Exercise-induced hypertension after repair of coarctation of the aorta: arm versus leg exercise.

The etiology of exercise-induced upper limb hypertension after repair of coarctation of the aorta is unknown. We hypothesized that blood flow across the coarctation repair site is a major determinant of such exercise-induced hypertension. Because arm ergometry should produce a smaller increase in descending aortic blood flow than treadmill exercise, we compared the changes in upper limb pressure and the coarctation gradient produced by each type of exercise at equivalent levels of heart rate and peak oxygen consumption in 28 children with repaired coarctation of the aorta. The children were classified into three groups: Group I, resting gradient less than 15 mm Hg and treadmill gradient less than 20 mm Hg; Group II, resting gradient less than 15 mm Hg and treadmill gradient greater than 20 mm Hg; and Group III, resting gradient greater than or equal to 15 mm Hg. Twelve children with no heart disease served as control subjects. All children were exercised to exhaustion with 45 minutes' rest between the two exercise protocols. There were no differences in maximal heart rate and oxygen consumption between the two types of exercise. In all groups, treadmill exercise produced a larger increase in arm systolic blood pressure and arm-leg gradient than did arm exercise. With treadmill exercise coarctation Groups II and III developed a greater rise in both arm-leg gradient and arm systolic pressure than was observed in the control subjects (p less than 0.05). However, with arm exercise, Group III developed a significantly greater rise in both arm pressure and arm-leg gradient (p less than 0.05) than was observed in the control subjects.

Obesity-induced hypertension in the dog.

To study the relationship between body weight and blood pressure, we have developed an animal model of obesity-induced hypertension. Nine adult mongrel dogs were chronically instrumented with aortic and vena caval catheters. After a 2-week control period, all dogs were made to gain weight by adding 2 lb/day of beef fat to their diet for 5 weeks. Blood pressure, heart rate, and body weight were measured daily before the addition of dietary fat, during the 5 weeks of the high fat diet, and for 6 weeks after the fat supplement was stopped. Plasma volume and cardiac output were measured prior to and after 5 weeks of the fat diet. During the 5-week high fat diet, the dogs' body weight increased from 22.2 +/- 2.1 to 27.4 +/- 3 kg (p less than 0.001); mean blood pressure increased from 90 +/- 5 to 112 +/- 6 mm Hg (p less than 0.01); and heart rate increased from 70 +/- 7 to 85 +/- 5 beats/min (p less than 0.05). Blood pressure, heart rate, and body weight returned to near control values after the fat diet was stopped. Over the 5-week fat diet, the dogs' plasma volume increased from 920 +/- 130 to 1059 +/- 195 ml (p less than 0.05); cardiac output increased from 2.5 +/- 0.4 to 3.1 +/- 0.3 L/min (p less than 0.05); and systemic vascular resistance increased from 35.3 +/- 8 to 38.9 +/- 9 mm Hg/L/min (p less than 0.1). Weight gain in the dogs was also associated with hyperinsulinemia and insulin resistance.(ABSTRACT TRUNCATED AT 250 WORDS)

Pathogenesis of weight-related changes in blood pressure in dogs.

We have previously shown that weight gain in the dog results in an increase in blood pressure. To study the pathogenesis of the rise in blood pressure associated with weight gain, we compared the serial changes in blood pressure, body weight, sodium balance, plasma volume, and three hormones known to affect sodium balance (norepinephrine, insulin, and aldosterone) in seven dogs fed a high fat diet for 6 weeks and seven dogs fed a control diet. The sodium content of both diets was equal. During a 2-week control period, no differences were noted between the two groups. Weight gain was associated with a progressive increase in blood pressure (mean pressure increased by 18.5 +/- 2.1 mm Hg in the high fat group) and plasma volume (plasma volume increased from 1,426 +/- 202 to 2,053 +/- 250 ml in the high fat group). Sodium retention occurred after 1 week of the high fat diet and persisted. Over the 6-week period, the dogs on the high fat diet increased their cumulative sodium balance by 2,024 +/- 462 meq versus an increase of only 289 +/- 97 meq for the dogs on the control diet. In the high fat diet group of dogs, there was a significant relation between change in cumulative sodium balance and the change in blood pressure and plasma volume. After 1 week of the high fat diet, norepinephrine was the only hormone that significantly increased from baseline. Over the next 5 weeks norepinephrine increased no further, whereas fasting insulin and aldosterone progressively increased.(ABSTRACT TRUNCATED AT 250 WORDS)

Insulin and renal sodium retention in obese adolescents.

