Values In Normal Subjects Research Articles

Increased plasma adrenomedullin levels in patients with acute myocardial infarction in proportion to the clinical severity

ObjectivesTo investigate the pathophysiological role of adrenomedullin in myocardial infarction.Patients and designPlasma concentrations of adrenomedullin, atrial natriuretic factor, and brain natriuretic peptide were measured by radioimmunoassay in 31 patients with...

Elevated cytosolic calcium and impaired proliferation of B lymphocytes in type II diabetes mellitus

Patients with diabetes mellitus have increased susceptibility to infection attributable, at least in part, to defective function of polymorphonuclear leukocytes (PMNLs) and B cells. Certain data suggest that cytosolic calcium ([Ca 2+]i) is elevated in various cells in diabetes, and high [Ca 2+]i adversely affects cell function. Indeed, the [Ca 2+]i of PMNLs of diabetic patients is elevated, and phagocytosis of the PMNLs is impaired. The current study examines whether the [Ca 2+]i of B cells is also elevated in diabetes and whether this derangement impairs B cell function. We studied 32 patients with non-insulin-dependent diabetes mellitus (NIDDM) and eight normal subjects. All patients had hyperglycemia (11.6 ± 0.80 mmol/L) and elevated HbAlc (13.2% ± 0.99%). The basal levels of [Ca 2+]i of the B cells (113 ± 3.3 nmol/L) were significantly ( P < 0.01) higher than the values in normal subjects (85 ± 1.7 nmol/L). There was a direct and significant correlation ( r = 0.88; P < 0.01) between the [Ca 2+]i of B cells and the blood levels of glucose. Proliferation of B cells in response to Staphylococcus aureus Cowan I (SAC) was significantly impaired in these patients (7.3 ± 0.48 × 10 3 cpm v 12.5 ± 0.61 × 10 3 cpm in normal subjects). Normalization of blood glucose with the hypoglycemic agents, glyburide, was associated with the return of both [Ca 2+]i of B cells and their proliferation in response to SAC to normal. The results show that hyperglycemia in type II diabetes mellitus is associated with a significant increase in [Ca 2+]i of B cells and with a decrease in their proliferation in response to mitogen. These derangements are reversed after the correction of the hyperglycemia. The data of the current study and those previously reported in PMNLs provide for a new pathogenetic process underlying the dysfunction of these cells in diabetes mellitus.

A Comparison of Retinal and Choroidal Hemodynamics in Patients With Primary Open-angle Glaucoma and Normal-pressure Glaucoma

To quantify, compare, and assess differences between retinal and choroidal hemodynamics in normal control subjects and patients with ocular hypertension, primary open-angle glaucoma, and normal-pressure glaucoma. Video fluorescein angiograms were made in 20 normal subjects, 11 patients with ocular hypertension, 45 patients with primary open-angle glaucoma, and 43 patients with normal-pressure glaucoma. Choroidal dye build-up curves were analyzed using an exponential model. The model time constant tau reflected the local blood refreshment time, the time needed to replace the blood volume in a tissue volume. Retinal arteriovenous passage time was estimated from the time lapse between retinal arterial and venous dye curves. The retinal arteriovenous passage time was longer in patients with primary open-angle glaucoma compared with normal subjects and patients with normal-pressure glaucoma; the average arteriovenous passage times (+/-SEM) in normal subjects and in patients with ocular hypertension, primary open-angle glaucoma, and normal-pressure glaucoma were, respectively, 2.44 +/- 0.19, 2.90 +/- 0.37, 3.02 +/- 0.17, and 2.55 +/- 0.15 seconds. Choroidal tau was longest in the normal-pressure glaucoma group but not as long in the primary open-angle glaucoma group; tau values in normal subjects and patients with ocular hypertension, primary open-angle glaucoma, and normal-pressure glaucoma were, respectively, 4.6 +/- 0.29, 5.6 +/- 0.69, 6.2 +/- 0.39, and 7.1 +/- 0.33 seconds. Whereas choroidal circulation is especially slower in patients with normal-pressure glaucoma, retinal circulation is delayed in patients with primary open-angle glaucoma. The choroidal and retinal vascular systems behave differently in primary open-angle and normal-pressure glaucoma, which may be important in the management of glaucoma.

