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

Two noninvasive methods for assessment of the compliance (1/E') of the aortic windkessel in man are presented and were tested for their ability to detect increases in stiffness of the aorta induced by atropine (0.012 and 0.024 mg/kg sequentially) in the presence and absence of a beta-blockade with propranolol 240 mg (n = 9). Method A, based on the calculation of the relation between pulse pressure and systolic storage volume of the aorta, requires measurement of blood pressure, systolic and diastolic time intervals and stroke volume. Method B, based on measurement of pulse wave velocity along the aorta also requires several anthropometric data (body surface area, age). Both methods were able to detect a dose-dependent increase in E' following atropine injections; method A has greater relative changes than method B. The average maximal increases were 90 and 40 percent of the baseline before atropine. The daily baselines of E' averaged 0.6 Torr x cm-3 for method A and 0.9 Torr x cm-3 for method B. Propranolol itself did not influence E' but dampened the atropine effects. The results from method A and B were correlated with r = 0.70 and 0.60 resp. (p < 0.01). The results suggest the use of these relatively simple techniques for evaluation of aortic compliance under influence of varying pathophysiological conditions or/and pharmacological interventions.
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PMID:Non-invasive assessments of compliance of the aortic wind-kessel in man derived from pulse pressure/storage volume ratio and from pulse wave velocity. 142 35

The preventive effects of long-term treatment with arotinolol on the development of cerebral stroke were examined in SHRSP fed a high salt diet. Arotinolol (4.87 mg/kg per day for 20 weeks) prevented cerebral lesions, reduced signs of stroke and delayed early mortality but did not alter blood pressure from control SHRSP, when the administration of the drug was started before the onset of hypertension. At dosage levels similar to arotinolol, both pindolol and labetalol were less effective in preventing cerebral lesions despite lower blood pressure. Propranolol produced no detectable effect on blood pressure or frequency of cerebral lesions. Furthermore, arotinolol (4.27 mg/kg per day) markedly inhibited the development of stroke without blood pressure reduction, when the administration was started after the onset of severe hypertension. These results suggest that arotinolol is more effective in preventing cerebral stroke than pindolol, labetalol and propranolol, and that factors other than blood pressure reduction may be involved in this preventive effect.
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PMID:Prevention of cerebral stroke by arotinolol in salt-loaded SHRSP. 172 31

Effects of a Senso (toad venom)-containing drug, KY, on cardiovascular system were examined in anesthetized open-chest dogs. KY increased aortic pressure, peak positive first derivative of left ventricular pressure, stroke work index, percent segment shortening in left ventricular myocardium and myocardial oxygen consumption, and decreased heart rate and total peripheral vascular resistance (TPR). Propranolol augmented the increase in aortic pressure with KY, inhibited the increase in aortic flow with KY and reversed KY-induced decrease in TPR to an increase. These results indicate that KY has positive inotropic and vasodilating actions possibly originating from both digitalis- and adrenaline-like action of a Senso.
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PMID:Effects of a senso (toad venom) containing drug on systemic hemodynamics, cardiac function and myocardial oxygen consumption in anesthetized dogs. 189 88

Peak aortic blood flow acceleration and velocity measured by Doppler echocardiography have been documented to be accurate descriptors of left ventricular systolic function. Both acceleration and velocity are reduced in the presence of beta-blockade at rest and during exercise. Whether and to what extent the simultaneous alterations in heart rate (HR) due to beta-blockade affect these parameters has received little study. In order to determine the influence of alterations in HR on Doppler measurements of velocity and acceleration, 10 healthy men were studied during upright exercise under control conditions, following propranolol administration, and following propranolol plus transesophageal atrial pacing. In addition, we assessed the response of stroke volume (measured as flow velocity integral) during beta-blocked and control exercise. Propranolol significantly reduced acceleration and velocity during all stages of exercise compared with control values (p less than 0.05). Increasing the HR during exercise via pacing had no effect on acceleration or velocity compared with propranolol administration alone, thus demonstrating that during upright exercise, changes in acceleration and velocity are independent of alterations in HR. At low levels of exercise, propranolol significantly reduced flow velocity integral (FVI) compared with control (-1.14 cm, p less than 0.05.). At high levels of exertion, however, FVI exceeded values obtained during control conditions (1.2 cm at stage 4). Pacing during beta-blockade reduced FVI at high levels of exercise but had no effect at lower levels. Our results suggest that during low levels of exercise stroke volume is increased as a consequence of both increased contractility and augmented left ventricular filling.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of beta-adrenergic blockade upon hemodynamic response to exercise assessed by Doppler echocardiography. 197 52

