Biomedical subjects

M Suzukawa

Publications and source records attributed to M Suzukawa.

At least 19 recordsLinked to original sources

PubMed1999

[Percutaneous dilational tracheostomy: report of 9 cases].

Nine patients with CNS damage who had been transferred to our critical care unit were treated with a commercially available kit for percutaneous dilational tracheostomy (PDT). The mean procedure time was about 11 minutes, and the perioperative complication rate was 22% (2/9). Only one complication, wound infection, occurred, and the patient was cured with conventional therapy. On the other hand, premature extubation of the translaryngeal tube occurred in one case. Long-term complications like tracheal stenosis and tracheal malacia were not experienced in two patients. They were discharged from the hospital after decannulation. In conclusion, the advantages of PDT include a short procedure time, the ability to perform the procedure at the bedside, and reduced stimulation of the trachea. Because of the safety and simplicity of the procedure, we recommend PDT for patients with CNS damage.

Adult↗

PubMed1998

Effect of supplementation with vitamin E on LDL oxidizability and prevention of atherosclerosis.

Supplementation of LDL with vitamin E is thought to protect LDL from oxidative modification and prevent the development of atherosclerosis. Large epidemiological studies have revealed that vitamin E levels in plasma are inversely correlated to the incidence of coronary heart disease. Double-blind placebo-controlled trials have reported that supplementation with vitamin E decreases the incidence of coronary events in coronary heart disease (CHD) patients. However, it is not clear how high a dose of vitamin E is needed to prevent formation of atherosclerosis. In animal studies, a diet containing 0.125% vitamin E increased its levels in plasma two-fold and prevented formation of early atherosclerotic lesions in the thoracic aorta of hypercholesterolemic rabbits. Dose-response studies in humans have reported that 400 IU/day vitamin E increased its levels in plasma two-fold and prolonged the lag time before LDL oxidation. It has been reported that oxidizability of LDL was correlated to the atherosclerotic score of coronary angiography in CHD patients. About 400 IU/day vitamin E, which increases its levels two-fold and prolongs sufficiently the lag time before LDL oxidation, might be beneficial in decreasing the individual risk of CHD.

Animals↗

PubMed1998

Vitamin E reduces cholesterol esterification and uptake of acetylated low density lipoprotein in macrophages.

The effects of vitamin E on cholesteryl ester (CE) metabolism in J774 cells were examined. Pretreatment of J774 cells with vitamin E at concentrations above 50 microM significantly decreased acetylated low density lipoprotein (LDL)-induced incorporation of [14C]oleate into CE in cells in a dose-dependent manner. This was partly due to vitamin E also significantly inhibiting the uptake of [3H]CE-labeled acetylated LDL by J774 cells. A trend existed toward suppression of acyl-CoA:cholesterol acyltransferase (ACAT) activity in the cell lysate at high vitamin E concentration, but there was no effect on hydrolysis of CE. These data indicate that vitamin E reduces the uptake of modified LDL and suppresses ACAT activity, resulting in less cholesterol esterification in macrophages: a novel mechanism underlying the antiatherogenic properties of vitamin E.

Animals↗

PubMed1998

Beneficial effect of gemfibrozil on the chemical composition and oxidative susceptibility of low density lipoprotein: a randomized, double-blind, placebo-controlled study.

Previous reports have shown that administration of fibrates can reduce coronary events and also improve plasma lipid levels. Oxidative modification of low density lipoprotein has been implicated in the pathogenesis of atherosclerosis, and the resistance of low density lipoprotein (LDL) to in vitro oxidation has been found to be correlated with the extent of atherosclerosis. We performed a double-blind, placebo-controlled intervention trial to establish whether gemfibrozil could improve resistance of LDL to oxidation in patients with hyperlipidemia. Patients were randomly assigned to treatment with gemfibrozil (450 mg, twice a day, n = 10) or placebo (n = 9) for 8 weeks. Blood samples were obtained after an overnight (12 h) fast. Gemfibrozil administration significantly reduced total plasma cholesterol and triglyceride levels and changed the LDL from small, dense particles (pattern B, < or = 25.5 nm) to larger, more buoyant particles (pattern A, > 25.5 nm). Gemfibrozil significantly increased the lag time of LDL oxidation in vitro by 18.2% from 45.5 +/- 8.0 min at week 0 to 53.4 +/- 11.4 min at week 8, but did not change LDL vitamin E and beta-carotene concentrations. Surprisingly, gemfibrozil significantly decreased LDL lipid peroxides by -33.1% and increased the LDL vitamin E/lipid peroxide ratio by 67.6% from 1.3 +/- 0.5 at week 0 to 2.1 +/- 0.9 at week 8. These results demonstrate that gemfibrozil treatment can render LDL less susceptible to oxidative modification while reducing plasma cholesterol and triglyceride and improving LDL subclass pattern. This antioxidative effect of gemfibrozil on LDL may be one of the factors which could delay the progression of atherosclerosis.