Body composition derived from whole body counting of potassium in growth hormone-deficient adults: a possible low intracellular potassium concentration.

The validity of total body potassium (TBK) measurement in estimating fat mass and fat-free mass (FFM) in GHD adults was assessed by comparison with the reference technique of dual energy x-ray absorptiometry (DEXA). The TBK and FFM values determined by DEXA were used to calculate the potassium concentration per kg FFM in GH-deficient (GHD) adults and compared with standard values for normal subjects of 59.6 mmol for females and 66.4 mmol for males. There were considerable differences between predicted and measured TBK values for both males (3972 vs. 3577 mmol; P < 0.001) and females (2526 vs. 2277 mmol; P < 0.001). Similarly, the estimation of FFM and fat mass by TBK measurement was significantly inaccurate for both sexes compared to values determined by DEXA. These discrepancies may be accounted for by the lower calculated potassium concentrations compared with standard values for both males (56.2 vs. 66.4 mmol; P < 0.001) and females (53.1 vs. 59.6 mmol; P < 0.001). These observations suggest that caution should be exercised in the interpretation of TBK in GHD adults, and the reduced potassium concentrations would alleviate inaccuracies in the estimation of body composition. Secondly, the decreased intracellular potassium concentration of GHD adults may account for the decreased muscle strength and ease of fatigueability seen in GHD adults.

Increased Circulating Hepatocyte Growth Factor in the Early Stage of Acute Myocardial Infarction

We measured serum hepatocyte growth factor (HGF) in patients with acute myocardial infarction, angina pectoris, and other heart diseases. In patients with acute myocardial infarction, blood was collected at the time of admission. Serum HGF was elevated within 3 hours in 8 of 10 patients (80%) with acute myocardial infarction after onset of chest pain (9.4 ± 3.2 ng/mL, mean ± SEM, values in normal subjects <0.39 ng/mL). Mean value of serum HGF was 11.0 ± 2.6 ng/mL (n = 11) in patients who admitted to the hospital between 6 and 9 hours and 13.1 ± 5.7 ng/mL between 12 and 24 hours after onset. Elevated HGF levels were significantly more frequent than those of creatine kinase within 3 hours, and elevated levels correlated well with those of serum creatine kinase at 6–9 hours after onset of acute myocardial infarction. No increase in serum HGF value was found in patients with angina pectoris or other heart diseases. Thus, measurement of HGF is a sensitive method for early diagnosis of acute myocardial infarction.

Inferior Vena Caval Syndrome and the Sniff Test for Elevated Central Venous Pressure and Its Contributing Factors

A prospective analysis of 50 apparently healthy subjects and intensive care subjects was performed to determine the reliability of two-dimensional ultrasound in the detection of elevated central venous pressure. The sniff technique was used as a means to determine the caval index of the inferior vena cava. Twodimensional images of the inferior vena cava were obtained 3.5 cm inferior to the right atrium where caval respiratory motion and elasticity were observed. Quantitative analysis (percent inspiratory collapse) was determined by measuring the antenor-to-posterior diameter of the inferor vena cava immediately upon the subject's rapid inspiration and expiration. The sniff test of the inferior vena cava has been found to be a sensitive index of central venous pressure-that is, with either increased vena caval dilatation or central venous pressure, the percent collapse of the inferior vena cava is expected to decrease upon the subject's inspiration. Twenty-two of 50 subjects (44%) tested positive with the use of the sniff technique for elevated central venous pressure with an associated abnormality rating of 90%. The full inspiratory method was found to yield caval indices 10-20% lower than the sniff test data and may be responsible for false-positive values in normal subjects. Two-dimensional ultrasound of the inferior vena cava using the sniff technique With examination of other organs may be a reliable diagnostic modality for the detection of elevated central venous pressure and its contributing factor(s).

