Biomedical subjects

Ritva Ylitalo

Publications and source records attributed to Ritva Ylitalo.

7 recordsLinked to original sources

PubMed2005

Effects of a mononitrate, a beta1-blocker and a dihydropyridine calcium channel blocker on cardiovascular responsiveness to passive orthostasis: a placebo-controlled double-blind study in normotensive volunteers.

OBJECTIVE: The aim of this study was to compare the influences of antianginal drugs such as mononitrate, beta-blocker and calcium channel blocker on cardiovascular responsiveness to orthostasis. METHODS: The responses to passive orthostasis (tilt provocation at 60 degrees for 3 min) were measured in normotensive healthy volunteers with whole-body impedance cardiography and finger blood-pressure monitoring after a single moderate oral dose of isosorbide-5-mononitrate (CAS 16051-77-7, 10 mg), the beta1-blocker bisoprolol fumarate (CAS 104344-23-2, 5 mg), the dihydropyridine calcium channel blocker nisoldipine (CAS 63675-72-9, 5 mg), and placebo in a randomised, double-blind fashion. RESULTS: In supine position, none of the drugs altered pre-tilt arterial pressure or heart rate (HR) when compared to placebo. Nisoldipine decreased systemic vascular resistance index (SVRI) when compared to either placebo or bisoprolol, and increased the cardiac index (CI) when compared to placebo. During the passive orthostasis, the mononitrate decreased SVRI when compared to placebo or bisoprolol. The mononitrate increased HR and pulse wave velocity (PWV) when compared to the other study groups, and decreased the stroke index when compared to placebo. In the bisoprolol group, the tilt responses of diastolic arterial pressure, HR, CI, left cardiac work index, and PWV decreased significantly compared to those in the placebo group. Nisoldipine did not alter the responses to orthostasis when compared to placebo. When compared to the mononitrate, both nisoldipine and bisoprolol decreased CI response to orthostasis. CONCLUSIONS: The mononitrate adversely affects the cardiovascular responsiveness to orthostasis. The beta-blocker reduces the responses and thus probably oxygen demand during orthostasis. The dihydropyridine calcium blocker seems to influence the responsiveness less than the mononitrate or beta-blocker.

Adrenergic beta-1 Receptor Antagonists↗

PubMed2005

Effects of adrenoceptor blocking drugs on cardiovascular responsiveness to passive orthostasis: a placebo-controlled double-blind study.

OBJECTIVE: To compare the acute effects of the beta-blocker propranolol (CAS 525-66-6), beta + alpha1-blocker carvedilol (CAS 72956-09-3) and alpha1-blocker tamsulosin (CAS 106463-17-6) on the cardiovascular responses to passive orthostasis. METHODS: The responses to passive orthostasis (tilt provocation at 60 degress for 8 min) were measured in normotensive healthy volunteers with finger-blood-pressure and whole-body impedance cardiography prior to drugs and three days after beginning the medications. The treatments were moderate oral doses of the beta-blocker propranolol HCl (40 mg twice daily, n = 7), (beta + alpha1-blocker carvedilol (12.5 mg once daily for two days and thereafter 25 mg daily, n = 7), alpha1-blocker tamsulosin HCl (0.4 mg once daily, n = 6), or placebo. The drugs were distributed in a randomised, double-blind fashion. RESULTS: When measured prior to the head-up tilt test, propranolol and carvedilol had decreased supine systolic arterial pressure (SAP) more than placebo, and heart rate (HR) more than placebo and tamsulosin. Propranolol had decreased also pulse wave velocity more than placebo. The cardiac index (CI), stroke index (SI) and systemic vascular resistance index (SVRI) were not changed with any drugs. During the head-up tilt, tamsulosin decreased SAP and SVRI and augmented CI but not SI. The SVRI response curve with tamsulosin differed from that with propranolol or carvedilol. Also, tamsulosin increased HR compared to the beta-blocking drugs. The propranolol and carvedilol groups did not differ from each other in terms of any parameter. CONCLUSIONS: Tamsulosin significantly decreases SAP in the passive head-up tilt, indicating that it is not purely uroselective alpha1-blocker. The responses with tamsulosin clearly differ from those with propranolol and carvedilol, the responses with the latter two being practically equal.