Adult↗

PubMed1998

Preoperative nocturnal desaturations as a risk factor for late postoperative nocturnal desaturations.

Severe postoperative hypoxaemia during sleep may increase the risk of postoperative cardiovascular complications. We hypothesized that the severity of hypoxic episodes after surgery are related to the presence of preoperative sleep-disordered breathing (SDB). We tested this hypothesis in a multicentre study designed to elucidate the major risk factors for development of postoperative nocturnal desaturations. We performed overnight oximetry before operation and for one night between the second and fourth day after operation in 80 patients undergoing major surgery. We calculated oximetry variables such as oxygen desaturation index (ODI), defined as the number of oxygen desaturations exceeding 4% below baseline, percentage time spent at SpO2 < 90% (CT90, %) and lowest SpO2 value. After operation, although the change in ODI was not significant (P = 0.34), deterioration in CT90 and lowest SpO2 values were significant (P = 0.036 and P = 0.007, respectively). Multivariate analysis of possible risk factors for postoperative desaturations revealed that preoperative hypoxaemia and apnoea witnessed by others were highly correlated with postoperative hypoxaemia.

Adult↗

PubMed1998

Effects of soy protein isolate (SPI) and casein on the postprandial lipemia in normolipidemic men.

To elucidate the effects of soybean protein and casein on postprandial lipemia, oral fat load tests were performed before and 3 weeks after the administration of soy protein isolate (SPI) and casein supplement to normolipidemic men. Eleven normolipidemic male subjects on otherwise identical controlled diets were assigned to either a 20 g/d soy protein isolate (SPI) dietary supplement or a casein dietary supplement for three weeks in a crossover design. Fat load tests with 40 g/m2 of bovine milk fat were carried out before and after 3 weeks on the experimental dietary supplements. Fasting plasma concentrations of lipids and apolipoproteins were not significantly different from baseline levels before or after the administration of SPI or casein supplemented diets. Neither SPI nor casein supplement affected the fasting plasma concentrations of lipids and apolipoproteins. The areas under the incremental curve (AUIC) of triglyceride (TG) and remnant-like particles triglyceride (RLP-TG) after both experimental diets were not significantly different from those before the experimental diets. However, the AUIC of remnant-like particles cholesterol (RLP-C) showed a tendency (p = 0.07) to decrease after administration of the diet supplemented with SPI than before the diet. The AUIC of RLP-C was significantly (p < 0.05) lower after the diet supplemented with SPI than after administration of the diet supplemented with casein. These results suggest that 3 weeks of 20 g/d SPI dietary supplement favorably affects the postprandial remnant lipoprotein response as compared to the casein dietary supplement.

Adult↗

PubMed1997

Effect of tea flavonoid supplementation on the susceptibility of low-density lipoprotein to oxidative modification.

Dietary flavonoid intake has been reported to be inversely associated with the incidence of coronary artery disease. To clarify the possible role of tea flavonoids in the prevention of atherosclerosis, we investigated the effects of tea flavonoids on the susceptibility of low-density lipoprotein (LDL) to oxidative modification. In an in vitro study, catechins or theaflavins (25-400 mumol/L) were added to plasma and incubated for 3 h at 37 degrees C. Then, the LDL fraction was separated by ultracentrifugation. The oxidizability of LDL was estimated by measuring conjugated diene, thiobarbituric acid-reactive substances (TBARS), and lipid peroxides after cupric sulfate was added. TBARS and lipid peroxides in the supernates were also measured after incubation with macrophages. Catechins significantly (P < 0.01 by ANOVA) and dose-dependently prolonged the lag time before initiation of oxidation. Among the catechins, epigallocatechin gallate exerted the most marked effect, prolonging the oxidation lag time more than vitamin E at the same molar concentration. Theaflavins exerted stronger inhibitory effects than catechins. Macrophage-mediated LDL oxidation was also inhibited by adding these tea flavonoids to the plasma samples. In an in vivo study, 14 healthy volunteers consumed 750 mL black tea/d for 4 wk. After the subjects had consumed tea for 4 wk, the lag time before LDL oxidation was significantly (P < 0.01) prolonged from 54 to 62 min. This minor prolongation occurred despite much lower plasma flavonoids than were used in vitro. No significant change was observed in eight control volunteers. LDL exposed to tea flavonoids in vitro or in vivo reduced oxidizability. We speculate that tea flavonoids may have a role in ameliorating atherosclerosis.