The effect of insulin on the renal handling of sodium was studied in obese and nonobese subjects by using euglycemic hyperinsulinemia. Seven water-loaded obese (14-19 years old) and five nonobese young adults (18-21 years old) had insulin given intravenously at a rate of 40 munits/m2/min. Blood glucose and creatinine clearance were not altered by euglycemic hyperinsulinemia in either the obese or the nonobese group. Hyperinsulinemia resulted in a significant decrease in urinary sodium excretion in both groups of subjects (by 54.2 +/- 3% [mean +/- SEM] in the obese and by 50.9 +/- 3.1% in the nonobese group). However, the amount of glucose required to maintain euglycemia was significantly less in the obese versus nonobese group, 89.5 +/- 6.2 versus 329.2 +/- 16 mg glucose/m2/min (p less than 0.001). There was no relation in either group between the amount of glucose required to maintain euglycemia and the change in urinary sodium excretion. On a separate day, all of the obese subjects underwent 3 hours of water diuresis but without insulin. There was no change in urinary sodium excretion with sustained water diuresis alone. However, when compared with the nonobese group, the obese group of subjects had a significantly higher resting mean arterial pressure, heart rate, and plasma norepinephrine concentration; during the insulin clamp, neither group experienced a significant change in mean arterial pressure or heart rate, and only the nonobese group experienced an increase in plasma norepinephrine. In obese subjects, we have found, despite the presence of insulin resistance to carbohydrate metabolism, that euglycemic hyperinsulinemia was associated with a normal decrease in urinary sodium excretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Hyperinsulinemia and the aldosterone and pressor responses to angiotensin II.

To determine whether hyperinsulinemia alters angiotensin II-mediated aldosterone secretion, the increase in plasma aldosterone after intravenous angiotensin II (5, 10, and 20 ng/kg/min for 15 minutes each) was measured before and after euglycemic hyperinsulinemia in seven chronically instrumented dogs. In a random sequence on 4 successive days, dogs received either 0, 2, 4, or 8 milliunits/kg/min insulin. Euglycemic hyperinsulinemia, at all insulin doses, resulted in a significantly greater (p less than 0.01) change in the angiotensin II-stimulated increments of plasma aldosterone than was observed when angiotensin II was administered alone. However, there was no dose-dependence of insulin's effect on angiotensin II-stimulated aldosterone. The effect of weight gain on the angiotensin II response was also evaluated in five dogs. After weight gain, euglycemic hyperinsulinemia augmented angiotensin II-stimulated aldosterone to the same magnitude that was observed before weight gain. Possible mechanisms whereby insulin could increase angiotensin II-stimulated aldosterone production include: increased intracellular potassium, reduced plasma free fatty acids, and a direct action of insulin to induce increased adrenal steroidogenesis. In addition to altering the angiotensin II-aldosterone dose-response curve, hyperinsulinemia also increased the pressor action of angiotensin II. In contrast to the angiotensin II-aldosterone response, progressive hyperinsulinemia resulted in a progressive increase in the pressor response to angiotensin II. The increased pressor response is probably due to an increased activation of the sympathetic nervous system by insulin.

Forearm resistance vessel abnormalities and insulin resistance in obese adolescents.

