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Biomedical subjects

D B Hunninghake

Publications and source records attributed to D B Hunninghake.

At least 127 records · Page 7Linked to original sources
PubMed1982

Recruitment from clinical studies.

Referrals from related clinical studies represent a recruitment source with a relatively low volume of initial contacts, moderate volume of entries, a high ratio of entries to initial contacts and a relatively low effort level requirement for the recipient recruitment team. In the CPPT, this source provided overall 1% of initial contacts, 9% of first protocol visits and 11% of entries. Referrals were obtained from three major clinical studies. Approximately two-thirds of the total entries from this source were derived from the Multiple Risk Factor Intervention Trial and almost three-fourths of these were accounted for by the Minnesota LRC. The recruitment campaign conducted at this center is highlighted. Recruitment costs were usually low with this strategy. The combination of low costs and high efficiency make clinical studies referrals attractive. Such referrals may not always be available, but if they are, every effort should be made to maximize their use.

Adult↗
PubMed1982

Population characteristics according to recruitment source.

Considerable variability was observed among recruitment sources and centers in the proportion of first protocol visits proceeding to entry. Some of the reasons for these differences are explored. Several characteristics of the participants were also analyzed to determine whether significant variability existed among recruitment sources. The variability encountered suggests that these characteristics might be exploited in selecting recruitment sources for clinical trials.

Adult↗
PubMed1981

Effect of colestipol and clofibrate on plasma lipid and lipoproteins in type IIa hyperlipoproteinemia.

The effects of 2.0 g of clofibrate and 15, 20 and 30 g of colestipol on plasma lipid and lipoprotein levels were evaluated in adult patients with Type IIa hyperlipoproteinemia. Clofibrate treatment was associated with decreases in 11.0% in plasma cholesterol. 15.2% in LDL cholesterol, 26.1% in triglycerides, and an 11.3% increase in HDL cholesterol. The reductions in total cholesterol with the various doses of colestipol ranged from 11.9 to 17.8% and reductions in LDL cholesterol ranged from 16.1 to 27.3%. Colestipol treatment was not associated with any significant change in HDL cholesterol levels and minor increases in triglycerides. The addition of clofibrate to patients receiving colestipol resulted in a significant increase in HDL cholesterol and a decrease in triglycerides, but no additional reduction in total or LDL cholesterol.

Adult↗
PubMed1981

Effect of colestipol and clofibrate, singly and in combination, on plasma lipid and lipoproteins in type IIb hyperlipoproteinemia.

The effect of colestipol, clofibrate and a combination of these two drugs on plasma lipid and lipoprotein levels was evaluated in 14 adult male patients with Type IIb hyperlipoproteinemia. A crossover design with each patient receiving all three treatments was utilized. Twenty g of colestipol per day reduced total and LDL cholesterol by 39.1 and 51.5 mg/dl, respectively (p less than 0.001). There was an associated rise in total triglycerides of 63.5 mg/dl (p less than 0.01) with no significant change in HDL cholesterol. Clofibrate, 2.0 g per day, did not significantly lower either total (-7.9 mg/dl) or LDL cholesterol (+8.7 mg/dl). There was marked interpatient variability in terms of the LDL cholesterol response to clofibrate, but the majority of patients demonstrated an increase. HDL cholesterol levels increased by 6.7 mg/dl (p less than 0.01) and total triglycerides were reduced by 94.6 mg/dl (p less than 0.001). Utilizing the same dosages of both drugs, the combination of colestipol and clofibrate were less effective in lowering total and LDL cholesterol than colestipol therapy alone, and increases in HDL cholesterol and decreases in triglycerides similar to those obtained with clofibrate were observed.

Adult↗
PubMed1981

TSH response to TRH in euthyroid, hypercholesterolemic patients treated with graded doses of dextrothyroxine.