Adult↗

PubMed1997

Beneficial effects of alcohol withdrawal on LDL particle size distribution and oxidative susceptibility in subjects with alcohol-induced hypertriglyceridemia.

LDL subclass pattern B, reported to have a higher prevalence in hypertriglyceridemics (HTGs), is considered to be associated with an increased risk for coronary artery disease, and the small dense LDL characteristic of this pattern is susceptible to oxidative modification. Alcohol is considered one of the most frequent causes of increases in plasma triglyceride (TG) levels. We investigated the effects of alcohol withdrawal on LDL subclass distribution and oxidizability in drinkers with different plasma TG levels. Thirty-seven male subjects with relatively heavy alcohol-consumption habits were divided into four groups; normotriglyceridemic (NTG)/withdrawal (n = 11), NTG/control (n = 8), hypertriglyceridemic (HTG)/withdrawal (n = 10), and HTG/control (n = 8). Both withdrawal groups abstained form alcohol for 4 weeks, while the control subjects maintained their usual intake of alcohol. Peak LDL particle diameter (PPD) was smaller in the combined HTG groups than in the combined NTG groups before abstinence, although PPD increased significantly (P < .01) from 25.5 to 26.1 nm in the HTG/withdrawal group. Before abstinence, lag times preceding LDL oxidation in the combined HTG groups were shorter than in the combined NTG groups; after withdrawal, lag time was prolonged significantly (P < .01) from 49.9 to 57.3 minutes in the HTG-withdrawal group. No significant changes in PPD and lag time were observed in the other three groups. Significant correlations (P < .05) were observed between the change (delta) in the lag time and delta TG and between delta lag time and delta PPD. We conclude that in alcohol-induced HTG subjects, alcohol withdrawal has beneficial effects on the LDL profile by shifting the particle size from smaller to larger and decreasing its susceptibility to oxidation.

Adult↗

PubMed1996

Enhanced capacity of n-3 fatty acid-enriched macrophages to oxidize low density lipoprotein mechanisms and effects of antioxidant vitamins.

We have investigated possible mechanisms by which n-3 fatty acid-enriched macrophages enhance the oxidation of low density lipoprotein (LDL), and the ability of antioxidant vitamins to prevent this. Macrophages were enriched with n-3 fatty acids (eicosapentaenoic acid, docosapentaenoic acid and docosahexaenoic acid) following incubation with fish oil. These macrophages produced large amount of TBARS in medium containing metals, and showed enhanced capacity to oxidize LDL (3-4 fold increase compared to control cells) and to accumulate the modified LDL. 5,8,11,14-eicosatetraynoic acid (ETYA, 15-lipoxygenase inhibitor) and superoxide dismutase (SOD) did not inhibit the enhanced capacity of n-3 fatty acid-enriched cells to oxidize LDL. However antioxidants, (vitamin E-enriched macrophages or vitamin C in the medium), inhibited this enhanced capacity. Medium conditioned by n-3 fatty acid-enriched cells had pro-oxidant effects on metal-initiated LDL oxidation. We conclude that n-3 fatty acid-enriched macrophages display increased oxidant capacity which is not inhibited by ETYA or SOD, and that antioxidant vitamins inhibit the enhanced capacity to oxidize LDL.

5,8,11,14-Eicosatetraynoic Acid↗

PubMed1996

Effects of beta-blockers on HMG CoA reductase and LDL receptor activity in cultured human skin fibroblasts.