MR quantification of muscle fatty replacement in McArdle's disease

McArdle's disease is an energy-dependant disorder of skeletal muscle caused by the inability to break down glycogen. The aim of this study was to quantify fatty replacement in patients with McArdle's disease. Calf and thigh axial spin echo T 1-weighted magnetic resonance (MR) images (repetition time 500 ms, echo time 25 ms) were obtained at 0.5 T in nine patients with McArdle's disease (age 51 ± 16 years, range 26–74) and nine sex- and age-matched healthy subjects (age 52 ± 16 years, range 29–78) to quantify intramuscular fat. Regions of interest were drawn manually, encompassing the largest cross section of muscle. A fatty replacement index (IF) was determined from histograms of signal in the regions of interest in calf and thigh muscles. In normal subjects, IF = 3.6 ± 2.8% in calf and 4.9 ± 2.3% in thigh. In patients, IF = 11 ± 9.3% in calf and 13.5 ± 10.4% in thigh, significantly different from IF values in normal subjects ( p = .03). IF correlated well with age in patients ( p = .03). In older patients, up to 25% of the muscle volume was replaced by fat. Patients with McArdle's disease, usually weakly disabled, exhibit significant muscle fatty replacement on MR images. These findings suggest a progressive muscle loss over time related to the disease process.

Urinary cyclic adenosine 3',5'-monophosphate response in McCune-Albright syndrome: clinical evidence for altered renal adenylate cyclase activity.

The recent finding of an activating mutation in the Gs alpha protein, the protein that couples receptors to stimulation of adenylate cyclase, from endocrine and nonendocrine tissues of patients with McCune-Albright syndrome (MAS) suggests that alterations in adenylate cyclase activity may account for the clinical abnormalities in these patients. Many patients with MAS have hypophosphatemia. This may result from the presence of the activating Gs alpha mutation in proximal renal tubules or the elaboration of a phosphaturic factor from fibrous dysplasia. We, therefore, sought to characterize renal cAMP generation and phosphate handling in MAS patients. Intravenous infusion of PTH is a classic clinical test used to evaluate hormonal responsiveness of renal proximal tubule adenylate cyclase and examine PTH-dependent phosphate clearance. We performed PTH infusion in 6 MAS patients, 10 normal subjects, and 6 patients with pseudohypoparathyroidism (PHP). The basal urinary cAMP (UcAMP) level in the MAS group [5.5 +/- 2.6 nmol/dL glomerular filtration (GF)] was elevated (P < 0.05) compared to those in both normal subjects (3.2 +/- 1.2 nmol/dL GF) and patients with PHP (1.9 +/- 0.6 nmol/dL GF). However, PTH-stimulated peak UcAMP (15.0 +/- 7.0 nmol/dL GF) and the peak/basal UcAMP ratio (3.1 +/- 1.7) in MAS were significantly lower than the respective values in normal subjects (30.8 +/- 16.9 nmol/dL GF and 9.3 +/- 2.9; P < 0.05 for both) and were statistically similar to the blunted levels in PHP (respectively, 3.1 +/- 1.5 nmol/dL GF and 2.0 +/- 1.7). By contrast, the PTH-induced phosphaturic response in MAS patients was similar to that in the normal subjects. Our study provides clinical evidence that MAS patients have altered renal adenylate cyclase activity, manifested by an elevated basal UcAMP, but a blunted UcAMP response to PTH stimulation. These observations are presumably due to a mutation in the Gs alpha protein in the renal tubules. Despite the blunted UcAMP excretion, the phosphaturic response to PTH in MAS patients is intact.

Verapamil reverses abnormal [Ca2+]i and carbohydrate metabolism of PMNL of dialysis patients

The basal levels of cytosolic calcium ([Ca2+]i) of polymorphonuclear leukocytes (PMNL) are elevated in hemodialysis (HD) patients, and this abnormality has been implicated in the dysfunction of the PMNL of these patients. The elevated [Ca2+]i appears to be due to PTH-induced entry of calcium into PMNL, an action that may be prevented by calcium channel blockers. We examined [Ca2+]i and carbohydrate metabolism of PMNL of normal subjects and of HD patients before, after eight to nine weeks of verapamil therapy (120 mg/day), and after eight to ten weeks of discontinuation of verapamil treatment. In HD patients, the basal levels of [Ca2+]i of PMNL are elevated and their glucose uptake, the activity of total and active forms of glycogen synthetase, and glycogen content are reduced compared to values in normal subjects (P < 0.01). These derangements were normalized after verapamil therapy and re-emerged after discontinuation of treatment with verapamil despite no change in blood levels of PTH. The results indicate that the elevation in [Ca2+]i of PMNL and the consequent derangements in carbohydrate metabolism of these cells are treatable with a calcium channel blocker. The data assign a valuable role for calcium channel blockers for the amelioration of some aspects of cell dysfunction of uremia.