The effect of beta-adrenergic blockade on stroke volume (SV) at increasing submaximal exercise intensities was studied in 12 endurance-trained normotensive and 12 untrained hypertensive (diastolic blood pressure greater than 95 mm Hg) men, aged 18 to 34 years. Subjects were assigned to each of 3 treatments in a double-blind, randomized order: placebo, propranolol (80 mg twice daily) and pindolol (10 mg twice daily) for 10 days, with a period of 48 to 60 hours from the initial dose to the first treadmill test and a 4-day washout period between drugs. Cardiac output was measured using the carbon dioxide rebreathing method and SV was calculated from cardiac output and heart rate as follows: SV = cardiac output/heart rate. Cardiac outputs were estimated at rest and while walking on a treadmill at 25, 45, 60 and 75% of the subject's previously determined maximal oxygen uptake (VO2max). No significant differences were found in cardiac output between either of the drugs and placebo at rest, or at any of the 4 rates of work. Propranolol significantly increased SV above placebo values (p less than 0.05) for both trained and untrained groups at the intensities of 45, 60 and 75%. Significant differences in SV were found between pindolol and placebo only at the intensities of 60 and 75% in the trained group. Contrary to expectations, SV showed no indication of a plateau with propranolol in the trained subjects throughout the 4 different exercise intensities, whereas a plateau was established under placebo conditions by 45% of VO2max in both trained and untrained subjects. These results suggest that both trained and untrained hypertensive persons can exercise with beta-adrenergic blockade at submaximal levels without compromised cardiac function.
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PMID:Stroke volume during submaximal exercise in endurance-trained normotensive subjects and in untrained hypertensive subjects with beta blockade (propranolol and pindolol). 199 67

The purpose of this study was to determine whether segment lengths measured from the right ventricular inflow and outflow tract regions of the right ventricle would accurately reflect true volume changes of the right ventricle and to determine the response of the right ventricle to afterload increases induced by both constricting the pulmonary artery (PAC) and embolizing the pulmonary circulation with glass beads (GBE). Three excised hearts were instrumented with segment-length crystals attached to the inflow and outflow tract regions, and saline was instilled into a balloon implanted inside the right ventricular cavity. The experiments showed a high correlation (r greater than or equal to 0.90 in all cases) between static segment lengths and volume instilled. In open chest, open pericardial canine experiments, vena caval occlusion reduced end-diastolic segments lengths and right ventricular systolic pressure consistent with a reduction in right ventricular end-diastolic volume. In a separate group of animals, volume loading with dextran increased inflow and outflow end-diastolic segment lengths and increased cardiac output. In two further groups of animals, one of which was pretreated intravenously with propranolol (Inderal), both forms of pressure overload increased end-diastolic lengths in both regions. However, GBE increased right ventricular stroke work compared with PAC. We conclude that end-diastolic segment lengths reflect true volume changes of the right ventricle. Furthermore, during acute pressure overload, the right ventricle dilates to compensate for the afterload change. However, ventricular function is better maintained after GBE.
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PMID:Pressure segment length analysis of right ventricular function: influence of loading conditions. 201 15

The authors investigated the cardiovascular effects of low doses of nitroprusside, dobutamine, and phenylephrine and a beta-adrenergic blocking dose of propranolol in conscious, healthy horses with and without prior atropine administration. A parasympathetic blocking dose of atropine produced significant increases in heart rate and arterial pressures, and decreased stroke volume, ejection fraction, pulse pressure, and right-ventricular end-diastolic pressure and volume. Cardiac output was not changed by atropine administration. Nitroprusside reduced arterial pressures to a greater extent in atropinized horses but increased heart rate in both atropinized and non-atropinized horses. Dobutamine increased mean arterial pressure in both non-atropinized and atropinized horses but increased heart rate, diastolic arterial pressure, and systemic vascular resistance only in atropinized horses. Propranolol did not affect any of the hemodynamic variables that were measured. Phenylephrine, in the presence of beta-adrenergic blockade, increased mean arterial pressure and reduced cardiac output. This study showed that low doses of nitroprusside, dobutamine, and phenylephrine produce significant hemodynamic effects in conscious, healthy horses and that these effects are modified by prevailing parasympathetic tone.
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PMID:Hemodynamic effects of atropine, dobutamine, nitroprusside, phenylephrine, and propranolol in conscious horses. 206 69