Previous reports, based on clinical trials and animal experiments, suggest that beta-blockers may be useful in the prevention of atherosclerosis. Betaxolol, a new beta1-selective blocker, was shown to decrease plasma total and LDL cholesterol levels or to have no adverse effect on those [1-4]. While many reports deal with metabolism of triglyceride and high density lipoprotein, fewer publications about cholesterol metabolism are currently available. To clarify the mechanism by which beta-blockers affect lipid metabolism, we examined the effects of beta-blockers on HMG CoA reductase and LDL receptor activity in cultured human skin fibroblasts. L-propranolol, a nonselective beta-blocker, increased HMG CoA reductase activity and decreased LDL receptor activity. However, d-propranolol had no major effects on HMG CoA reductase activity. These results suggest that beta-blockers act on HMG CoA reductase through the beta receptors. Beta1-blocking action should decrease HMG CoA reductase activity and increase LDL receptor activity. In fact, betaxolol, a beta1-selective blocker, decreased HMG CoA reductase activity and increased LDL receptor activity, but metoprolol had no major effect. We speculate that the discrepancy between betaxolol and metoprolol in the effect on HMG CoA reductase and the LDL receptor might be due to the difference of the extent of beta1-selectivity. We conclude that beta1-selective blockers are antihypertensive agents potentially valuable in the prevention of atherosclerosis.

Adrenergic beta-Antagonists↗

PubMed1995

Effect of in-vivo supplementation with low-dose vitamin E on susceptibility of low-density lipoprotein and high-density lipoprotein to oxidative modification.

OBJECTIVES: We have examined the effects of in-vivo supplementation with low-dose vitamin E on the susceptibility of low-density lipoprotein (LDL) and high-density lipoprotein (HDL) to oxidative modification, and compared the oxidizability of HDL with that of LDL. METHODS: Normal humans (n = 8) ingested vitamin E (150 mg/day for 1 week, followed by 300 mg/day for 3 weeks) in divided doses with meals. The subjects did not use any medications or vitamins before being enrolled in this study. Fasting blood samples were drawn before and at the end of supplementation. LDL and HDL were separated by sequential ultracentrifugation and susceptability to copper-mediated oxidation was measured. RESULTS: After vitamin E supplementation, vitamin E content of LDL increased 1.9-fold and that of HDL increased 1.8-fold. Lag time before initiation of LDL oxidation lengthened significantly (+20%, p < 0.01), and the propagation rate of LDL decreased significantly (-10%, p < 0.05). The lag time of HDL oxidation did not change significantly, but the propagation rate of HDL oxidation decreased significantly (-24%, p < 0.001). The lag time of HDL oxidation was shorter than that of LDL. HDL contained the same or higher concentrations of vitamin E relative to lipid mass as LDL, but contained lower concentration of CoQ10 relative to lipid mass and fewer molecules of vitamin E and beta-carotene per particle than LDL. CONCLUSIONS: We conclude that in-vivo supplementation of low-dose vitamin E protects LDL against oxidative modification and decreases the propagation rate of HDL oxidation significantly. We suggest that supplementation with low-dose vitamin E would be beneficial for ameliorating atherosclerosis.

Adult↗

PubMed1995

Effects of Ca-antagonists on oxidative susceptibility of low density lipoprotein (LDL).

Twelve adults (age 32-61 years) with essential hypertension were recruited from the outpatient clinics of National Defense Medical College hospital to serve as subjects in the present study. They were treated with nilvadipine, a Ca-antagonist, 4 mg b.i.d. for 4 weeks. LDL samples were isolated by ultracentrifugation at the beginning (week 0) and at the end (week 4) of the treatment regimen. The formation of conjugated dienes was measured by incubating 100 micrograms of LDL protein with 2 mumol CuSO4 in 2 ml phosphate buffered saline (PBS). There were no significant differences between lipids levels, composition and anti-oxidant levels of LDL at weeks 0 and 4. The lag time of LDL oxidation was 71.1 +/- 11.3 min at week 0 and 81.3 +/- 13.2 min at week 4 (p < 0.05). In vitro studies of LDL oxidation, evaluated by thiobarbituric acid reactive substances (TBARS) and by agarose electrophoretic mobility, indicated that nilvadipine inhibited the oxidative modification of LDL while amlodipine, used as control, did not. Nilvadipine, a lipophilic Ca-antagonist, significantly prolonged the lag time of conjugated diene formation of LDL by 12.6% but amlodipine, a hydrophilic Ca-antagonist, had no major effect on LDL oxidation. These results suggest that Ca-antagonists are effective for the prevention of atherosclerosis but the effect is dependent upon the lipophilicity of the drugs.

Adult↗

PubMed1995

Effects of fish oil fatty acids on low density lipoprotein size, oxidizability, and uptake by macrophages.