Retinal thickness change after focal laser treatment of diabetic macular oedema.

Laser photocoagulation has been used successfully for the treatment of clinically significant macular oedema to reduce the risk of loss of vision in diabetic patients. A quantitative method for measuring retinal thickness was applied to 20 patients with diabetic macular oedema before and 4 months after focal laser treatment to assess the reduction in retinal thickening and its relation to visual acuity. The degree of thickening at each location, defined by thickness index, was determined relative to the corresponding average value in normal subjects. Comparison of quantitative retinal thickness measurements before and after treatment demonstrated that treatment at thickness indices of approximately 1.6 (60% thickening) has nearly 50% probability for reversal of thickening to within the normal range (< or = 1.3), whereas at thickness indices greater than 2.8 (180% thickening) there is less than 2.5% probability that reversal will occur. The level of foveal thickening before treatment strongly correlated with the degree of thickening after treatment. Most of the eyes with an improvement in visual acuity had a foveal thickness within the normal range at 4 months' follow up. These findings suggest that quantitative retinal thickness measurement provides an objective assessment of the degree of macular oedema and can be useful for monitoring the efficacy of focal laser treatment in reducing the thickening and relating the latter to visual outcome.

Proinsulin by immunochemiluminometric assay for the diagnosis of insulinoma.

We used a newly developed immunochemiluminometric assay of proinsulin to determine its relative utility vis-à-vis C-peptide and insulin for the diagnosis of insulinoma. The evaluation was conducted in 20 consecutive patients with histologically confirmed insulinoma and 22 normal subjects who underwent a prolonged fast according to a standard protocol. Patients with insulinoma fasted to the point of demonstrating Whipple's triad; normal subjects fasted to 72 h. At the end of the prolonged fast, when the glucose value was 2.8 mmol/L or less (50 mg/dL), all three hormones had equal sensitivity (100%) in detecting insulinoma with no overlap with the values of normal subjects. When glucose levels were between 2.8 mmol/L (50 mg/dL) and 3.3 mmol/L (60 mg/dL) at the end of the prolonged fast, proinsulin was better than C-peptide and insulin in the diagnosis of insulinoma. The sensitivity was 90% for proinsulin and 85% for both C-peptide and insulin. Therefore, proinsulin not only is useful for the diagnosis of insulinoma, but it may have greater diagnostic accuracy than C-peptide and insulin.

Serial changes in atrial and brain natriuretic peptides in patients with acute myocardial infarction treated with early coronary angioplasty

To examine the role of brain natriuretic peptide (BNP) in acute myocardial infarction (AMI), we measured the plasma concentration of immunoreactive (ir) BNP together with that of atrial natriuretic peptide (ANP) over the 4-week course of AMI in 16 patients treated with early coronary angioplasty. Both the plasma ir-ANP and ir-BNP levels were increased on the first day of the infarction compared with the values in normal subjects. During the clinical course of the infarction, the plasma ir-ANP concentration soon decreased, while the plasma ir-BNP level remained elevated at 2 weeks after the infarction, also exhibiting a high level at 4 weeks. Plasma ir-BNP levels on day 1 or days 14 and 28 were inversely correlated with left ventricular ejection fraction obtained by left ventriculography at the acute or chronic phase, respectively. Plasma ir-BNP concentrations on days 14 and 28 were positively correlated with the maximal myosin light chain I level, an indicator of infarct size. These observations suggest that the plasma ir-BNP level increased to compensate for the ventricular dysfunction associated with the size of the infarct in AMI. BNP may act as a cardiac hormone in AMI, differing somewhat from ANP in its synthetic, secretory, or clearance behavior.

Direct in vivo comparison of calcium-regulated parathyroid hormone secretion in normal volunteers and patients with secondary hyperparathyroidism.