To determine if structural changes in forearm resistance vessels are associated with insulin resistance, we evaluated the relation between minimum forearm vascular resistance and insulin resistance in 95 obese adolescents before and after weight loss. Insulin resistance was assessed by fasting insulin levels and sum of insulin values after an oral glucose tolerance test in all 95 subjects and whole body glucose uptake during euglycemic hyperinsulinemia in 35 of 95 subjects. Structural changes in forearm vessels were assessed by measurement of minimum forearm vascular resistance during 10 minutes of ischemic exercise. As compared with our normal values, obese adolescents had a significantly (p less than 0.01) decreased maximal forearm blood flow (41.6 +/- 1.4 versus 67.1 +/- 2.4 ml/min/100 ml) and increased minimum forearm vascular resistance (2.9 +/- 0.4 versus 1.6 +/- 0.7 mm Hg/ml/min/100 ml). There was a significant relation (p less than 0.01) between minimum forearm vascular resistance and fasting insulin, sum of insulins, and whole body glucose uptake. After a 20-week weight-loss program, minimum forearm vascular resistance decreased (3.0 +/- 0.3 versus 2.0 +/- 0.2, p less than 0.01), maximal forearm blood flow increased (41 +/- 2.3 versus 57.4 +/- 3.9, p less than 0.01), and forearm volume remained unchanged. We also observed a significant (p less than 0.01) relation between the decrease in minimum forearm vascular resistance and the decrease in fasting insulin (r = 0.29), decrease in sum of insulins (r = 0.42), and increase in whole body glucose uptake (r = 0.63).(ABSTRACT TRUNCATED AT 250 WORDS)

Basal metabolism of obese adolescents: inconsistent diet and exercise effects.

Effects of 20 wk of diet-plus-behavior (DB) therapy or exercise-plus-diet-plus-behavior (EDB) therapy on changes in basal energy expenditure (BEE) were studied in 36 obese male and female adolescents. BEE was assessed by open-circuit spirometry and body composition by hydrostatic weighing. Dietary restriction was based on the dietary-exchange program. Behavioral treatment included record-keeping, stimulus-control, and reinforcement techniques. EDB therapy included 50 min/d, 3 d/wk of aerobics. A time-by-group (2 X 3) repeated-measures ANOVA was used to analyze pre-to-postintervention differences between groups (DB, EDB, and control). Results revealed small but statistically significant (p less than 0.05) differences in body composition between the two experimental groups and control subjects. There were no differences in body composition between the DB and EDB groups, although all control subjects gained body mass (p less than 0.05). There was no group-by-time interaction for BEE. Moderate correlations of r = less than or equal to 0.61 were obtained between change in BEE and change in body composition for the subjects in the experimental groups.

Oxygen uptake and energy output during walking of obese male and female adolescents.

Oxygen uptake and steady-rate energy output of 7 obese male and 13 obese female adolescents (greater than 178% ideal body weight) walking at four different speeds (1.167, 1.5667, 1.7833, and 2.125 m/s) were studied. Body composition was measured by hydrostatic weighing, and steady-rate energy output by open circuit spirometry. Energy output was expressed as kJ/min (kcal/min) and indexed to body mass and fat-free mass. A 2-by-4 ANOVA (sex by speed) revealed significant differences in the energy output between the speed conditions. There was no significant difference between the sexes. A nonlinear increase in calorie output with increasing speed indicated a decreasing efficiency with increasing speed of walking. Possible reasons include biomechanical factors such as increased upper-body forward lean needed to maintain balance at faster speeds of movement, increased energy output due to increased inertia, extra energy output needed to accelerate the limbs and torso, and increased body fat.

Coronary risk incidence of obese adolescents: reduction by exercise plus diet intervention.

The incidence of coronary heart disease risk factors and the effects of 20 weeks of diet and exercise were studied in 36 obese adolescents. Values for the following risk factors were determined: serum triglyceride level, high-density lipoprotein-cholesterol level, total cholesterol level, systolic and diastolic BP, maximum work capacity, obesity, and presence of coronary heart disease in the family history. Of the subjects, 97% had four or more risk factors. Two subjects possessed all eight risk factors. The adolescents were randomly assigned to either a control, diet therapy and behavior change, or exercise, diet therapy, and behavior change group. From pre- to posttreatment, a 14.8% and 41.4% reduction in multiple risk was noted for the latter two groups, respectively. No significant difference between the control group and the diet and behavior change group was found. In contrast, the exercise-diet-behavior change group reduced multiple risk (P less than .01) more than either of the other groups. It was concluded that obese adolescents are at high risk for the development of coronary heart disease and that exercise in addition to moderate dietary restriction can result in the reduction of multiple coronary heart disease risk.

