Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The cardiovascular effects of lysine acetylsalicylate and/or propranolol were studied in 26 dogs. All animals were maintained under anaesthesia with halothane 0.75 per cent, supplemented by the intravenous administration of succinylcholine to allow controlled ventilation during a two hour period of monitoring. Cardiac output, stroke volume, heart rate, mean arterial pressure, pulse pressure, central venous pressure, total peripheral resistance, pH, Paco2, pao2 and base deficit were measured in each dog. Lysine acetylsalicylate 50 mg . kg-1, administered alone as a single bolus, significantly (P less than 0.05) increased the cardiac output and stroke volume and significantly decreased the heart rate, central venous pressure and total peripheral resistance in dogs under halothane anaesthesia. Propranolol hydrochloride 0.5 mg . kg-1 as a single intravenous bolus was followed by a significant decrease in cardiac output, heart rate and mean arterial pressure and a significant increase in central venous pressure and total peripheral resistance. The administration of propranolol prior to lysine acetylsalicylate resulted in a significant decrease in cardiac output and heart rate. Pretreatment with propranolol was effective in inhibiting the positive inotropic effect of lysine acetylsalicylate.
 ...
PMID:Inhibition of the cardiovascular effects of lysine acetylsalicylate by propranolol in dogs during halothane anaesthesia. 680 96

Propranolol has been found to have a protective effect in experimental myocardial ischemia. Protection of ischemic kidneys was subsequently demonstrated following treatment with propranolol and its weaker beta blocking isomer, d-propranolol. The objective of the present investigation was to study the effects of propranolol (i.e., racemic d,1 mixture) and d-propranolol upon regional cerebral blood flow (rCBF) and early ischemic changes following experimental middle cerebral artery (MCA) occlusion. Thirty adult cats, lightly anesthetized with ketamine hydrochloride, underwent 3 hours or right MCA occlusion. Ten cats were untreated. Ten cats were given a continuous infusion of propranolol (1 mg/kg/hr) for 4 hours beginning 1 hour before MCA occlusion and a 4 mg/kg bolus immediately before occlusion. Ten cats were given a continuous infusion of d-propranolol (0.5 mg/kg/hr) for 4 hours beginning 1 hour before MCA occlusion and a 2 mg/kg bolus immediately before occlusion. The therapeutic agents were injected directly into the right carotid artery. The rCBF in the right Sylvian region was not significantly different in the 3 groups. EEG changes also were similar. Carbon filling defects were found to be smallest in the d-propranolol-treated group. Light microscopic studies demonstrated a reduction in infarct size in the propranolol and d-propranolol groups. The findings of the investigation indicated that propranolol and d-propranolol do not have a deleterious effect on rCBF after MCA occlusion and suggested that these agents have a protective effect upon ischemic cerebral tissue.
Stroke
PMID:Treatment of acute focal cerebral ischemia with propranolol. 708 Jan 22

Aortic rigidity, plasma noradrenaline and adrenaline, and hemodynamic parameters were measured in 48 essential hypertensive patients, 25 younger than 45 (Group I) and 23 of 45 years and over (Group II). Aortic rigidity was determined by the ratio of pulse pressure over stroke volume. Aortic rigidity and hemodynamic parameters were also determined after combined alpha-beta receptor blockade induced by Labetalol (mg 100 IV) or by Propranolol (mg 10 IV) plus Phentolamine (mg 10 IV). The aortic rigidity index was significantly higher in Group II, systolic arterial pressure being significantly higher. All other data, including plasma noradrenaline and adrenaline, were not significantly different in the two groups. In Group II a significant correlation (r = 0.62) was noted between aortic rigidity indexes and plasma noradrenaline values. The alpha-beta receptor blockade induced a decrease of aortic rigidity particularly in Group II, owing to a more marked decrease of systolic arterial pressure. A highly significant correlation was noted in Group II between the changes in aortic rigidity index and the basal plasma noradrenaline levels (r = 0.81). Therefore, the aortic rigidity in essential hypertensive patients older than 45 is influenced by the sympathetic nervous system activity, as judged by plasma noradrenaline levels. This influence seems related to an increase with age of aortic responsiveness to sympathetic stimulation.
 ...
PMID:Aortic rigidity and plasma catecholamines in essential hypertensive patients. 711 58

Basal hemodynamics and plasma catecholamines were measured in 10 patients with systolic hypertension, 7 males and 3 females, aged 38-69 years (Group 1), and in 10 patients with systolic and diastolic hypertension, 7 males and 3 females, aged 40-65 years (Group 2); the same measurements were repeated after acute pharmacological alpha and beta-blockade with Labetalol, 100 mg iv, or Propranolol, 10 mg iv, plus Phentolamine, 10 mg iv. In patients of Group 1 plasma noradrenaline was inversely related to systolic arterial pressure and to stroke index and was directly related to heart rate. In patients of Group 2 plasma noradrenaline was directly related to systolic arterial pressure. After acute alpha and beta-blockade the degree of reduction of systolic arterial pressure was directly related to basal plasma noradrenaline in both groups; systolic arterial pressure was reduced to normotensive levels in 5 patients of Group 1 who had high basal plasma noradrenaline values. These results confirm some of our previous findings and suggest that in some patients with systolic hypertension adrenergic activity is increased and may have a significant role in maintaining high blood pressure values.
 ...
PMID:Adrenergic activity in systolic hypertension. 711 59