The regulation of PTH secretion by calcium is altered in patients with primary hyperparathyroidism. A similar disturbance may occur in secondary hyperparathyroidism, but direct in vivo comparisons of PTH secretion in normal subjects and those with secondary hyperparathyroidism have not been made. Thus, 13 patients with end-stage renal failure and secondary hyperparathyroidism and 20 healthy volunteers underwent dynamic tests of PTH secretion. Changes in ionized calcium were induced by 2-h iv infusions of calcium gluconate or sodium citrate on consecutive days, and the sigmoidal relationship between serum ionized calcium and PTH levels was examined. During sodium citrate infusions, serum ionized calcium levels decreased by 0.21 +/- 0.04 and 0.20 +/- 0.05 mmol/L, respectively (mean +/- SD), in normal volunteers and dialyzed patients (P = NS). Serum PTH levels rose from 27 +/- 7 to 107 +/- 33 pg/mL in controls and from 480 +/- 238 to 859 +/- 412 pg/mL in dialyzed subjects; thus, maximum PTH levels were 396% of preinfusion values in normal subjects, but only 79% greater than baseline values in dialyzed patients (P < 0.001). During the first 30 min of calcium infusions, the increase in serum ionized calcium did not differ between groups, but PTH levels fell more rapidly in normal volunteers; values were 24% of preinfusion levels in controls, but only 56% of the baseline in dialyzed patients (P < 0.01) after 30 min. Minimum PTH levels were attained after 50 min of calcium infusion in normal volunteers and after 70 min in dialyzed patients. The derived values for set-point were 1.21 +/- 0.04 and 1.24 +/- 0.06 mmol/L, respectively, in control and dialyzed subjects (P = NS). These results do not support the contention that the set-point for calcium-regulated PTH secretion is greater than normal in patients with secondary hyperparathyroidism due to end-stage renal disease.

Motor unit estimation: Reproducibility of the spike‐triggered averaging technique in normal and ALS subjects

Reproducibility of the spike-triggered averaging technique of motor unit estimation (MUE) was assessed in biceps-brachialis muscle in 10 normal subjects and 15 subjects with amyotrophic lateral sclerosis (ALS). MUE was calculated by dividing the compound muscle action potential by the mean amplitude of 15 surface motor unit potentials (S-MUPs) of low recruitment threshold. Averaged MUE values in normal subjects were higher than in ALS subjects, with few values overlapping. Differences between test and retest MUE values were not significant for either subject group. The relative differences between test-retest values were 45.3% for normal subjects and 32.6% for ALS subjects. Correlation coefficients between test and retest values were low (r = 0.07) for normal subjects when influential outlying points were removed, and higher (r = 0.65) for ALS subjects when individuals with MUE values within the normal range were removed. The higher correlation of test-retest MUE values in ALS subjects compared to normal subjects may be due to a greater probability of resampling among the smaller number of motor units in ALS subjects. In summary, the reproducibility and technical aspects of the spike-triggered averaging technique are similar to those reported for other MUE techniques.

Direct quantitation of right and left ventricular volumes with nuclear magnetic resonance imaging in patients with primary pulmonary hypertension

To test the utility of electrocardiographically gated spin echo nuclear magnetic resonance (NMR) imaging in quantitating right and left ventricular volumes and function in patients with primary pulmonary hypertension, right and left ventricular end-diastolic and end-systolic volumes, stroke volumes and ejection fractions were determined in 11 patients with primary pulmonary hypertension and in 10 subjects with normal echocardiographic findings. Ventricular chamber volumes were computed by summing the ventricular chamber volumes of each NMR slice at enddiastole and end-systole. This technique was verified by comparison of results obtained by this method and with the water displacement volumes of eight water-filled latex balloons and ventricular casts of eight excised bovine hearts.In the patients with primary pulmonary hypertension, right ventricular volume indexes were 121 ± 45 ml/m2at end-diastole and 70.1 ± 41.6 ml/m2at end-systole; both values were significantly greater than values in the normal subjects (67.9 ± 13.4 and 27.9 ± 7.5 ml/m2, respectively). Left ventricular end-diastolic volume index was significantly less in the patients (44.9 ± 9.7 ml/m2) than in the normal subjects (68.9 ± 13.1 ml/m2). There was no significant difference in left ventricular end-systolic volume between the two groups (24.4 ± 8.6 and 27.1 ± 7.8 ml/m2, respectively). Right and left ventricular ejection fractions in the patients with primary pulmonary hypertension (0.43 ± 0.21 and 0.46 ± 0.15, respectively) were significantly less than values in normal subjects (0.59 ± 0.09 and 0.6 ± 0.11, respectively).The ratio of right to left ventricular stroke volume indexes was 0.97 ± 0.1 in the normal subjects, not significantly different from the expected value of 1. In the patients with primary pulmonary hypertension, this ratio was significantly greater (3.17 ± 2.3), in part reflecting the presence of tricuspid regurgitation in these patients. Intra- and interobserver errors in the computation of ventricular volumes were low but were greater in patients with primary pulmonary hypertension. Nuclear magnetic resonance imaging provides a means of ventricular volume determination in the normal and failing ventricle.