Urine sodium excretion in response to an oral glucose tolerance test in obese and nonobese adolescents.

To determine if physiologic changes of insulin are capable of inducing sodium retention in insulin-resistant patients, we evaluated the ability of an oral glucose tolerance test to alter urine sodium excretion in 32 obese subjects (13.3 +/- 1 years, weight 82 +/- 5 kg, mean arterial pressure 89.3 +/- 1.5 mm Hg) and 13 nonobese subjects (13.8 +/- 2 years, weight 46 +/- 4 kg, mean arterial pressure 74.5 +/- 2.6 mm Hg). After an overnight fast, subjects were placed in water diuresis and fasting insulin and glucose levels were drawn. Three 30-minute urine collections were obtained for baseline urine sodium excretion. The oral glucose tolerance test was administered with glucose and insulin levels drawn at 15, 30, 45, 60, 90, and 120 minutes. During the oral glucose tolerance test, four 30-minute urine collections were obtained for urine sodium excretion. Serum glucose levels at baseline and throughout the glucose tolerance test did not differ between obese and nonobese subjects. Baseline insulin levels were elevated significantly in the obese (20 +/- 3 microU/mL) compared with the nonobese (5 +/- 0.7 microU/mL) subjects. Furthermore, insulin levels remained significantly elevated in the obese subjects compared with the nonobese subjects throughout the glucose tolerance test (118 +/- 19 vs 49 +/- 6 microU/mL, obese vs nonobese subjects at 1-hour post-glucose tolerance test).(ABSTRACT TRUNCATED AT 250 WORDS)

Role for aldosterone in blood pressure regulation of obese adolescents.

To determine the role of aldosterone in the regulation of blood pressure (BP) in obese adolescents, supine and 2-hour upright plasma renin activity (PRA), and aldosterone and cortisol were measured in 10 nonobese and 30 obese adolescents before and after a 20-week weight loss program. The obese adolescents had significantly higher supine and 2-hour upright plasma aldosterone concentrations (17 +/- 8 vs 6 +/- 2 ng/dl [p less than 0.01 supine obese vs nonobese] and 30 +/- 11 vs 14 +/- 8 ng/dl [p less than 0.01 2-hour upright]). Although PRA was not significantly different between the 2 groups of children, a given increment in PRA produced a greater increment in aldosterone in the obese adolescents. In addition, obese subjects had a significantly increased mean BP (93 +/- 12 vs 74 +/- 8, p less than 0.005) and a weak correlation between BP and plasma aldosterone concentration. Compared with an obese control group, weight loss resulted in a significant decrease in plasma aldosterone (p less than 0.01) without an associated decrease in PRA. After weight loss there was also a significant decrease in the slope of the posture-induced relation between PRA and aldosterone. In addition to weight loss being associated with a significant decrease in BP (p less than 0.01), there was a significant correlation between the change in plasma aldosterone and the change in mean BP (r = 0.538; p less than 0.002 change in upright aldosterone vs change in mean BP). Obese adolescents have an increased plasma aldosterone concentration that may be important in the regulation of their BP.

Comparison of hospital charges for balloon angioplasty and surgical repair in children with native coarctation of the aorta.

A retrospective review of hospital charges was performed in children > 1 year old with native coarctation of the aorta who underwent balloon angioplasty, primary surgical repair, or elective surgical repair after unsuccessful balloon angioplasty. Hospital charges were less overall in the balloon angioplasty group, although the failure rate was higher.

Hemodynamic determinants of exercise-induced ST-segment depression in children with valvar aortic stenosis.

