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Biomedical subjects

T J Moore

Publications and source records attributed to T J Moore.

At least 91 records · Page 5Linked to original sources
PubMed1987

Renal abnormalities in nonmodulating essential hypertension.

Hypertensives with low renin levels are known to be sensitive to salt intake and diuretics. The subset of hypertensives sensitive to salt and having normal or high renin levels are termed nonmodulators. These are patients with essential hypertension who fail to modulate their renal blood flow and aldosterone responsiveness to angiotensin II when dietary sodium is changed. The result of nonmodulation is a pressor response to a short-term sodium load that results from a failure to excrete the sodium appropriately and that is presumably secondary to the defect in renal blood supply. On a high sodium load only nonmodulators have a decrease in BP in response to short-term treatment with an angiotensin-converting enzyme (ACE) inhibitor, which indicates an abnormality in intrarenal angiotensin II levels or in the renal angiotensin II receptor.

Adrenal Glands↗
PubMed1986

Adrenal imaging with technetium-99m-labelled low density lipoproteins.

Evaluation of adrenal cortical function by external imaging is currently accomplished by injection of radiolabelled analogs of cholesterol. Although the adrenals do utilized exogenous cholesterol for steroid hormone synthesis, the cholesterol is delivered to the glands not as free cholesterol but through the uptake of low density lipoproteins (LDL), which are subsequently degraded within the adrenal cortical cells to provide cholesterol. Thus, we sought to assess the use of 99mTc-labelled LDL injected into rabbits to obtain external images of the adrenal glands. Adrenal images of all nine rabbits tested were obtained within 18 to 21 hours after injection of 99mTc-LDL. Seven of the rabbits were subjected to adrenal cortical suppression with dexamethasone and then all nine rabbits were imaged a second time. In the untreated animals, visualization of the adrenal glands was accompanied by normal serum cortisol concentrations and accumulation of radiolabel in the adrenals, whereas in the dexamethasone-treated animals, lack of visualization of the adrenal glands was correlated with low serum cortisols, and greatly decreased accumulation of the radionuclide in the adrenals. These findings demonstrate for the first time that LDL, when labelled with 99mTc, can be used to evaluate adrenal cortical function by external imaging.

Adrenal Cortex Function Tests↗
PubMed1984

Captopril enhances vascular and adrenal responsiveness to angiotensin II in essential hypertension.

The converting-enzyme inhibitor captopril (25-50 mg orally every 6 h for 66 h) was used to dissociate the circulating levels of angiotensin II (ANG II) from changes in sodium balance in 11 patients with normal renin essential hypertension on 10 mmol of sodium/day intake. Pressor, renal vascular and adrenal responses to graded infusions of ANG II (0.3, 1 and 3 pmol kg-1 min-1) were measured before and after captopril administration. Systemic vascular responses were assessed by measuring diastolic blood pressure (DBP), renovascular responses by measuring p-aminohippurate (PAH) clearance and adrenal responses by measuring plasma aldosterone. After receiving captopril for 66 h the hypertensive subjects showed a significantly (P less than 0.004) enhanced blood pressure response to the infused ANG II but not to noradrenaline when compared with the response before captopril. ANG II (3 pmol kg-1 min-1) also produced a significantly (P less than 0.03) greater reduction in PAH clearance after (-194 +/- 40 ml/min) compared with before (-104 +/- 15 ml/min) captopril. These results suggest that the responsiveness to ANG II in these two target tissues is determined by the circulating ANG II level. In the adrenal gland the aldosterone responses to ANG II also were significantly greater after (P less than 0.01) than before captopril (increment at 3 pmol kg-1 min-1: 660 +/- 88 vs 381 +/- 94 pmol/l). These results are in distinct contrast with the responses previously reported for normotensive subjects and support the hypothesis that the regulation of aldosterone secretion is altered in subjects with essential hypertension.

Adrenal Glands↗
PubMed1984

Human platelet angiotensin II receptors: regulation by the circulating angiotensin level.

Human platelets possess angiotensin II (AII) receptors which increase in number in response to sodium loading, a response similar to that reported for animal smooth muscle and renal AII receptors. In these studies, we studied platelet AII binding (by Scatchard analysis of competitive binding curves) in normal subjects as they changed their dietary sodium intake from 200 to 10 to 200 meq/day. Binding capacity fell significantly after 24 h of sodium restriction and furosemide diuresis, declining to a nadir of 40% of the binding capacity found during sodium loading (from 23 to 10 fmol AII/10(9) platelets). Binding increased again after 24 h of sodium loading. There were no significant changes in receptor affinity during either low or high salt intake. The binding changes were significantly inversely correlated with the changes in plasma AII levels (r = -0.87), suggesting that AII itself is the regulator of the platelet AII receptor. Short term increases in AII level (by furosemide administration or AII infusion) did not alter platelet AII binding, indicating that the changes in platelet binding were not due simply to receptor occupancy changes. These results show that platelets have the capacity for dynamic rapid up- and down-regulated of their AII receptors and that these receptor changes are regulated by the plasma AII level.