Measurement of right ventricular mass in normal and dilated cardiomyopathic ventricles using cine magnetic resonance imaging

The accurate quantification of right ventricular (RV) mass has eluded conventional imaging modalities. Accordingly, cine magnetic resonance imaging was used for quantification of RV as well as left ventricular (LV) mass in 10 normal subjects and in 10 patients with dilated cardiomyopathy with an LV ejection fraction < 0.40. Hearts were imaged with 10 mm thick short-axis slices from apex to base with a short echo delay time of 5 ms. Each slice was partitioned into 3 sections: RV free wall, ventricular septum and LV free wall, for calculation of end-diastolic and end-systolic mass and LV:RV free wall ratio. RV end-diastolic mass in normal subjects was 45 ± 8 g, which was similar to the values determined in previously published postmortem studies, mean 46 g (range 23 to 68). The value determined in patients with dilated cardiomyopathy was higher (50 ± 11 g), but this difference was not significant. LV:RV free wall ratio in cardiomyopathy (3.6 ± 1.0) was greater than in normal subjects (2.4 ± 0.3), because of the greater LV free wall mass in dilated cardiomyopathy, where LV free wall end-diastolic mass was 173 ± 40 g vs 107.1 ± 19.9 g in normal subjects (p < 0.05). RV mass measurements had 6.4 ± 3.6% interobserver and 7.3 ± 6.1% intraobserver variability. There were no significant differences between end-diastolic and end-systolic mass measurements. Thus, cine magnetic resonance imaging can reproducibly calculate RV mass. The values in normal subjects correspond to previously reported postmortem values for a population without heart disease.

Diabetes mellitus induces red blood cell plasma membrane alterations possibly affecting the aging process

Various alterations of red blood cell (RBC) plasma membrane appear both in diabetes mellitus and during the physiological aging process. Diabetes mellitus decreases RBC life-span; therefore, it may change the plasma membrane by acting through its effect on the aging process. In order to clarify the issue, RBCs from normal subjects and insulin-dependent diabetic patients were fractionated in five subpopulations of different mean age (fraction 1: early young RBC, fraction 5: mature RBC). Thereafter, plasma membranes were prepared and enzymatic activities, membrane fluidity and lipid peroxidation were evaluated. NA+, K(+)-ATPase activity decreased during aging and it was higher in all RBC subpopulations from normal subjects in comparison to diabetic patients. Next, lipid peroxidation and fluidity increased during aging in both the study groups; in this case, however, in all subpopulations, except for that from fraction 1, RBCs from diabetic patients showed higher membrane fluidity and lipid peroxidation in comparison to normal subjects. Data herein reported suggest that diabetes mellitus affects the plasma membrane independently of (lipid peroxidation and fluidity) or dependently on (Na+, K(+)-ATPase) its effect on aging. In the case of lipid peroxidation and fluidity diabetes mellitus seems to affect the membrane by decreasing RBC life span, whereas in the case of Na+K(+)-ATPase it seems to alter this enzymatic activity which in turn might affect RBC aging. Acetylcholinesterase activity decreased during aging in RBCs from normal subjects, but it increased in RBCs from diabetic patients; RBC subpopulation from fraction 1, on the other hand, showed similar values in normal subjects and diabetic patients. In this case the effect of diabetes mellitus appears only during aging.

