High blood pressure. Causes, symptoms, treatments

Effects of dipyridamole on Plasmodium falciparum-infected erythrocytes.


Effects of azelnidipine, a dihydropyridine derivative, on stunned myocardium were examined in anesthetized open-chest dogs. The left anterior descending (LAD) coronary artery was ligated for 20 min and then released for 60 min. Dimethyl sulfoxide (DMSO), the solvent of azelnidipine, or azelnidipine (0.03, 0.1 or 0.3 mg/kg) was injected i.v. 20 min before ligation. Segment shortening was determined by sonomicrometry. The levels of high-energy phosphate were measured in 60-min reperfused hearts. Azelnidipine at 0.1 and 0.3 mg/kg significantly decreased diastolic blood pressure and increased % segment shortening. The increase in % segment shortening due to azelnidipine appeared to be abolished by propranolol and atropine pretreatment. Ischemia significantly decreased % segment shortening in all groups. The % segment shortening that had been decreased by ischemia recovered during reperfusion, but did not reach its preischemic level in each group. In the 0.1 and 0.3 mg/kg of azelnidipine-treated dogs, a significant enhancement of % segment shortening recovery during reperfusion was observed, as compared with that in the DMSO-treated dogs. Azelnidipine did not affect the high-energy phosphate levels in 60-min reperfused hearts. In conclusion, azelnidipine improved the contractile dysfunction in stunned myocardium, without any preservation of high-energy phosphate.

Propranolol causes splanchnic arterial vasoconstriction owing to the unopposed alpha vasoconstriction resulting from the blockade of beta-2 adrenoceptors. It is therefore hypothesized that this drug may cause vasoconstriction in the splenic arterial circulation and, thus, modify the manifestations of hypersplenism, such as thrombocytopenia. The aim of the present study was to test this hypothesis.

The aim of this work was to study effect of fosinopril combined with propranolol or cytomack on ecoendotoxicosis, size of myocardial infarction (MI), left ventricular (LV) systolic function, and clinical picture of stationary phase MI in patients working in environmentally unfriendly conditions. 42 patients aged 30-70 yr presenting with MI and initial Q-wave were randomized into 2 groups of 21 subjects each. In group 1, they were given fosinopril with propranolol, in group 2 fosinopril with cytomack. Mean age of group 1 and 2 patients was 57.8 +/- 2.1 and 56.9 +/- 23 yr respectively. All the patients were hospitalized within 6 hr after onset of the disease and received heparin. They underwent PETG and echoCG, also studied were endotoxicosis (PSD), central hemodynamics, left ventricular systolic functions (ESV, EDV, EF), size of MI (total ST, AST, total Rh), and clynical symptoms. It was shown that patients working in environmentally unfriendly conditions were characterized by high degree of PSD. In group 1 they exhibited reduction of PSD, total ST, AST, ESV, EDV and increase of total Rh and EF. Decreased systolic and diastolic AP did not lead to clinically significant hypotension. Patients of group 2 showed stabilization of AP, decrease of PSD, total ST, AST, ESV, EDV and increase of total Rh and EF that prevented the development of cardiac insufficiency in the phase of stationary rehabilitation of MI. Characteristics of groups 1 and 2 were not significantly different. The clinical course of IM in patients given fosinopril with cytomack was more favourable than in those treated with fosinopril and propranolol. Two patients of group 1 suffered cardiac insufficiency.

Octreotide enhances HVPG reduction induced by propranolol in cirrhotic patients.

Propranolol is one of the most commonly prescribed drugs for migraine prophylaxis.

To explore sex differences in the regulation of lipolysis during exercise, the lipid-mobilizing mechanisms in the subcutaneous adipose tissue (SCAT) of overweight men and women were studied using microdialysis.

The Biopharmaceutical Classification System (BCS) guidance issued by the FDA allows waivers for in vivo bioavailability and bioequivalence studies for immediate-release (IR) solid oral dosage forms only for BCS class I drugs. However, a number of drugs within BCS class III have been proposed to be eligible for biowaivers. The World Health Organization (WHO) has shortened the requisite dissolution time of BCS class III drugs on their Essential Medicine List (EML) from 30 to 15 min for extended biowaivers; however, the impact of the shorter dissolution time on AUC(0-inf) and C(max) is unknown. The objectives of this investigation were to assess the ability of gastrointestinal simulation software to predict the oral absorption of the BCS class I drugs propranolol and metoprolol and the BCS class III drugs cimetidine, atenolol, and amoxicillin, and to perform in silico bioequivalence studies to assess the feasibility of extending biowaivers to BCS class III drugs. The drug absorption from the gastrointestinal tract was predicted using physicochemical and pharmacokinetic properties of test drugs provided by GastroPlus (version 6.0). Virtual trials with a 200 mL dose volume at different drug release rates (T(85%) = 15 to 180 min) were performed to predict the oral absorption (C(max) and AUC(0-inf)) of the above drugs. Both BCS class I drugs satisfied bioequivalence with regard to the release rates up to 120 min. The results with BCS class III drugs demonstrated bioequivalence using the prolonged release rate, T(85%) = 45 or 60 min, indicating that the dissolution standard for bioequivalence is dependent on the intestinal membrane permeability and permeability profile throughout the gastrointestinal tract. The results of GastroPlus simulations indicate that the dissolution rate of BCS class III drugs could be prolonged to the point where dissolution, rather than permeability, would control the overall absorption. For BCS class III drugs with intestinal absorption patterns similar to those of cimetidine, atenolol or amoxicillin, the dissolution criteria for extension of biowaivers to BCS class III drugs warrants further investigation.