In order to assess the hemodynamic effects of medical (propranolol) and surgical (transaortal subvalvular myectomy) therapy, we determined in 20 patients with hypertrophic obstructive cardiomyopathy the following circulatory parameters at rest and during maximal exercise before and after therapy: heart rate, stroke volume, cardiac output, and pulmonary artery pressure. 9 patients were re-investigated after medical therapy of 3.5 weeks to 7 months (averaging 3 months) with a daily dose of 120 to 360 mg (mean 198 +/- 80 mg) propranolol, 11 patients 1 week to 28 months (averaging 7.5 months) after operation. Propranolol induced a significant reduction of heart rate and cardiac output averaging 20.9% and 20.3%, respectively (p in both cases < 0.0001) at equal exercise levels, no change in stroke volume, and a slight increase in the pathologically elevated exercise mean pulmonary artery pressure, with the pulmonary vascular resistance remaining unchanged. Although 3 of the 9 patients reported a slight subjective improvement, exercise capacity did not change significantly from a mean of 66.7 to 69.4 watts. Myectomy, on the other hand, induced no change in heart rate, but a significant increase in exercise stroke volume by 14.9% (p < 0.025) and a distinct increase in cardiac output by an average of 11.2% (not significant), whereas the pathologically elevated exercise mean pulmonary artery pressure fell significantly by 23.8% from a mean of 45.0 to 34.3 mm Hg (p < 0.025). 10 of the 11 surgically treated patients reported a usually marked subjective improvement, and the exercise capacity increased from an average of 61.4 to 81.8 watts (p < 0.01). Thus, the clinical and functional result of surgical therapy was significantly better than that of medical therapy and included, in contrast to medical therapy, a significant hemodynamic improvement and increase in exercise capacity.
 ...
PMID:[Hemodynamic effects of medical and surgical therapy of hypertrophic obstructive cardiomyopathy (author's transl)]. 719 56

The effect of oral propranolol on left ventricular ejection fraction, left ventricular volumes, cardiac output, and segmental wall motion was assessed with multigated blood pool imaging both at rest and during supine exercise in 15 patients with angina pectoris. Propranolol had no effect on resting left ventricular ejection fractions. Before propranolol, they did not change during exercise, whereas after propranolol the ejection fractions increased slightly. Exercise left ventricular ejection fractions increased with propranolol in three patients with resting left ventricular ejection fractions of less than 40 per cent. More specifically, left ventricular end-diastolic volume index, end-systolic volume index, stroke volume index, and cardiac index were not altered significantly at rest or during exercise by propranolol. Exercise left ventricular ejection fractions were increased in five and unchanged in eight patients by propranolol. Those patients with increases in left ventricular ejection fractions had a greater change in left ventricular end-diastolic volume indices and a greater change in left ventricular end-systolic volume indices during exercise while on propranolol. Left ventricular segmental wall motion was not altered significantly during exercise by propranolol. We conclude that: (1) Left ventricular functional responses to propranolol during exercise are heterogeneous and not easily predicted; (2) propranolol causes no consistent deterioration in exercise left ventricular ejection fraction even in patients with resting ventricular ejection fractions less than 40 per cent; (3) increased exercise left ventricular ejection fraction with propranolol is contributed to by significant increases in end-diastolic volume during exercise; and (4) gated blood pool imaging is a useful method for characterising rest and exercise left ventricular ejection fractions and left ventricular volumes during propranolol therapy.
 ...
PMID:Effect of oral propranolol on rest and exercise left ventricular ejection fraction, volumes, and segmental wall motion in patients with angina pectoris. Assessment with equilibrium gated blood pool imaging. 725 15

Haemodynamic investigations were performed in 40 patients with acute myocardial infarction before and after intravenous application of 6 mg propranolol. Cardiac index was significantly decreased caused by reduction of cardiac frequency and stroke volume. Pulmonary capillary pressure increased significantly. As a consequence pulmonary and peripheral vascular resistance increased. Arterial blood pressure remained largely unaffected. Propranolol showed a haemodynamically beneficial decrease of left ventricular stroke work without signs of negative cardiodepression at a cardiac index of more than 3.0 l/min . m2. At a cardiac index of less than 3.0 l/min . m2 a haemodynamically detrimental lowering of cardiac index to ranges of insufficiency of 2.0 l/min . m2 on average occurred. Thus cardiac index is an important factor for the decision of use of beta-blocking agents in acute myocardial infarction. Indiscriminate use of beta-blocking substances should not be accepted.
 ...
PMID:[Risks of treatment with beta-blocking agents in acute myocardial infarction (author's transl)]. 729 32

