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At least 1,099 records · Page 61Linked to original sources
PubMed1988

Lipid alterations and decline in the incidence of coronary heart disease in the Helsinki Heart Study.

In the Helsinki Heart Study, a randomized five-year, double-blind trial, a 34% reduction in the incidence of coronary heart disease (CHD) was observed in dyslipidemic men treated with gemfibrozil. Averaged over the five years of the trial, gemfibrozil therapy produced, compared with placebo, mean decreases of 10% in serum total cholesterol level, 14% in non-high-density lipoprotein (HDL) cholesterol level, 11% in low-density lipoprotein (LDL) cholesterol level, 35% in triglyceride level, and a mean increase of 11% in HDL cholesterol level from baseline levels measured prior to treatment. While changes in HDL cholesterol level were similar in all Fredrickson types, the effect on concentrations of total cholesterol and LDL cholesterol was largest in type IIA and on LDL minimal in type IV. The reduction of CHD incidence over placebo was largest in type IIB and smallest in type IIA. The lipid changes were dependent on lipid levels prior to treatment and on compliance with the medication regimen. When risk factors for CHD, including age, blood pressure, smoking and drinking habits, baseline lipid levels, and exercise and relative weight, were controlled by applying the Cox proportional hazards model, the changes in serum HDL and LDL cholesterol levels were both statistically significantly associated with the decline in CHD incidence within the gemfibrozil-treated group. The large decrease in serum triglyceride levels had relatively small effect on CHD incidence. Thus, the results of this study, together with earlier observations, suggest that both elevating HDL and lowering LDL cholesterol levels are effective in the primary prevention of CHD.

Adult↗
PubMed1985

Apolipoprotein changes associated with the plasma lipid-regulating activity of gemfibrozil in cholesterol-fed rats.

Gemfibrozil (Lopid) is a new plasma lipid-regulating drug that decreases very low and low density lipoprotein (VLD/LDL) and increases high density lipoprotein (HDL) concentrations in man. The present experiments tested the effects of gemfibrozil on plasma lipoproteins and apolipoproteins in rats fed high fat/high cholesterol diets. Compared to chow-fed rats, cholesterol feeding for 2 weeks (20% olive oil/2% cholesterol) produced the expected increases in VLDL and intermediate density lipoprotein (IDL) while lowering plasma HDL. This was documented by using three methods of lipoprotein isolation: sequential ultracentrifugation, density gradient ultracentrifugation, and agarose gel filtration. Gemfibrozil gavaged at 50 mg/kg per day for 2 weeks during cholesterol feeding prevented these changes such that lipoprotein patterns were similar to those in chow-fed animals. Whole plasma apoE and apoA-I concentrations were decreased and apoB increased due to cholesterol feeding as determined by electroimmunoassay, but again gemfibrozil treatment prevented these diet-induced alterations. Gradient polyacrylamide gel electrophoresis patterns of the total d less than 1.21 g/ml lipoprotein fractions reflected the changes in apolipoprotein concentrations and further demonstrated a greater increase of apoBl compared to apoBh in cholesterol-fed rats. Gemfibrozil lowered the concentration of both apoB variants and prevented the shift of apoE from HDL to lower density lipoproteins. Changes in the distribution of apoE were confirmed using agarose gel column chromatography followed by electroimmunoassay. These methods also revealed a shift of apoA-IV from HDL to the d greater than 1.21 g/ml, lipoprotein-free fraction with gemfibrozil treatment when blood was taken from fasted or postabsorptive animals. Since it was also noted that in chow-fed rats more apoA-IV was present in the d greater than 1.21 g/ml fraction in the postabsorptive or fed state compared to fasted animals, it could be postulated that the shift of apoA-IV into this fraction in gemfibrozil-treated rats is related to an accelerated clearance of chylomicrons. It is concluded that gemfibrozil largely prevents the accumulation of abnormal lipoproteins in this model of dyslipoproteinemia, and that apoE may play a critical role in this normalization process.

Animals↗
PubMed1994

Age-dependent appearance of synaptic currents in rat neocortical neurons in culture.

Rat neocortical neurons grown in dissociated cell culture were recorded with the whole-cell patch-clamp technique. Spontaneous inward currents were observed in cells that were held at a membrane potential of -80 mV in medium containing tetrodotoxin and Cd2+. These currents displayed amplitudes up to 140 pA and rise time of 1.8 +/- 0.2 ms (mean +/- SD, n = 15). They reversed near 0 mV and showed no voltage-dependent frequency of occurrence. Hence, they were presumably due to spontaneous release of transmitter. The inward currents appeared around day 10 in culture and were detected up to 4 weeks. When cells of different ages were compared, the maximal probability of recording these inward events occurred at around 3 weeks in culture. The inward currents were not reduced by application of bicuculline methiodide which is a competitive antagonist of the GABAA receptor, but were blocked by the broad-spectrum glutamate receptor antagonist kynurenic acid. Moreover, spontaneous inward events were not affected by DL-2-aminophosphono-valerate (NMDA receptor antagonist) but disappeared following application of the non-NMDA receptors antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). Our observations indicate that the inward currents represent miniature synaptic events that are primarily mediated by non-NMDA excitatory amino acid receptor subtypes. Furthermore, our findings indicate that they develop over time and are not present in neurons that are grown in culture for less than 10 days.

2-Amino-5-phosphonovalerate↗
PubMed1993

NMDA and non-NMDA receptors mediating nociceptive and non-nociceptive transmission in spinal cord of cat.

The effects of excitatory amino acid (EAA) receptor agonists and blockers on the nociceptive and non-nociceptive transmission in cat spinal dorsal horn neurons were studied. About 80% of neurons were facilitated by iontophoretic injection of EAA receptor agonists (10-100 nA), such as N-methyl-D-aspartate (NMDA), quisqualic acid (QA), kainic acid (KA), and DL-homocysteic acid (DLH). The nociceptive responses, irregular spontaneous discharges, and C afferent induced-response of dorsal horn neuron, were reduced by the different EAA receptor blockers (35-150 nA), such as DL-2-amino-5-phosphono-valerate (APV), ketamine, 6,7-dinitro-quinoxaline-2, 3-dion (DNQX), and kynurenic acid (Kyn). Ketamine and Kyn had different effects on the long-lasting response and the short-lasting response of neurons induced by stimulation of A afferent fiber of the tibial nerve. The long-lasting response in 8/12 neurons was reduced by Kyn, but not by ketamine, and the short-lasting response was reduced by neither Kyn nor ketamine. The DLH-induced excitations were reduced by DNQX and, to a less extent, by APV. The results suggest that both NMDA and non-NMDA receptors are involved in spinal nociception; the non-nociceptive information is in part mediated by non-NMDA receptors.

Animals↗