) in steps from 2 to 6 volumes %, was highly dependent on the kind of anesthesia, being greatest under halothane and least under nitrous oxide. Reactivity to CO2 in halothane-anesthetized animals also depended on arterial blood pressure, being greatest when pressure was below 70 mm Hg. Intravenous atropine blocked the increase in reactivity in halothane-anesthetized animals at low blood pressures. Conversely, intravenous eserine (physostigmine) greatly increased the reactivity to CO2 in nitrous oxide-anesthetized animals. Precollicular decerebration considerably decreased CO2 reactivity of halothane-anesthetized rabbits, while partial brain stem lesions that spared midline structures had no effect on CO2 reactivity. It is concluded that a central neurogenic mechanism with a cholinergic link may be responsible, at least in part, for the cerebrovascular effect of CO2. Moreover, the cerebrovascular effects of halothane may result from stimulation of the same system.
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PMID:Cerebrovascular CO2 reactivity: role of a cholinergic mechanism modulated by anesthesia. 64 10

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.
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PMID:Rat brain osmolality during barbiturate anesthesia and global brain ischemia. 64 23

Cardiovascular effects of venous alveolar concentrations of halothane in oxygen were studied in 8 young, healthy horses under conditions of constant arterial carbon dioxide tension. The alveolar concentration of halothane was expressed as a multiple of the minimal alveolar concentration (MAC) which was known for each animal. Increasing alveolar halothane concentrations to MAC 2.0 resulted in a progressive and significant (P less than 0.05) decline in systemic arterial pressure and left ventricular work. Cardiac output decreased between MAC 1.0 and MAC 2.0 as a result of a significant (P less than 0.05) decrease in stroke volume. Heart rate, total peripheral resistance, pulmonary artery pressure, hematocrit, plasma protein concentration, arterial oxygen tension, and arterial pH remained constant over the same range of anesthetic dosages. Continuation of anesthesia, spontaneous ventilation, and the accompanying rise in arterial carbon dioxide tension and electrical stimulation of the horse's oral mucous membranes produced varying degrees of stimulation of cardiovascular function at MAC 1.5.
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PMID:Cardiovascular effects of halothane in the horse. 64 95


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