Adrenergic Antagonists↗

PubMed2005

Microcrystalline chitosan is ineffective to decrease plasma lipids in both apolipoprotein E epsilon 4 carriers and non-carriers: a long-term placebo-controlled trial in hypercholesterolaemic volunteers.

Chitosan is a deacetylated product of chitin. Microcrystalline form of chitosan has a large adsorption area claimed to decrease gastrointestinal absorption of cholesterol. However, the long-term effect of chitosan on plasma lipids is variable, the averaged influence being negligible or lacking in mildly-to-moderately hypercholesterolaemic (4.8-6.8 mmol/l) subjects. We evaluated whether this variation and inefficacy depend on apolipoprotein E genotype. 130 middle-aged, otherwise healthy men (n=55) and women (n=75) were randomized into two treatment groups for a 7 month trial. During a 1 month run-in period all participants received placebo. Subsequently, one half first took placebo twice daily for 3 months and then 1.2 g chitosan twice daily for 3 months, and the other half vice versa in a cross-over way. Altogether 84 participants completed the study. Plasma lipids and glucose were determined at the end of each phase of the study, and all subjects undergone to the cross-over phases were apolipoprotein E genotyped. Chitosan altered plasma total, low- and high density cholesterol, triglycerides, and blood glucose in neither apolipoprotein E epsilon 4 allele carriers (n=29) nor non-carriers (n=55), compared to placebo. In conclusions, chitosan is ineffective to decrease plasma lipids in apolipoprotein E epsilon 4 carrier and non-carrier phenotypes with mildly-to-moderately increased plasma cholesterol.

Adolescent↗

PubMed2004

The vasodilatory effect of alfuzosin and tamsulosin in passive orthostasis: a randomised, double-blind, placebo-controlled study.

OBJECTIVE: To compare in details the effects of urologically used alpha(1)-blockers alfuzosin and tamsulosin on the cardiovascular responses to passive orthostasis. METHODS: The responses to passive orthostasis (tilt provocation at 60 degrees for 8 min) were measured in normotensive healthy volunteers with finger blood pressure method and whole-body impedance cardiography prior to the administration of the drugs as well as three days after the beginning of the randomised, double-blind medications. The parallel treatments were standard clinically used doses of alpha(1)-blockers alfuzosin (5 mg twice daily, n=10), tamsulosin (0.4 mg once daily, n=10), or placebo (n=11). RESULTS: When measured prior to the head-up tilt test in supine position, neither alfuzosin nor tamsulosin significantly changed any of the cardiovascular variables. During the passive orthostasis, however, both tamsulosin and alfuzosin reduced systemic vascular resistance index compared to pre-drug responses (-540 and -462 dyns/cm(5)m(2), respectively, p<0.05). Both drugs also augmented orthostatic responses of heart rate (11 and 9 bpm, respectively, p<0.05) and cardiac index (0.50 and 0.40 l/min/m(2), respectively, p<0.05) but not those of stroke index when compared to the responses during placebo or before the administration of the drugs. The alfuzosin and tamsulosin groups did not significantly differ from each other in terms of any parameter. CONCLUSIONS: Both alfuzosin and tamsulosin have clear cardiovascular effects, which are most strikingly evident in the influences on systemic vascular resistance and cardiac output.

Adrenergic alpha-Antagonists↗

PubMed2003

The effect of long-term microcrystalline chitosan therapy on plasma lipids and glucose concentrations in subjects with increased plasma total cholesterol: a randomised placebo-controlled double-blind crossover trial in healthy men and women.