Delayed postischemic brain hypoperfusion and hypermetabolism are likely detrimental factors to neurologic recovery after transient global brain ischemia and may be mediated by catecholamines acting via adrenergic receptors. We evaluated the effects of alpha and beta receptor blockade on cerebral blood flow (CBF) and metabolism after 16 min transient global brain ischemia. Ischemia was induced by arterial hypotension and a high pressure neck tourniquet in 13 anesthetized cats. Six cats were untreated, 4 received propranolol 1 mg/kg, IV and 3 a combination of propranolol and phentolamine, one mg/kg injected one min before recirculation. Total CBF was measured by continuous monitoring of cerebral venous 133Xe clearance after bolus intra-arterial injection. Arterial and cerebral venous oxygen, glucose and lactate were measured. Cerebral cortex glucose and lactate were measured 3 hours post-ischemia after in situ freezing with liquid N2. The cerebral cortex of 3 cats anesthetized, but not subjected to ischemia, was similarly frozen and analyzed for glucose and lactate. Total CBF was relatively constant for up to 3 h post-ischemia in all groups, but significant changes in fast and slow-flow rates and compartment sizes were observed. In untreated cats, the normal 60/40 percent relative weight of the fast and slow-flow compartments was reversed to 30/70 percent by 1 hr post-ischemia. Propranolol attenuated the size of the fast-flow compartment in the first 30 min post-ischemia which was partially restored by phentolamine. Brain oxygen consumption increased 2 to 3-fold by 1 h post-ischemia in all groups. Propranolol compromised CBF and impaired glucose and lactate oxidation which was partly reversed by phentolamine. We concluded that within the first 30 min post-ischemia, beta, and to a lesser extent, alpha receptors predominate in the modulation of cerebrovascular tone. By 1 h post-ischemia, however, adrenergic modulation of cerebrovascular tone is lost. Delayed post-ischemic hypermetabolism unlike stress-induced, but like hypoxia-induced hypermetabolism is only partially affected by beta blockade. Propranolol apparently compromises brain oxygen consumption secondary to a reduction in brain O2 supply while phentolamine improves perfusion and oxygen consumption.
Stroke
PMID:Post-ischemic hypermetabolism in cat brain. 730 55

A catheter-tip velocity transducer with two high-fidelity pressure manometers was used to evaluate the left ventricular (LV) hemodynamic effects of intravenous propranolol (10 mg). Nine patients without clinical evidence of heart failure were studied. Pulsatile ascending aortic blood flow velocity and pressure and LV pressure were measured continuously during drug administration. Beat-to-beat changes in stroke volume index, stroke work index, LV end-diastolic pressure, maximum blood flow velocity and acceleration, and maximum LV dP/dt were determined. Propranolol produced a decrease in maximum blood flow velocity (from 58 +/- 4.7 to 42 +/- 5.1 cm/sec, p less than 0.002), and acceleration (from 1181 +/- 130 to 847 +/- 117 cm/sec2, p less than 0.002, max dP/dt (from 1361 +/- 70 to 1146 +/- 63 mm Hg/sec, p less than 0.002), stroke volume index (from 47 +/- 3.0 to 38 +/- 3.2 ml/m2, p less than 0.002) and total stroke work index (from 702 +/- 33 to 603 +/- 44 mJ/m2 p less than 0.04), with little change in mean aortic pressure, peak systolic pressure and LV end-diastolic pressure. Depression in myocardial function was detectable within 1 minute after initiation of propranolol and persisted when negative chronotropic effects were eliminated by atrial pacing. The multisensor catheter technique allows rapid and safe detection of changes in cardiovascular function during propranolol administration in conscious man.
 ...
PMID:Use of catheter-tip velocity--pressure transducer to evaluate left ventricular function in man: effects of intravenous propranolol. 736 37

Left ventricular systolic pressure (LVSP) and stress in the outer layers of the left ventricular wall were directly recorded in 10 anaesthetised, open-chested dogs. Left ventricular oxygen consumption (VO2) was calculated from the difference in oxygen content in the arterial and in the coronary sinus blood and from the left ventricular coronary flow (LVCF). LVCF was measured in the shunt between the carotid artery and left coronary artery (2 experiments) or in the shunt between the coronary sinus and jugular vein. Tension-time index was calculated either as the product of the mean LVSP and time (TTI(P)), or as the product of mean systolic stress and time (TTI(sigma)). Both TTIs were changed within the broad range by means of exsanguination and blood infusion. Contractility was changed by means of Inderal or noradrenaline infusion. In all experimental conditions VO2/100 g/stroke correlated linearly (P less than 0.01) with TTI(sigma), with correlation coefficient r greater than 0.8. When TTI(P) was used, correlation coefficient r was less than 0.6 and no correlation was found in one series of experiments with noradrenaline infusion. It is concluded that TTI calculated from the directly measured wall stress is a very good correlate of the VO2, which is not the case when the 'classical' TTI is used.
 ...
PMID:Directly measured tension-time index as a correlate of myocardial oxygen consumption. 736 21


<< Previous 1 2 3 4 5 6 7 Next >>