Adult↗
PubMed1984

Evaluating the impact of a conference.

A comprehensive five-phase evaluation of the first Conference on Citizen CPR was implemented to measure its educational value and impact on attitudes regarding key issues in the lay CPR movement. Pre- and post-conference surveys of 480 members of the national CPR community and 165 conference participants along with an on-site evaluation of 152 participants indicated that participants felt that new and relevant information was presented and the conference resulted in little change in the attitudes of either participants or members of the national CPR community. The data reaffirm the educational value of conferences as new information was disseminated easily. However, the data raise questions about the impact conferences have upon attitudes, as only minor changes were reported. Weaknesses in the evaluation design are discussed, and recommendations for future conference evaluations are presented.

Community Participation↗
PubMed1984

External fixation for the uninfected angulated nonunion of the tibia.

External skeletal fixation is an effective method of stabilizing angulated ununited fractures of the tibia. In 14 patients who were not infected, realignment was accomplished by: closed-fracture-site manipulation (five cases); fibular osteotomy and closed manipulation (six cases); or fibular osteotomy and open reduction (three cases). External fixation was selected instead of internal fixation for patients in whom there was: risk of reactivating quiescent sepsis; thin secondary epithelium adherent to bone that might slough after surgical dissection; a very proximal or a very distal nonunion, where internal fixation is technically difficult; or a bulky, angulated delayed union or nonunion or one in bayonet apposition that would require excessive plate contouring. On the average, patients were corrected from 17.3 degrees (either varus or valgus) to 2.3 degrees. Two patients did not unite with the fixator/orthosis treatment plan, but neither one lost correction during subsequent management. The technique is not suitable for atrophic nonunions.

Adolescent↗
PubMed1983

Dopaminergic blockade of the renin-angiotensin-aldosterone system: effect of high and low sodium intakes.

Recent investigations suggest that dopamine inhibits aldosterone secretion. To test the hypothesis that dopamine contributes to the reduced aldosterone secretion on a high sodium intake, eight normal subjects were studied in metabolic balance on both 200 and 10 mmol sodium diets. On each diet, the subjects received a constant 4 h intravenous infusion of the dopamine antagonist, metoclopramide (MCP). Although MCP significantly increased plasma aldosterone (PA) throughout the infusion on both diets, the maximum increment in PA was greater on the low (37 +/- 5 ng/dl) than on the high (14 +/- 4 ng/dl) sodium intake (P less than 0.02). The greater response on the low sodium intake could not be ascribed to changes in potassium, cortisol or ACTH. However, plasma renin activity (PRA) and angiotensin II (AII) levels were significantly (P less than 0.01) increased by MCP while on the low but not the high sodium intake. We conclude that the rise in PA while on a high sodium intake reflects dopaminergic antagonism by MCP directly at the level of the adrenal gland. On the low sodium intake, the enhanced PA response to MCP probably reflects both a direct adrenal effect and an indirect effect mediated via activation of the renin-angiotensin system.

Adult↗
PubMed1983

Defect in the sodium-modulated tissue responsiveness to angiotensin II in essential hypertension.

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 (greater than 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 (less than 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 less than 0.001, chi-square) 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 less than 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). The adrenal responses to sodium intake and infused AII also differed in the two subgroups. In the NR, the adrenal response to AII was significantly greater (P = 0.011, Wilcoxon signed rank test) after sodium restriction. In contrast, there was no significant difference in the aldosterone response to AII infusion between the low and high sodium diets in the AbR. Thus, a substantial subgroup of essential hypertensives has an abnormality in responsiveness to AII in two systems central to volume homeostasis: the kidney and adrenal. They fail to modulate their renal blood flow and aldosterone responses to AII with changes in dietary sodium intake. Moreover, basal renal blood flow does not increase appropriately with increased sodium intake. These abnormalities, which may be due to an increased local production of AII or a defect in the AII receptors in these three target tissues, could contribute to the elevated blood pressure.

Adolescent↗
PubMed1983

Dopaminergic modulation of aldosterone responsiveness to angiotensin II with changes in sodium intake.