In an attempt to determine the minimum dose of D-Thyroxine (D-T4) which will suppress pituitary TSH response to TRH, we have treated 6 euthyroid, hypercholesterolemic patients with graded doses of D-T4. TSH response was suppressed in 3 patients with 3 mg and in the remaining 3 patients with 4 mg D-T4 administered once daily. The mean TSH suppressive dose of 3.5 mg, as determined in this study, is considerably less than the 6 mg daily dose given to patients treated with D-T4 in the Coronary Drug Project. This suggests that the adverse effects observed with D-T4 treatment in the Coronary Drug Project may have been due to mild, undetected hyperthryroidism. D-T4 treatment in our patients was not associated with an increase in heart rate or ventricular ectopic beats as determined by Holter monitoring. However, bile samples obtained at the time of TSH suppression showed a significant increase in lithogenic index. In four patients, TSH suppressive doses of D-T4 were associated with a 12% decrease in mean cholesterol and a 17% decrease in mean LDL cholesterol concentrations.

Adult↗
PubMed1981

Effects of thiazide diuretics on plasma lipids and lipoproteins in mildly hypertensive patients: a double-blind controlled trial.

A blood lipid-lipoprotein elevating effect of the diuretics hydrochlorothiazide and chlorthalidone in mildly hypertensive men has been established by a cross-over, randomized controlled trial, confirming previous clinical observations. Compared to baseline, plasma total cholesterol increased 6% and 8% and triglycerides 17% and 15% under treatment with hydrochlorothiazide and chlorthalidone, respectively. A cholesterol-lowering diet largely prevents this increase. Because these effects may be long-lasting and may cancel part of the potential benefit of blood pressure control in mildly hypertensive patients, with thiazide diuretics attention should be given to prescription of a cholesterol-lowering diet and to periodic monitoring of blood lipid levels. Different antihypertensive agents might be considered in patients with elevated blood lipid levels. Other antihypertensive agents currently in use need to be studied for potential effects on lipid metabolism.

Adult↗
PubMed1980

Effect of probucol on plasma lipids and lipoproteins in type IIb hyperlipoproteinemia.

Probucol was administered for 4 months in 20 adult males with Type IIb HLP in a total daily dose of 1.0 g per day. All patients had achieved a stable weight and diet response prior to entering the study. Plasma lipid and lipoprotein determinations were done at monthly intervals. Probucol produced mean reductions to TPC of -38.8 mg/dl (P < 0.0001), in LDL of -26.7 mg/dl (P < 0.001) and HDL of -8.1 mg/dl (P < 0.0001) for the entire treatment period. The mean LDL/HDL ratio increased from 5.43 to 6.08 (P < 0.02). There was no significant change in TG levels. During the study a progressive decrease in mean HDL levels from 38.9 to 29.2 mg/dl was noted. A progressive increase in the LDL/HDL ratio from 5.43 to 6.35 was also observed. These findings suggest that probucol should be used cautiously in patients with Type IIb HLP, because an inverse relationship between HDL levels and IHD incidence has been demonstrated in epidemiologic studies.

Adult↗
PubMed1980

Cimetidine blockade of histamine-induced insulin secretion.

The effects of an H2-histamine receptor antagonist, cimetidine, on histamine-induced changes in plasma levels of insulin, free fatty acids (FFAs), and glucose was examined in a randomized, double-blind study in six fasted men. The intravenous infusion of histamine at an average rate of 0.13 microgram/kg/min for 20 min caused a rapid rise in plasma insulin levels throughout the infusion period (p < 0.05). Insulin levels rose 23% above baseline after 5 min of infusion and continued to 51% above baseline 10 min after the infusion ended. Cimetidine pretreatment (300 mg intravenously) inhibited histamine-induced insulin secretion by 98% or more at each point during the infusion (p < 0.05), but did not inhibit an effect of histamine to elevate plasma FFA levels. Plasma FFA levels were increased 33% by histamine alone and 41% by histamine when subjects had been pretreated with cimetidine (p < 0.05). Plasma glucose levels were not affected by histamine or cimetidine. These findings demonstrate that histamine is capable of inducing insulin secretion in man at low doses. Blockade of this effect with cimedine suggests that the mechanism of histamine-induced insulin secretion involves the H2-histamine receptor.