Dipyridamole vasodilator response after human orthotopic heart transplantation: Quantification by oxygen-15-labeled water and positron emission tomography

To assess coronary vasodilator restore after orthotopic heart transplantation, regional myocardial perfusion was measured with oxygen-15-labeled water and dynamic positron emission tomography in 14 cardiac allograft recipients who were not experiencing rejection and who had no angiographic evidence of epicardial coronary sclerosis 15 to 73 months (mean ± SD 43 ± 19) after transplantation (group I). Twelve normal men with an average age of 31 years (group II) served as a control group. Regional perfusion was measured at rest and after the intravenous administration of 0.6 mg/kg body weight of dipyridamole.Rest regional myocardial blood flow was homogeneously distributed throughout the left ventricle and was significantly higher in transplant recipients (mean 1.16 ± 0.26 ml/g per min [range 0.8 to 1.73] than in normal subjects mean 0.85 ± 0.13 ml/g per min [range 0.57 to 0.99); p = 0.001) as was rest heart rate-systoll blood pressure product (rate-pressure product 11,255 ± 2,540 vs. 7,073 ± 1,306; p < 0.001). After dipyridamole, perfusion in the transplant recipients was homogeneous and slightly lower (2.73 ±1.03 vs. 3.40 ± 1.09 ml/g per min; p = NS), whereas rate-pressure product was slightly higher (12,179 ± 2,266 vs. 10,885 ± 1,895: p = NS) than the value in normal subjects.Dipyridamole vasodilator response (dipyridamole/rest myocardial blood flow) ranged from 1.23 to 4.92 (mean 2.50 ± 1.13) in group I and from 2.65 to 5.45 (3.97 ± 0.89) in group II (p = 0.001). Rate-pressure product change (dipyridammole/rest rate-pressure product) was markedly attenuated in transplant recipients compred with the value in normal subjects (1.09 ± 0.09 vs. 1.56 ± 0.27 ml/g/per min; p < 0,001).Normalization for the difference in rest rate-pressure product for each individual subject showed that the adjusted rest show values (group 11.19 ± 0.27, group II 1.39 ± 0.31 ml/g per min; p = NS) and the dipyridamole-vasodilator response data (group I 2.45 ± 0.64, group II 2.47 ± 1.23, p = NS) in the two groups were not significantly different. Thus, in transplant recipients who are not experiencing rejection, the respons iveness of the coronary vasculature to dipyridamole-mediated vasodilation is uniformly preserved among all regions of the left ventricular myocardium.

Neuropeptide production by small cell carcinoma: vasopressin and oxytocin as plasma markers of disease.

Vasopressin (VP) and oxytocin (OT) were evaluated as tumor markers for small cell carcinoma of the lung by measuring the concentrations of these hormones in plasma samples obtained from patients at the onset of therapy and during treatment. Patient levels of VP before treatment ranged from 0.9-116 pmol/L, and this hormone was elevated (greater than 2.4 times) in 37 of 80 patients (46%) when values were compared to those of 25 healthy volunteers (normal mean, 2.13 +/- 0.15 pmol/L). Seventeen patients with elevated arginine VP displayed symptoms of the syndrome of inappropriate secretion of antidiuretic hormone. Patient levels of OT ranged from 0.3-124 pmol/L, and OT was elevated (greater than 2.4 times) in 14 of 72 patients (19%) compared with values in normal subjects (normal mean, 2.23 +/- 0.34 pmol/L). Both hormones were elevated in 6 patients. A positive response to treatment (partial or complete remission) was associated with reductions of elevated VP to 34.6 +/- 4.0% and of elevated OT to 34.7 +/- 7.5%, of values before treatment. Relapse was associated with an increase to 334 +/- 93% of remission values for VP (6 patients) and to 307% for OT (1 patient). These results indicate that VP and OT may be suitable plasma markers for a majority of small cell tumors. In most cases, an elevated concentration of hormone was associated with an elevation of the biosynthetically related neurophysin and vice versa. However, there were a number of exceptions, so that an elevated plasma concentration of VP, OT, or a neurophysin was found for 88% of patients with extensive disease and 70% of patients with limited disease.

Regional cerebral blood flow asymmetries in a group of 189 normal subjects at rest

Regional cerebral blood flow (rCBF) asymmetries were studied in 189 subjects (96 males and 93 females) at rest with the 133Xenon inhalation method using a fixed detector system. rCBF asymmetries in the resting condition were very small, nevertheless a significant (p less than 0.001) effect for their topographical distribution was present, reflecting higher rCBF in the right fronto-temporal and left parieto-occipital regions. rCBF asymmetries were not correlated with age, and there were no significant differences between males and females. Asymmetries are therefore useful from a statistical point of view in detecting rCBF abnormalities in the resting condition: they are more stable than absolute values in normal subjects and no matching according to age or sex is required when statistical comparisons are performed.