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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 lidoflazine were studied in 12 young healthy subjects who received the drug orally (240 mg daily) for 8 weeks. During exercise after lidoflazine, heart rate (-2.6%), mean arterial pressure (-3.1%), arterio-venous oxygen (A-V02) difference (-3.4%), pressure rate product (-6.2%), and systemic vascular resistance (-8.6%) were significantly lower, while cardiac output (+5.4%) and stroke volume (+8.3%) were significantly greater. The maximal heart rate was lower after lidoflazine (-6 beats/min) but the maximal oxygen intake (VO2max) was not affected by the drug. The major hemodynamic effects of lidoflazine appear to be, on the one hand, an unexplained decrease in heart rate, and on the other, a decrease in systemic vascular resistance; the latter, which was expected from a vasodilator, could account for the greater stroke volume and contributes to the decrease of the pressure rate product. Lidoflazine has another unexplained effect, i.e. a decrease of the A-VO2 difference, suggesting a decreased peripheral extraction of oxygen at rest as well as during submaximal and maximal exercise.
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PMID:Hemodynamic effects of lidoflazine during graded levels of bicycle exercise in normal subjects. 127 6

Lidoflazine, a piperazine derivative with known selectivity for vascular smooth muscle, was evaluated as a possible agent for prophylaxis of cerebral vascular contraction induced by subarachnoid perfusion with serotonin. The animals treated with serotonin (5 X 10(-6) M), had a 60% reduction in the diameter of basilar artery but when pretreated with Lidoflazine (1 mg/kg) intravenously, only had a 20% reduction in diameter (p less than 0.01). Lidoflazine, when administered intravenously at a slow rate will not adversely lower systemic blood pressure and can prevent the contraction of cerebral vessels when the stimulus for contraction is in the subarachnoid space.
Stroke
PMID:The effect of intravenous lidoflazine on serotonin-induced cerebral vascular contraction--an in vivo study. 373 57

Lidoflazine, a calcium channel blocker, was administered to dogs following twelve minutes of cerebral ischemia, induced by aortic cross-clamping. The effects of lidoflazine (1 mg/kg i.v.) on cerebral blood flow following ischemia was studied in 15 anesthetized, mechanically ventilated dogs. Cerebral blood flow was measured with the radiolabelled microsphere technique before and 10, 30, 60, 90 and 150 minutes following ischemia. Cerebral blood flow increased in all brain regions following ischemia, but by 60 minutes had decreased to control values. Lidoflazine had no effect on this reperfusion phenomenon, or on the distribution of blood flow within the brain. Regional cerebral blood flow was also not altered by lidoflazine therapy. Our data demonstrate that this dose of lidoflazine has no effect on regional or total cerebral blood flow following 12 minutes of cerebral ischemia in dogs. These data do not support perfusion preservation as a mechanism of amelioration of neurologic injury after ischemia by this calcium channel blocker.
Stroke
PMID:Effect of lidoflazine on cerebral blood flow following twelve minutes total cerebral ischemia. 642 83

The clinical situation of heterogeneous cardioplegia was simulated in a canine model by temporary ligation of the circumflex coronary artery during a three-hour interval of cardioplegic arrest. Nifedipine and lidoflazine, administered prior to aortic clamping, were evaluated as adjuncts to cold (2 degrees C) crystalloid cardioplegia. Assessment was made of regional function (sonomicrometer systolic shortening) and of global function by measuring left atrial (LA) pressure at constant cardiac output (CO), aortic pressure, and heart rate, and by measuring stroke work at constant LA pressure, aortic pressure, and heart rate. Among 14 control dogs, only 7 could achieve a CO of 5 liters per minute following cardioplegic arrest. Left anterior descending coronary arterial systolic shortening recovered to only 86% of prearrest values (p less than 0.05), circumflex coronary arterial systolic shortening recovered only 28% (p less than 0.01), stroke work recovered 59% (p less than 0.01), and LA pressure was 6.7 mm Hg higher (p less than 0.01) than prior to cardioplegic arrest. Lidoflazine provided no statistically significant benefit in these animals (N = 4). However, dogs given nifedipine (N = 6) had very little change in left anterior descending coronary arterial systolic shortening (99% recovery), stroke work (93% recovery), and LA pressure (delta = 0.4 mm Hg). None of these changes was statistically significant. There was some deterioration in circumflex coronary arterial systolic shortening (56% recovery; p less than 0.05). All 6 dogs given nifedipine achieved a CO of 5 L/min following cardioplegic arrest. Clinical cardioplegia is typically heterogeneous cardioplegia. Calcium-channel blockade appears to be useful in this situation.
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PMID:Calcium-channel blockade as an adjunct to heterogeneous delivery of cardioplegia. 686 5