Adult↗
PubMed1980

Alterations of plasma high-density lipoprotein cholesterol levels associated with consumption of selected medications. The Lipid Research Clinics Program Prevalence Study.

From the 10 North American study populations of the Lipid Research Clinics Program, mean levels of plasma high-density (HDL) cholesterol were contrasted between users of eight categories of prescribed medications and a control group of nonusers of those categories matched for age, sex, study population and ponderosity. Women taking propranolol had a mean HDL cholesterol level 12 mg/dl lower than nonusers (p < 0.05). Men taking phenytoin had a mean HDL cholesterol level more than 18 mg/dl higher than nonusers (p < 0.05). Men taking benzodiazepine derivatives had a mean HDL cholesterol level 3.3 mg/dl lower than nonusers (p < 0.05). No significant differences were found between users and nonusers of thiazide diuretics, chlorthalidone, barbiturates, sympathomimetics or antihistamines.

Barbiturates↗
PubMed1979

Altered plasma lipid and lipoprotein levels associated with oral contraceptive and oestrogen use. Report from the Medications Working Group of the Lipid Research Clinics Program.

In a study of women attending ten North American Lipid Research Clinics plasma total cholesterol, triglyceride, low density (L.D.L.), very low density (V.L.D.L.), and high density (H.D.L.) lipoprotein levels in those taking oral contraceptives (O.C.) and in those taking oestrogens for menopausal symptoms were compared with those in women not taking gonadal hormones, after adjustment for age, educational attainment, and body-mass index, O.C. and oestrogen users were leaner than non-users. Compared with controls, O.C. users showed increased cholesterol, triglyceride, and L.D.L.-cholesterol and V.L.D.L.-cholesterol levels, but H.D.L.-cholesterol levels were similar. Cholesterol, triglyceride, and H.D.L.-cholesterol and V.L.D.L.-cholesterol levels were positively associated with the quantity of the oestrogen component of the O.C. preparations. Compared with non-users, menopausal oestrogen users had slightly lower cholesterol and triglyceride levels, significant decreases in L.D.L.-cholesterol and V.L.D.L.-cholesterol, and a significant increase in H.D.L.-cholesterol.

Adolescent↗
PubMed1979

Effects of a vigorous walking program on body composition, and carbohydrate and lipid metabolism of obese young men.

With no attempt made to influence their diet, six sedentary obese men ages 19 to 31 completed 16 weeks of vigorous walking 90 min, 5 days/week, on a treadmill at up to 3.2 mph on a 10% grade, expending about 1100 kcal per session. Body composition studies indicated a loss of 5.9 kg of body fat and a gain of 0.2 kg of lean tissue for a net loss of 5.7 kg. Percentage body fat decreased from 23.3 to 17.4. Monitored food intake initially increased, then progressively decreased below pretraining levels. Work capacity and cardiovascular efficiency improved with training. Plasma cholesterol and triglyceride concentrations were not significantly changed; however, high density lipoprotein cholesterol progressively increased to 15.6% above pretraining levels and the high/low density lipoprotein ratio increased 25.9%. Fasting blood sugar was significantly lower after training. Blood glucose concentrations after a glucose challenge did not significantly change, but a 43% reduction in plasma radioimmunoassay insulin levels and a 36% decrease in the ratio of insulin/glucose concentration occurred. Thus, vigorous regular walking resulted in a reduction of body fate stores, endogenous insulin requirements, and food intake, and perhaps improved the ability to eliminate cholestrol by increasing the plasma high density lipoprotein fraction.

Adipose Tissue↗
PubMed1979

Sensitivity of the canine pancreatic intraductal pressure to subclinical reduction in cholinesterase acitivity.