To evaluate the hemodynamic factors associated with treadmill-induced ST-segment depression in children with valvar aortic stenosis, 12 patients (mean age 13 years) with ST-segment depression during treadmill exercise and 5 patients (mean age 13 years) without ST-segment depression during treadmill exercise underwent exercise testing during cardiac catheterization. The left ventricular (LV) systolic pressure and LV outflow tract gradient at rest (177 +/- 25 vs 138 +/- 8 mm Hg and 59 +/- 18 vs 23 +/- 7 mm Hg, respectively) and corresponding pressures during maximal supine exercise (248 +/- 37 vs 189 +/- 17 mm Hg and 112 +/- 34 vs 52 +/- 14 mm Hg) were significantly greater (p less than 0.01) in the patients with exercise-induced ST-segment depression, although overlap existed. The LV-O2 supply-demand ratio during maximal supine exercise was significantly less (6.4 +/- 2.7 vs 11.8 +/- 0.7; p less than 0.005) in patients with than in those without exercise-induced ST-segment depression. In fact, an LV-O2 supply-demand ratio less than 11.0 was 100% sensitive and specific in predicting treadmill-induced ST-segment depression. These results suggest that although the development of ST-segment depression during treadmill exercise is related to LV systolic pressure and LV outflow gradient, its major hemodynamic determinant is the LV-O2 supply-demand ratio.

A balloon-dilatable pulmonary artery band in the dog. Results at one year.

Increased pulmonary blood flow and pulmonary hypertension are frequent problems in infants with congenital heart disease. Although the use of pulmonary artery banding to limit pulmonary blood flow has decreased, the procedure may still be beneficial in certain forms of complex heart disease. The ability to noninvasively relieve the obstruction caused by the band may significantly reduce later operative complexity or even avoid reoperation entirely. The present study evaluated the effectiveness of a balloon-dilatable pulmonary artery band. Twenty 1-week-old dogs had a band of an absorbable suture material (Vicryl; Ethicon, Inc., Somerville, N.J.) placed around the main pulmonary artery. Eight dogs underwent angioplasty 6 months after band placement and also underwent follow-up catheterizations 3 and 6 months after angioplasty. Balloon angioplasty acutely reduced both the right ventricle-pulmonary artery pressure gradient (from 37 +/- 7 mm Hg to 3 +/- 1 mm Hg, p less than 0.001) and the right ventricular systolic pressure (from 62 +/- 8 mm Hg to 32 +/- 2 mm Hg, p less than 0.01). At follow-up the gradient remained low, measuring 4 +/- 1 mm Hg at 3 months and 3 +/- 1 mm Hg at 6 months. Twelve dogs did not undergo balloon dilatation until 12 months after band placement to determine whether any obstruction persisted and whether the band could be relieved after long-term placement. These 12 dogs had progressive increases in right ventricle-pulmonary artery gradient, from 27 +/- 3 mm Hg at 6 months to 43 +/- 4 mm Hg at 12 months. Ten of these dogs underwent dilation 1 year after pulmonary artery band placement. This dilation significantly reduced the right ventricular outflow tract gradient (from 43 +/- 4 mm Hg to 1 +/- 1 mm Hg, p less than 0.001). The remaining two dogs underwent successful partial dilation of the band 12 months after placement. This study demonstrated that a pulmonary artery band of absorbable suture material maintains effective right ventricular outflow tract obstruction for at least 1 year. Additionally, the effect of the pulmonary band can be successfully and persistently relieved.

Relationship between insulin resistance and abnormal lipid profile in obese adolescents.

OBJECTIVE: To determine whether the lipid abnormalities observed in obese adolescents are associated with insulin resistance. METHODS: We evaluated the relationship between lipid levels and insulin resistance in 82 obese adolescents. Insulin resistance was assessed by fasting insulin level and sum of the insulin values after an oral glucose tolerance test in all 82, and were compared with data from 40 nonobese adolescents. Whole-body glucose uptake during euglycemic hyperinsulinemia (M value) was performed in 19 of the obese adolescents and compared with that of 24 nonobese young adults. RESULTS: The obese adolescents had significantly elevated low-density lipoprotein cholesterol (LDL-C) (3.09 +/- 0.73 mmol/L; 119 +/- 28.2 mg/dl) and triglycerides (1.22 +/- 0.62 mmol/L; 108 +/- 54.6 mg/dl) and low high-density lipoprotein cholesterol (HDL-C) levels (0.94 +/- 0.24 mmol/L; 36 +/- 9.1 mg/dl) when compared with values in the nonobese subjects. M values were significantly depressed in the obese compared with the nonobese subjects. Adiposity significantly correlated with low HDL-C and elevated triglyceride values. From the variables representing insulin resistance, the strongest correlation with the abnormal lipid profile was found for the M value. A stepwise multiple regression analysis revealed that the M value was the only step entered into the relationship for triglycerides and LDL-C, and both M value and fasting insulin were entered for HDL-C. CONCLUSION: In obese adolescents the degree of insulin resistance explains a significant portion of the variance in the levels of triglycerides, LDL-C, and HDL-C.

