High blood pressure. Causes, symptoms, treatments

Neuroprotective Effects of Cistanches Herba Therapy on Patients with Moderate Alzheimer's Disease.

2017-04-10

Ibudilast shows a better curative effect than loratadine in the improvement of the total scores on clinical symptom and signs(P<0.05). Scores of symptoms and signs in Ibudilast group after 3, 7, 14 days decreased significantly by means of square analysis of single factor (P<0.01). No complication was observed.

Cold contact urticaria is the second most common subtype of physical urticaria. Cold stimulation standardized tests are mandatory to confirm the diagnosis. The aim of this study is to define the utility of determining thresholds (critical time and temperature) in assessment of the clinical course of typical acquired cold contact urticaria. Nineteen adult patients (10 women and 9 men; mean age 45 years) were included in the study and the diagnosis was confirmed with the ice-cube test and TempTest 3.0. Patients were treated continuously for 1 year with 20 mg/day rupatadine (anti-H1). Thresholds measurements were made before and after treatment. Improvements in temperature and critical time thresholds were found in the study sample, demonstrating the efficacy of continuous treatment with rupatadine. In most cases association with a clinical improvement was found. We propose an algorithm for the management of acquired cold contact urticaria based on these results.

Studies were performed on isolated cerebral and peripheral arterial segments from the rat to define contractile receptors for 5-hydroxytryptamine (5-HT) and to elucidate the responses to calcium channel blockers in relation to their effects on potassium-induced contractions. 5-HT induced strong contraction of the middle cerebral artery, arteries forming the circle of Willis, basilar artery and tail artery in the mentioned order of relative potency and with an intrinsic activity in the brain vessels approximately 70% of that caused by 124 mM potassium in the buffer solution. Ketanserin inhibited the contraction both in the basilar and tail arteries competitively, with pA2 = 9.35 and 9.09, respectively, suggesting mediation by 5-HT2 receptors. The inhibition by cyproheptadine and methysergide (of the response in the basilar artery) was noncompetitive. High potassium in the buffer solution contracted the basilar and tail arteries biphasically, including prazosin-sensitive alpha-adrenoceptor activation in the latter. Cyproheptadine, nimodipine, verapamil and diltiazem inhibited the 5-HT-induced contraction in the mentioned order of potency. Verapamil was more potent than diltiazem, also in the tail artery, but nimodipine inhibited the contraction only by 35%. Also the (tonic) contraction induced by high potassium concentration was attenuated, with the same relative potency as in the presence of 5-HT except for cyproheptadine, which was less efficient than nimodipine. The transient potassium-induced contraction was inhibited less effectively by the calcium antagonists. The IC50 values were characteristically lower in the basilar than in the tail artery, irrespective of whether the contraction had been produced by 5-HT or high potassium.(ABSTRACT TRUNCATED AT 250 WORDS)

Basophil activation test should be performed as early as possible after taking the blood sample, preferably within 4 h. In contrast to the skin test, BAT can be performed in patients undergoing treatment with antihistamines. For reasons of multiple influencing factors, BAT should be performed only at validated laboratories.

A 4-year-old girl was admitted 25 h after accidentally ingesting approximately 27 pills of sibutramine (15 mg, approximately 23 mg/kg). The child developed clinical features suggestive of SS, including diaphoresis, tachycardia, hypertension, agitation, insomnia, incoordination, hypertonia (lower limbs > upper limbs), and hallucinations. Serum creatine phosphokinase levels reached a peak on day 3 (2,577 U/L, reference value <145), suggesting mild rhabdomyolysis. No relevant changes were detected in other laboratory examinations or in the electrocardiogram throughout the period of hospitalization. The quantification of sibutramine and the active metabolites, M1 (mono-desmethyl sibutramine) and M2 (di-desmethyl sibutramine), by liquid chromatography/electrospray ionization tandem mass spectrometry in six sequential samples collected from 25 to 147 h post-ingestion revealed a nonlinear decrease in the log-scale plasma concentrations. Treatment was only supportive and involved prolonged sedation to control the agitation, sleeplessness, and hypertension; no cyproheptadine was used. The patient was discharged on day 6 and follow-up revealed no sequelae.

Fifteen minutes after the last drug administration, groups of mice were presented with sweetened chow and the amount of food consumed was recorded at 0.5,1,2, 3 and 4h time intervals.

The studies showed CMC could be applied to investigate drug-receptor interactions.

Bothrops jararaca venom (30 micrograms/site) triggered a marked inflammatory reaction in the pleural cavity that was long-lasting and reproducible. In the first 1 h after pleurisy induction, a significant decrease of total and differential cell count was observed in comparison with control values, despite the gradual enhancement of fluid leakage. A significant increase of cell migration was observed after 3 h of pleurisy induction, due to mononuclear and neutrophil cells that peaked 8 h later and this was followed by a gradual decrease, remaining elevated up to 24 h. In parallel with cell influx, a significant increase of fluid leakage that peaked between 1 and 8 h was observed, being completely abolished after 12 h following pleurisy induction. This inflammatory response was not associated in parallel with significant changes in circulating leucocyte cells and it was significantly inhibited by compound 48/80, cyproheptadine, pyrilamine, dexamethasone, indomethacin and phenidone. Preheating of the venom (100 degrees C) caused a significant decrease of both leakage of fluid and cell migration in the pleural cavity 8 h after pleurisy induction. Previous exposure to the venom (30 micrograms/site, 5 days before) produced a significant decrease of both cell migration and fluid leakage 4 h after triggering pleurisy with the same dose of the venom. Otherwise, prior daily treatment with the venom (10 micrograms/site, 4 days) resulted only in marked fluid leakage reduction 1 h after treating the animals with BJV (30 micrograms/site). These results show that the venom elicits pro-inflammatory effects in the rat pleural cavity which involve the participation of several mediators, including histamine, 5-hydroxytryptamine and products of arachidonic pathways.