OBJECTIVE: To evaluate the long-term effect of microcrystalline chitosan (MCC) on plasma lipids, especially the concentration of low-density lipoprotein (LDL) cholesterol, in subjects with a moderately increased concentration of plasma total cholesterol. METHODS: A total of 130 middle-aged men and women without severe disease and with a total cholesterol of 4.8-6.8 mmol/l and triglycerides below 3.0 mmol/l were randomised into two treatment groups. At the beginning of the 10-month trial, all participants received placebo 1.2 g twice daily during a 1-month run-in period. Subsequently, group 1 first received 1.2 g placebo twice daily for 3 months and then 1.2 g MCC twice daily for 3 months. Correspondingly, group 2 received 1.2 g MCC twice daily during the first and 1.2 g placebo twice daily during the second 3-month period. During the final 3-month follow-up period, both groups received MCC. Altogether, 83 participants completed the study. RESULTS: No difference was detected in the change in the LDL-cholesterol concentration between the treatments during the crossover trial ( P=0.98 for interaction between time period and treatment group, repeated-measures analysis of variance for crossover design). In an otherwise similar analysis, no differences were detected between the treatments in the concentrations of total cholesterol, high-density lipoprotein cholesterol, triglycerides and glucose. CONCLUSIONS: Treatment with MCC had no effect on the concentrations of plasma lipids or glucose in healthy middle-aged men and women with moderately increased plasma cholesterol concentrations.

Adjuvants, Pharmaceutic↗

PubMed2002

Suppression of immunoreactive macrophages in atheromatous lesions of rabbits by clodronate.

Bisphosphonates inhibit the development of experimental atherosclerosis and decrease the intima-media thickness of human carotid artery. Since arterial macrophages have a key role in atherogenesis, we studied whether clodronate, an antiatherogenic bisphosphonate, will suppress the appearance of macrophages generated by atheromatous process in the rabbit aorta. The atherosclerosis was caused in rabbits by means of a high-cholesterol (1%) diet, and the animals were treated simultaneously with saline (n = 11) or 25 mg/kg of clodronate disodium (n= 12) intravenously twice a week for 6 to 12 weeks. The cholesterol diet for 6 weeks caused no visible atheromatous plaques in the aorta, but feeding for 6 more weeks produced progressively atheromatous lesions. Immunohistochemistry with specific antimacrophage antibody showed an intensive accumulation of macrophages in the subendothelial layer of the aorta in cholesterol-fed rabbits treated with saline or clodronate for 6 weeks. In the aorta of rabbits treated with cholesterol diet + saline for 12 weeks, the area of immunoreactive macrophages extended from the internal elastic lamina up to the luminal surface of the aorta. However, far less immunoreactive macrophages were present in the atheromatous regions of the aorta of rabbits medicated with clodronate for 12 weeks; in the clodronate-treated animals the macrophages were located closer to the luminal surface of the aorta than in controls on saline. No atheromatous lesions and macrophages appeared in the aorta of rabbits on standard diet (n = 7). The results suggest that clodronate suppresses the appearance of cholesterol-phagocyting macrophages in arterial walls during atherogenesis.

Animals↗

PubMed2002

Cholesterol-lowering properties and safety of chitosan.

Chitosan (CAS 9012-76-4) is derived by alkaline deacetylation from chitin, an abundant polymeric product of natural biosynthesis especially in crustaceans. It is available in a primary, unorganised structure, but also in a microcrystalline form. As a dietary supplement, chitosan has been claimed to control obesity and to lower serum cholesterol. A variety of chitosan products have been freely available worldwide in health stores and pharmacies. This review summarises the current knowledge about cholesterol-lowering and safety properties of chitosan and focuses its possible application for the treatment of hypercholesterolaemia. Chitosan behaves as a polycationic(+) cellulose-like fibrillar biopolymer that forms films with negatively charged surfaces. It is not specifically hydrolysed by digestive enzymes in man, but limited digestion of chitosan due to bacterial flora and to the unspecific enzymes might occur. Negatively charged molecules in stomach attach strongly to the positive charged tertiary amino group (-NH3+) of chitosan. Therefore, chitosan reduces fat absorption from gastrointestinal tract by binding with anionic carboxyl groups of fatty and bile acids, and it interferes with emulsification of neutral lipids (i.e., cholesterol, other sterols) by binding them with hydrophobic bonds. In short-term animal studies the safety of chitosan has been good. There are only few studies with chitosan in humans. In man, dietary chitosan has been reported to reduce serum total cholesterol levels by 5.8-42.6% and low-density lipoprotein levels by 15.1-35.1%. In short-term trials up to 12 weeks, no clinically significant symptoms have been observed with chitosan compared to placebo. Mild and transitory nausea and constipation have been reported in 2.6-5.4% of subjects. Although chitosan has been clinically well tolerated, it cannot be recommended to people allergic to crustaceans.

Animals↗