Transcutaneous oxygen monitoring. Its use in the treatment of outpatients with congenital heart disease.

To validate transcutaneous Po2 (TcPo2) monitoring for outpatient use in cyanotic congenital heart disease (CCHD), TcPo2 was compared with simultaneous arterial Po2 at cardiac catheterization and with arterial Po2 obtained by puncture. Over a 40-month period, 1,493 outpatient TcPo2 determinations were made in 461 patients to diagnose the presence or absence of hypoxemia in newly referred patients and to help assess oxygen delivery in patients with known CCHD. Clinical decisions regarding the need for further diagnostic study and the adequacy of oxygen delivery were made based on these determinations.

Gender dimorphism in size, shape and body composition of child-onset obese and nonobese adolescents.

Gender dimorphism (percent GD) for stature (S), body size, body mass (BM) distribution and body composition for obese and nonobese male and female adolescents (mean age 12.7 years, range 10.5-14.5) was compared for 22 girths, 13 bony widths, five skin + fat folds (SF), fat mass (FM), fat free mass (FFM), body density (Db), and calculated variables (BMI, BSA, unit-size mass, waist:hip ratio (WHR), and FFM/S). BM distribution was computed with the ponderal mass equivalent somatogram. There was significant (P less than or equal to 0.05) percent GD for FM, FFM, Db, for the nonobese, but not obese. Only the neck, forearm and wrist girths revealed small but significant (P less than or equal to 0.05) percent GD for the obese. There was no girth percent GD for the nonobese. The elbow, wrist and ankle diameters revealed significant (P less than or equal to 0.05) percent GD for the obese; there was no significant percent GD for the nonobese for the same bony widths. Only the subscapula and iliac SF revealed significant (P less than or equal to 0.05) percent GD for the obese. For nonobese, percent GD was significant (P less than or equal to 0.05) for the triceps, subscapula and thigh SF, Comparisons between obese and nonobese indicated significant (P less than or equal to 0.05) differences between obese and nonobese males and females for FM, FFM, all girths and SF, but not S. Surprisingly, the obese and nonobese had nearly identical trunk diameters; the sum of biacromion, chest, biilac, and bitrochanter diameters were different by only 4.6 percent (n.s.) for the obese and nonobese males, and 1.3 percent (n.s.) for the obese and nonobese females. Thus, a large central frame-size cannot be used to justify the acquisition or maintenance of a larger than average BM for the obese. The ponderal equivalent analyses revealed that the obese's abdomen was the size of a person projected to have a BM in excess of 100 kg. The use of surface anthropometry in the study of adolescent obesity was supported.

Transhepatic cardiac catheterization in children. Evaluation of efficacy and safety.

