AB S T R A C T In normal subjects, dietary sodium intake modulates renovascular, adrenal, and pressor responses to infused angiotensin II (AII). To examine the hypothesis that this modulation is abnormal in some patients with essential hypertension, we studied 18 hypertensives and 9 normal subjects twice-during dietary sodium restriction and during loading. Paraaminohippurate (PAH) clearance was used to assess renal plasma flow. AII was infused in graded doses (0.3-3.0 ng/kg per min). Plasma aldosterone, cortisol, renin activity, AII, sodium, potassium, and PAH clearance were measured at the onset and end of each AII dose.During dietary sodium repletion, eight of the subjects with essential hypertension showed a normal renovascular response (>125 ml/min per 1.73 m2) to AII infusion (3 ng/kg per min). The decrement in renal blood flow in these normal responders (NR) was 168±10, which was comparable to the range in normotensive subjects (206±25 ml/min per 1.73 m2). All of the remaining hypertensive patients, designated abnormal responders (AbR), had lower (<125) renal blood flow responses to the same dose of infused AII (mean decrement: 84±11 ml/min per 1.73 m2) compared with the NR and normotensive subjects. Renal blood flow responses to all AII doses were statistically greater on a high-vs.-low salt diet in the NR (P < 0.001, chisquare) and normotensives (P = 0.004, chi-square) but sodium intake had no effect on this response in the AbR. Basal renal blood flow in NR increased significantly (P < 0.001, paired t test) with dietary sodium repletion, from 491±36 (low salt) to 602±40 ml/min per 1.73 m2 (high salt), but was almost identical in the AbR on differing dietary sodium intakes (429±24 vs. 425±26 ml/min per 1.73 m2).
SUMMARY This retrospective study correlates electrocardiographic and histopathologic findings in 24 patients with single wellcircumscribed infarcts to determine 1) whether ECG terms commonly used to describe the location of myocardial infarcts are significant, and 2) whether the extent of infarct can be determined using QRS characteristics. Transverse sections of the hearts were photographed. Based on histologic sections, the infarct was outlined on the photograph and each section was planimetered via a sonic digitizer into a computer that was programmed to divide the left ventricle into 8 radial sectors and also into basal, mesial, and apical thirds. The percentage of infarct in each of these areas was then calculated.Of the 24 hearts evaluated 12 had posterior infarcts and 12 had anterior infarcts. Posterior infarcts principally involved the basal and THE DIAGNOSIS OF MYOCARDIAL INFARCTION has been complicated by the large number of terms that are used to specify the location of infarction based on electrocardiographic (ECG) interpretation. These include anterior, septal, lateral, high lateral, inferior, posterior, diaphragmatic, apical, basal, transmural and subendocardial. The accuracy of these distinctions remains unclear despite prior studies correlating electrocardiographic and postmortem findings."'21A wide variety of interventions, both medical and surgical, that may affect the quantity of irreversibly damaged myocardium are currently being examined. Thus there is a need for noninvasively determined descriptors of the extent of infarcted myocardium. Although exacting criteria for quantifying infarct size electrocardiographically have been proposed,22 these criteria have not been validated by anatomic observation.Because of these considerations we have developed a technique to accurately localize and determine the extent of infarcts in postmortem hearts. The purpose of the present study was to employ this technique to correlate anatomic findings with the ECG under optimal diagnostic conditions by including only those hearts with single, wellcircumscribed, anterior or posterior infarcts. mesial levels, whereas the anterior infarcts were more extensive in the apical and mesial thirds, with relative or total sparing of the base. Posterior infarcts were associated with Q waves in leads II, III and aVF in 11 instances. The other posterior infarct was associated with markedly diminished R waves in leads II, III and aVF in the presence of a horizontal axis. All anterior infarcts were associated with Q waves or markedly diminished R waves in the right precordial leads. Eight of the anterior infarcts exhibited circumferential apical involvement and all eight were associated with Q waves or markedly diminished R waves in the left precordial leads.This study documents the electrocardiographic identification of anterior, posterior, and apical infarcts by correlation with pathologic anatomy. Methods Study PopulationHearts of deceased patients who had been evaluated in either the Duke Cardiac Care Unit or Cardiac Cath...