The effect of fish oil and corn oil supplementation on plasma lipids and lipoproteins and on low density lipoprotein (LDL) oxidation was examined in 20 treated hypertensive subjects. The randomized double-blind crossover study consisted of two 6-week interventions with 4 g/day of a highly purified fish oil or corn oil. Fish oil significantly (-24%, P < 0.01) reduced plasma triglyceride, and increased LDL-cholesterol (+6%, P < 0.01 compared to corn oil). LDL particles were larger (P < 0.01) after fish oil compared to baseline and LDL size was inversely correlated with plasma triglyceride (P < 0.001) both before and after fish oil supplementation, and positively correlated with high density lipoprotein cholesterol (P < 0.01). Fish oil reduced lag time before onset of copper-induced LDL oxidation (-25%, P < 0.001) and significantly increased production of thiobarbituric acid-reactive substances (TBARS) during oxidation, compared with corn oil. Corn oil had no significant effect on lag time and oxidation rate. Fish oil increased macrophage uptake of copper-oxidized LDL and of macrophage-modified LDL. Corn oil was without effect. Additionally, macrophages that were supplemented with fish oil fatty acids in vitro displayed a significantly (P < 0.001) higher capacity to oxidize LDL than either control cells or cells supplemented with corn oil fatty acids. We conclude that from the standpoint of atherosclerosis, fish oil fatty acids adversely raise the susceptibility of LDL to copper-induced and macrophage-mediated oxidation but that the increase in plasma LDL cholesterol concentration reflects an increase in size that may be favorable.

Aged↗

PubMed1994

Effects of supplementing with vitamin E on the uptake of low density lipoprotein and the stimulation of cholesteryl ester formation in macrophages.

Vitamin E supplementation has been reported to protect low density lipoprotein (LDL) from copper-induced oxidation and macrophage-mediated oxidation. We investigated the effect of in vitro vitamin E enrichment of LDL on the accumulation of [3H]cholesteryl ester (CE)-LDL and stimulation of cholesteryl ester formation in J774 macrophages. Vitamin E supplementation prolonged lag time (2.9-fold) before the initiation of copper-induced LDL oxidation. LDL, preincubated with 5 microM copper or with macrophages in Ham's F10 medium, accumulated in macrophages much more than did native LDL. However, following vitamin E enrichment, LDL accumulation was significantly reduced following oxidative stress. Vitamin E-enriched LDL also reduced the stimulation of cholesteryl ester formation in macrophages. Moreover, vitamin E enrichment of macrophages reduced the ability of the cells to oxidize LDL. The present results indicate that vitamin E supplementation protects LDL against copper-induced and macrophage-mediated oxidation, inhibits oxidation-dependent accumulation of LDL in macrophages, and prevents stimulation of cholesteryl ester formation in macrophages. Additionally we have provided evidence that intra-cellular enrichment with vitamin E prevents oxidative modification of LDL by macrophages.

Arteriosclerosis↗

PubMed1994

Effects of alcohol consumption on antioxidant content and susceptibility of low-density lipoprotein to oxidative modification.

OBJECTIVE: The effects of moderate alcohol intake on antioxidant content of low-density lipoprotein (LDL) and the susceptibility of LDL to oxidative modification were examined in 12 healthy adult males. DESIGN: Volunteers abstained from alcohol for 3 weeks and then 12 subjects (alcohol intake group) consumed alcohol (0.5 g/kg/day) as brandy for 4 weeks; 4 subjects (control abstinence group) did not consume any alcohol for the entire study. RESULTS: In the alcohol intake group, plasma total cholesterol (TC), triglyceride (TG), phospholipids (PL), free cholesterol (FC) and apoprotein B (apoB) levels in LDL decreased significantly after alcohol intake; however, since TC/apoB, TG/apoB, PL/apoB and FC/apoB ratios did not change significantly, it is clear that LDL particle numbers decreased. Vitamin E and vitamin A levels in plasma, and vitamin E content of LDL also did not change significantly. Beta-carotene levels in plasma and in LDL decreased significantly in the alcohol intake group. In the abstinence group, lipid levels and vitamin levels did not change. Lag time before the onset of LDL oxidation and propagation rate of LDL oxidation in the alcohol intake group did not change significantly. CONCLUSIONS: Moderate alcohol intake decreases particle numbers of LDL without any changes in chemical composition, vitamin E content and susceptibility of LDL to oxidative modification. However, beta-carotene content was decreased significantly by even moderate alcohol intake.