BACKGROUND: In some children with congenital heart disease, conventional venous access is unavailable for cardiac catheterization. This study investigates a novel transhepatic venous approach to cardiac catheterization in children and evaluates its efficacy and safety. METHODS AND RESULTS: Percutaneous transhepatic puncture was performed using a 22-gauge Chiba needle under fluoroscopic guidance. After wire exchanges were performed, a 5F to 8F sheath was positioned in the low right atrium and cardiac catheterization was performed. On completion of the catheterization, the sheath was withdrawn and a 3-mm steel coil was placed in the parenchymal tract between the hepatic vein and liver capsule. Liver enzyme studies were obtained before and after transhepatic catheterization, and an abdominal ultrasound was performed to evaluate the liver 24 hours after the procedure. Percutaneous transhepatic cardiac catheterization was performed successfully in 17 of 18 children in whom it was attempted. Patient age was 30 +/- 8 months (mean +/- SEM; range, 1 day to 9 years), weight was 10.5 +/- 1.5 kg (3.1 to 27.5 kg), and mean right atrial pressure was 10 +/- 1 mm Hg (5 to 19 mm Hg). Time from initial needle puncture to right atrial entry was 6.2 +/- 1.2 minutes. Diagnostic catheterization was performed successfully in all 17 children, and additional interventional procedures were performed in 5 children. The total catheterization time was 2.0 +/- 0.2 hours. Serum aspartate aminotransferase increased from 57 +/- 15 to 78 +/- 8 IU/L (P = .06), but alanine aminotransferase and gamma-glutamyl transpeptidase did not change. Ultrasound was performed 24 hours after transhepatic catheterization, and no evidence was found in any patient of hemorrhage or subcapsular hematoma. CONCLUSIONS: These data suggest that this novel transhepatic approach provides an effective and safe route for diagnostic and interventional cardiac catheterization in children.

Increased forearm vascular reactivity in patients with hypertension after repair of coarctation.

To determine whether altered vascular reactivity could contribute to hypertension after repair of coarctation, the change in forearm and calf vascular resistances to small intra-arterial infusions of norepinephrine were measured in six patients who had undergone surgical correction of coarctation of the aorta but still had upper extremity hypertension and compared with similar measurements made in five normotensive patients with mild heart disease. Only the mean upper extremity pressure was significantly greater in the group that underwent repair of coarctation (102 +/- 11 vs 83 +/- 5 mm Hg, p less than .05, for mean arm pressures and 96 +/- 13 vs 83 +/- 7 mm Hg for mean leg pressures in patients who had coarctation vs normotensive patients, respectively). Forearm and calf blood flows were measured in the right arm and leg with a mercury-in-plastic strain-gauge plethysmograph. Forearm and calf vascular resistances were calculated by dividing mean arterial pressure of the appropriate extremity by the blood flow of that extremity. Norepinephrine was infused into the right brachial and femoral arteries of the patients at doses of 0.02, 0.05, 0.1, 0.2, 0.3, 0.5, and 0.7 microgram/min. Resting forearm and calf vascular resistances were similar in both groups of patients. The norepinephrine dose-response curves showed that control patients required more than three times the norepinephrine to produce the same percent increase in forearm vascular resistance (after 0.2 microgram/min forearm vascular resistance increased by 55% in the coarctation group, while the resistance in the control group increased by only 3%, p less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Reduced short-term thermic effects of a meal in obese adolescent girls.

Post-meal energy expenditure (TEM) was compared for 14 healthy obese (body fat = 45.3%, body mass index, BMI = 35.9 kg m-2) and 9 healthy nonobese (body fat = 20.7%, BMI = 17.8 kg m-2) adolescent girls. The test meal for both groups was a standard 3348.8-kJ, 0.473-1 chocolate milkshake of 15% protein (casein), 40% fat (polyunsaturated/saturated ratio = 0.05; 75 mg cholesterol) and 45% carbohydrate (lactose and sucrose). Glucose, insulin and resting energy expenditure (RMR) were measured at rest prior to meal consumption and 20, 40, 60, 90, and 120 min after the meal. Cumulative net TEM was calculated as the integrated area under the TEM curve with RMR as baseline. Reliability was assessed by retesting 4 subjects, and a placebo effect was tested by administering a flavored energy-free drink. Results indicated high reliability and no placebo effect. The meal resulted in a greater rise in insulin and glucose for the obese compared to the nonobese subjects (P < or = 0.05), and a significant TEM for both groups (P < or = 0.05). The cumulative TEM (W kg-1) was 61.9% greater for the nonobese (P < 0.01) when expressed relative to body mass, and 33.2% greater for the nonobese (P < or = 0.01) when expressed relative to the fat-free body mass. Expressed relative to the meal, the TEM was 25.5% less for the obese (P < 0.01). The data support an energy conservation hypothesis for obese female adolescents.