SUMMARY To determine whether prostaglandins contribute to the depressor response to the converting enzyme inhibitor, captopril, we measured the plasma prostaglandln levels by radioimmunoassay before and after captopril administration, and then examined the effect of prostaglandin synthetase inhibition on captopril's antihypertensive effect. When a single oral captopril dose (25-100 mg) was given to 31 sodium-restricted patients with essential hypertension, the levels of the stable transformation product of prostacyclin remained immeasurable and that of thromboxane A, did not change, while the metabolite of PGE, (PGE-M) increased by 53% (34 ± 4 pg/ml pre-captopril, 52 ± 5 pg/ral after; p < 0.001). As expected, blood pressure (BP) and angiotensin II (AH) levels fell, and kinin levels rose (all changesp < 0.001). We then blocked prostaglandin synthesis in 18 of these subjects for 24 hours with either indomethacin (n = 10) or aspirin (n = 8) before repeating the captopril dose, to assess the importance of these PGE-M increments. The PGE-M responses to captopril were effectively blocked in nine of 10 subjects receiving indomethacin and four of eight receiving aspirin. In these 13 patients, the depressor response to captopril was significantly blunted (-20 ± 3 mm Hg pre-synthetase inhibition vs -13 ± 2 mm Hg post; p < 0.05). When these agents did not block the PGE-M response to captopril, the BP response was also unchanged (-15 ± 4 mm Hg pre, -18 ± 5 mm Hg post). Neither indomethacin nor aspirin changed the AH or kinin responses to captopril. We conclude that the prostaglandins may be important mediators of captopril's antihypertensive effect in the sodium-restricted state. hormones, the prostaglandins, may also be involved. It is known that bradykinin releases prostaglandins from several tissues, 1 " 7 and it has been postulated that inhibition of kininase II with CEI could increase endogenous kinin levels, permitting more kinin-mediated prostaglandin release. Murthy et al. 8 have provided indirect evidence in rabbits supporting this postulate by showing that prostaglandin synthetase inhibition partially blocks the hypotensive response to bradykinin after CEI. Vinci et al. 9 found that the peptide CEI, SQ 20,881, increased plasma immunoreactive prostaglandin E levels in some hypertensive subjects.In the studies reported here, we examined the potential importance of the prostaglandins in mediating the depressor response to the oral CEI, captopril, in hypertensive patients both by measuring the changes in plasma prostaglandin levels after CEI and by assessing the effect of prostaglandin synthetase inhibition on the response to CEI. Our results show that captopril does increase endogenous prostaglandin production and that prostaglandins contribute to captopril's antihypertensive effect.
Neuropathological studies of Huntington’s disease reveal neuronal atrophy, lipofuscin accumulation and other findings characteristic of the aged brain, although the onset of disease is only the fourth decade. The pathology is limited to specific areas such as the caudate nucleus, cerebral cortex and hypothalamus. 14 patients with documented Huntington’s disease (mean age of 44.4 years with a range of 27–79 years) were studied by oral glucose tolerance tests (GTT) and intravenous arginine tolerance tests performed under standardized metabolic conditions. Seven of the 14 patients had impaired carbohydrate tolerance. Mean plasma glucose level at 2 h was 90.4 ± 6.2 mg/l00 ml in the patients with a normal GTT and 148.1 ± 8.9 mg/l00 ml in the patients with a diabetic type GTT. Mean peak insulin level in the nondiabetic group occurred at 1/2 h and was 60.2 ± 10.1 μ U/ml, but in the diabetic group the peak insulin level occurred at 2h and was 155.9 ± 33.8 μU/ ml. There was failure of suppression of growth hormone during the GTT, with a rise to abnormally high levels at 5 h (18.6 ± 5.6 ng/ml). Arginine infusion resulted in normal glucose and insulin rise in the nondiabetic patients with Huntington’s disease. However, arginine infusion provoked an elevated insulin response in those with a diabetic GTT, and an exaggerated growth hormone response in the majority of the patients. It is uncertain whether these observations are related to abnormal cerebral aging per se, direct hypothalamic neuronal degeneration, or perhaps a relative imbalance of intracerebral neurotransmitters including dopamine.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.