Adult↗

PubMed1993

Pulmonary capillary pressure measured with a pulmonary arterial double port catheter in surgical patients.

We developed a pulmonary artery (PA) double port catheter technique for reliable clinical measurements of pulmonary capillary pressure (Ppc). In seven elective surgical patients, the PA double port catheter with the second PA port 1 cm proximal to the balloon was inserted. The two PA ports, connected to identical pressure measuring systems, provided the pulmonary arterial pressures (Ppa) distal and proximal to the balloon. After general anesthesia was stabilized, the two Ppas were measured simultaneously during a PA occlusion maneuver during 10 s of apnea. The instant of occlusion was determined precisely as the time when the two Ppa traces sharply diverged. A single exponential equation was fitted to the segment of distal Ppa tracing starting 0.3 s after the instant of occlusion. Ppc was determined as the value of the exponential fit extrapolated to time 0. In six of seven patients, PA occlusion occurred consistently in the early systolic phase regardless of the timing of balloon inflation. Mean Ppa, Ppc, and pulmonary arterial wedge pressure were 16.6, 11.8, and 7.6 torr. The ratio of venous to total resistance ranged from 0.37 to 0.54 (mean:0.46). We conclude that this technique is clinically feasible and valuable in precise definition of the instant of PA occlusion. By defining PA occlusion consistently, this technique can provide reliable Ppc estimation in the clinical settings.

Catheterization, Swan-Ganz↗

PubMed1993

[Atherosclerosis, with special reference to vitamin E].

The relationship between atherosclerosis and fat soluble vitamin, especially vitamin E is reviewed on the basis of oxidised modification of low density lipoprotein (LDL). Data now support the notion that the oxidised LDL is present in the blood and arterial wall and antioxidant drugs such as probucol and vitamin E, beta-carotene, may prevent the progression of atherosclerosis. LDL alpha-tocopherol levels are generally correlated to the plasma concentrations and supplementation with alpha-tocopherol increases its content in LDL. There is a significant correlation between the LDL alpha-tocopherol level and the resistance to oxidative modification. Epidemiological data also shows the relation between low levels of plasma vitamin E and the increased incidence of coronary heart disease. Clinical application of vitamin E should be clarified in detail to inhibit the progression of atherosclerosis.

Animals↗

PubMed1990

Effects of ketanserin tartrate on 3-hydroxy, 3-methylglutaryl coenzyme A reductase activity in cultured human skin fibroblasts.

Ketanserin tartrate (ketanserin) is a new antihypertensive drug that is a selective 5HT2 serotonergic receptor antagonist and at high concentrations antagonizes the alpha 1-adrenergic receptor. Several reports have indicated that ketanserin clinically decreases plasma low density lipoprotein (LDL) cholesterol. In order to clarify the mechanisms of this LDL cholesterol reduction by ketanserin, we investigated the effects of ketanserin on 3-hydroxy, 3-methylglutaryl coenzyme A(HMG CoA) reductase activity to cultured human skin fibroblasts. We also studied the effects of ritanserin (a 5HT2 serotonergic receptor antagonist) and prazosin HCl (an alpha 1-adrenergic receptor antagonist) on HMG CoA reductase activity in cultured human skin fibroblasts. Human skin fibroblasts were cultured in Dulbecco's modified Eagle's (DME) medium containing 10% fetal calf serum. Before the cells reached confluence, the medium was changed to DME containing 10% lipoprotein-deficient serum. After incubation for 48-72 hours, the drugs under investigation were added to the medium. The cells were incubated for 14 hours and harvested after washing with phosphate buffered saline. In our study, ketanserin decreased HMG CoA reductase activity in a dose-dependent manner up to 300 ng/ml (550 nM). Prazosin also decreased HMG CoA reductase activity in a dose-dependent manner up to 40 ng/ml (95 nM); ritanserin decreased HMG CoA reductase activity at concentrations of 100 nM and 200 nM. These findings suggest that the combination of alpha 1-adrenergic receptor and 5HT2 serotonergic receptor antagonist effects of ketanserin inhibits HMG CoA reductase activity and that this suppression is probably one of the mechanisms for the plasma LDL cholesterol reduction resulting from ketanserin treatment.

Adrenergic alpha-Antagonists↗