As a continuation of work from this laboratory on anticholinesterase induced pancreatitis, a study of the relationship between reduced serum cholinesterase activity and changes in pancreatic intraductal pressure was undertaken. Pharmakokinetic studies in three dogs revealed rapid reduction in serum cholinesterase activity following an IV bolus dose of the cholinesterase inhibitor 0,0-diethyl-0-(2-isopropyl-6-methyl-4-pyrimidinyl)phosphorothioate. Following each dose of cholinesterase inhibitor, stable levels of cholinesterase inhibition were reached in 30 minutes. In four dogs the pancreatic duct was perfused from the tail of the ventral pancreas and intraductal pressures measured. A total of 25 mg/kg of the cholinesterase inhibitor was given in 5 mg/kg doses 30 minutes apart, and serum cholinesterase measured 30 minutes after each dose. Mean pressures were established over a 15 minute interval. Linear regression analysis of 23 data points revealed a significant (p < 0.001) cumulative dose-related increase in pancreatic intraductal pressure [Pressure (cm saline) = 14.2 + 1.03 x Cumulative Dose (mg/kg)] and significant (p< 0.001) negative correlation between serum cholinesterase activity and intraductal pressure [Pressure (cm saline) = 48.0 - 0.057 x Esterase Activity (mU/ml)]. These data suggest that, in dogs, reduced cholinesterase activity is directly related to increased pancreatic intraductal pressure, and it may be a factor in the pathogenesis of pancreatitis.

Animals↗
PubMed1976

Histamine-induced lipid mobilization in humans and dogs.

The effect of histamine on serum free fatty acid (FFA) and glycerol levels was examined in humans and dogs in vivo. By the end of a 15-minute infusion of histamine diphosphate (11 mug of histamine per min i.v.), FFA levels in six male human volunteers had risen from basal values of 424 +/- 41 (mean +/- S.E.M.) to 909 +/- 45 muEq/1, and glycerol levels had risen from 66 +/- 5.5 to 124 +/- 9.3 mumol/1. These effects in man were not blocked by diphenhydramine, an H1-receptor antagonist, but were entirely blocked by propranolol, a beta adrenergic antagonist. Similar infusions of histamine (11 mug/min i.v.) in six anesthetized dogs caused FFA levels to rise from 189 +/- 13 to 461 +/- 92 muEq/1 and glycerol levels to rise from 58 +/- 3.7 to 157 +/- 22.4 mumol/1. These effects in the dog were not blocked by diphenhydramine or by propranolol but were entirely blocked by metiamide, an H2-receptor antagonist. These observations illustrate that low levels of histamine in vivo can produce significant elevations of serum FFA and glycerol levels in both humans and dogs. These results further suggest that the action of histamine in humans is indirect whereas the effect in dogs may be due to a direct action of histamine at the H2-receptor in canine adipose tissue.

Adult↗
PubMed1975

Histamine receptors in adipose tissue: involvement of cyclic adenosine monophosphate and the H2-receptor in the lipolytic response to histamine in isolated canine fat cells.

The effects of histamine on lipolysis and associated changes in adenosine 3',5'-monophosphate (cyclic AMP) levels were examined in the isolated canine fat cell. Histamine, like norepinephrine, caused a dose-dependent increase in free fatty acid (FFA) and glycerol levels. The lipolytic response to histamine was preceded by a rise in the levels of cyclic AMP and was greatly potentiated by the addition of theophylline. In isolated canine fat cells, histamine (2 muM) caused a 7-fold increase in FFA levels. This effect was inhibited more than 50% in the presence of insulin (0.4 mmu/ml) or prostaglandin E1 (2.8 muM). In similar experiments, cyclic AMP Levels were increased 11-fold by histamine (2 muM) in the presence of 1 mM theophylline. Burimamide (0.1 mM), a histamine H2-receptor antagonist, reduced the effect of histamine (2 muM) on FFA levels as well as the effect on cyclic AMP levels greater than 95% but did not inhibit the lipolytic response to norepinephrine (2 muM). Propranolol (0.01 mM), a beta adrenergic antagonist, reduced the lipolytic response to norepinephrine by 97% but did not inhibit the effects of histamine on FFA or cyclic AMP levels. Tripelennamine and 1,5-diphenyl-3-dimethylaminopyrrolidine, histamine H1-receptor antagonists, inhibited neither the lipolytic response to histamine nor the effect on cyclic AMP levels. It was concluded that histamine induces lipolysis in canine fat cells by a mechanism involving cyclic AMP and the histamine H2-receptor.

Adipose Tissue↗