Postnatal olfactory learning produces both a conditioned behavioral response and a modified olfactory bulb neural response to the learned odor. The present report describes the role of norepinephrine (NE) on both of these learned responses in neonatal rat pups. Pups received olfactory classical conditioning training from postnatal days (PN) 1-18. Training consisted of 18 trials with an intertrial interval of 24 hr. For the experimental group, a trial consisted of a pairing of unconditioned stimulus (UCS, stroking/tactile stimulation) and the conditioned stimulus (CS, odor). Control groups received either only the CS (Odor only) or only the UCS (Stroke only). Within each training condition, pups were injected with either the NE beta-receptor agonist isoproterenol (1, 20, or 4 mg/kg), the NE beta-receptor antagonist propranolol (10, 20, 40 mg/kg), or saline 30 min prior to training. On day 20, pups received one of the following tests: (1) behavioral conditioned responding, (2) injection with 14C-2-deoxyglucose (2-DG) and exposed to the CS odor, or (3) tested for olfactory bulb mitral/tufted cell single-unit responses to the CS odor. The results indicated that training with either: (1) Odor-Stroke-Saline, (2) Odor-Stroke-Isoproterenol-Propranolol, or (3) Odor only-Isoproterenol (2 mg/kg) was sufficient to produce a learned behavioral odor preference, enhanced uptake of 14C-2-DG in the odor-specific foci within the bulb, and a modified output signal from the bulb as measured by single-cell recordings of mitral/tufted cells. Moreover, propranolol injected prior to Odor-Stroke training blocked the acquisition of both the learned behavior and olfactory bulb responses. Thus, NE is sufficient and may be necessary for the acquisition of both learned olfactory behavior and olfactory bulb responses.
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PMID:Norepinephrine and learning-induced plasticity in infant rat olfactory system. 258 63

The influence of alloxan-induced diabetes on the adrenergic constriction of the rat cerebral vasculature was investigated in the in situ perfused brain preparation. The preparation was perfused with an artificial medium at a constant flow rate and the change in perfusion pressure was measured. Norepinephrine (NE) and serotonin produced a dose-dependent increase in the perfusion pressure, but only the effect of NE was significantly enhanced in the diabetic rats. Such an enhancement of NE-induced vasoconstriction was not observed in the perfused hindquarter preparations from the diabetic rats. Propranolol (1 microM) potentiated the cerebrovascular constriction by NE and abolished the difference between diabetic and control rats at low doses of NE. However, vasoconstriction by the higher doses of NE in the diabetic rats was still enhanced even in the presence of propranolol. The cerebrovascular constriction by phenylephrine was also enhanced in the diabetic rats, while the vasoconstricting effects of clonidine, xylazine and oxymetazoline were not affected by diabetes. These results suggest that the enhanced cerebrovascular constriction by NE may be due to either the reduced response through beta-adrenoceptors or the enhanced response through alpha 1-adrenoceptors. The enhanced adrenergic constriction of the cerebral vasculature might be concerned with the high incidence of neurological deficit in stroke patients with diabetes.
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PMID:Enhanced adrenergic response of the cerebral vasculature in alloxan-induced diabetic rats. 263 66

Acute right ventricular pressure overload shifts the interventricular septum leftward and decreases systolic shortening of the left ventricular (LV) septal-lateral diameter. These changes should alter regional shortening in the LV minor axis. To test this hypothesis, LV minor axis circumferential segment lengths of the septum and anterior, lateral, and posterior walls were measured during pulmonary artery or venae caval constriction in seven open-chest dogs with intact pericardia. Starting at an end-diastolic pressure of 10 mm Hg, venae caval constriction decreased LV end-systolic pressure by 19 +/- 6% and stroke volume by 40 +/- 15% and produced uniform decreases in systolic shortening and end-diastolic length around the minor axis. However, during pulmonary artery constriction resulting in similar decreases in end-systolic pressure (22 +/- 7%) and stroke volume (39 +/- 11%), decreases in systolic shortening were significantly larger in the anterior (-34 +/- 10%) and posterior (-33 +/- 21%) walls than in the septum (-10 +/- 9%) or lateral wall (-8 +/- 13%). The mechanisms of these large anterior and posterior shortening decreases differed: anterior end-diastolic length decreased more than posterior and lateral end-diastolic lengths, while posterior end-systolic length decreased less than anterior and lateral end-systolic lengths. Similar changes were seen at starting end-diastolic pressures of 5 and 15 mm Hg. Propranolol did not alter this nonuniform response, while pericardiectomy attenuated the regional variations. Thus, changes in LV geometry during acute right ventricular pressure overload are associated with nonuniform regional changes in systolic shortening in the LV minor axis that are enhanced by the pericardium.
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PMID:Nonhomogeneous left ventricular regional shortening during acute right ventricular pressure overload. 273 38


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