The aldosterone response to infused angiotensin II (AII) is blunted by sodium (Na) loading. Since dopamine levels increase on a high Na diet and dopamine can inhibit aldosterone secretion, it is possible that dopamine mediates the blunted aldosterone secretion in this setting. To test this hypothesis, we assessed whether the dopamine antagonist, metoclopramide (MCP) would enhance the aldosterone response to infused AII. Six normal subjects received graded infusions of AII when they were in metabolic balance on diets containing both 10 and 200 meq Na/day (control infusions). The infusions were then repeated (on the same diets) during the administration of MCP (0.1 mg/kg iv bolus, then 0.05 mg/kg . h). During the control AII infusions, the aldosterone response to the highest dose of AII was significantly less on the 200 meq Na intake than on 10 meq (plasma aldosterone levels increased 17 +/- 5 vs. 30 +/- 8 ng/dl respectively; P less than 0.01). However, MCP administration eliminated this difference in aldosterone responsiveness by significantly enhancing (P less than 0.02) the response to infused AII during the 200 meq Na intake (plasma aldosterone increment of 25 +/- 9 ng/dl). This effect of MCP was limited to the adrenal response to AII: on a given Na intake, the mean blood pressure response to AII was similar both with and without concomitant MCP. These results suggest that dopamine may be an important regulator of the alterations in aldosterone responsiveness to AII that occur during changes in dietary sodium intake.

Adult↗
PubMed1983

Endogenous angiotensin II as a determinant of sodium-modulated changes in tissue responsiveness to angiotensin II in normal man.

Dietary sodium restriction reduces vascular smooth muscle, particularly renovascular, responsiveness to infused angiotensin II (AII), while the responsiveness of the adrenal and the AII-renin short feedback loop to AII is enhanced. To determine whether circulating AII mediates these changes in responsiveness, we studied 11 sodium-restricted and 9 sodium-replete normal subjects before and after 75 h of converting enzyme inhibitor pretreatment with MK421. All subjects received infusions of paraaminohippurate (PAH) to assess renal plasma flow during graded AII infusion (0.3-10 ng/kg X min) before and after MK421 administration. Plasma aldosterone, cortisol, PRA, AII, sodium, potassium, and PAH clearance were measured at the onset and end of each AII dose. In sodium-restricted subjects, preinfusion AII and aldosterone levels were significantly reduced, (P less than 0.001) to the range found in sodium-replete subjects, after 75 h of MK421 administration, whereas blood pressure and PAH responses to infused AII were significantly enhanced (P less than 0.01). Blood pressure and PAH responses to infused AII in sodium-replete subjects were not significantly modified by MK421 treatment, confirming that the drug effect was specific. In contrast, the plasma aldosterone increment and PRA decrement after AII infusion were similar before and after MK421 on both diets. Thus, sodium-modulated changes in PAH and blood pressure responsiveness to infused AII depend on circulating AII levels. However, circulating AII does not mediate sodium modulation of adrenal or PRA short-feedback loop responsiveness to infused AII. Two different mechanisms determine sodium modulation of tissue responsiveness to AII; in one, circulating AII via a receptor mechanism is the mediator, and in the other, some other factor(s) also linked to sodium intake must be responsible.

Adolescent↗
PubMed1982

Successful arterial embolization of an insulinoma.

A 38-year-old woman had fasting hypoglycemia, hyperinsulinemia, and an arteriographically demonstrable insulinoma. One year after surgical resection, however, hypoglycemia recurred and an arteriogram demonstrated a recurrent intrapancreatic vascular mass. Because of anticipated complications of another surgical approach, we elected to embolize the tumor arteriographically, using microfibrillar collagen. The patient's fasting blood glucose and insulin levels improved rapidly. Eleven months after embolization, the patient remains well, with normal blood glucose levels.

Adenoma, Islet Cell↗
PubMed1982

Angiotensin II receptors on human platelets.

The investigation of the interaction between angiotensin II and its receptors in human subjects has been hampered by the inaccessibility of human tissue containing angiotensin II receptors. In order to find a more accessible angiotensin II-binding tissue, we studied angiotensin II binding to platelets in normal human volunteers. Platelet preparations purified on Ficoll: Isopaque gradients were incubated with 125I-angiotensin II (30 pm), with and without unlabeled angiotensin at 22 degrees C, separating bound from free hormone by microcentrifugation. Binding was linearly related to the number of platelets incubated, and, at 8 X 10(5) cells/microliters, specific binding ranged from 0.8 to 10%. Scatchard analysis indicated a binding site with a Kd of 2.4 +/- 0.3 X 10(-10) m which agreed well with the Kd by displacement analysis (3.1 X 10(-10) m). The relative binding potencies for angiotensin II and analogues were: angiotensin II = des-Asp1 an angiotensin II greater than [Sar1, Ala8] angiotensin II greater than des-Asp1-[Ile8] angiotensin II greater than angiotensin I. The effect of high and low sodium (Na) intake (200 vs. 10 mEq/day) on platelet angiotensin II binding was studied in nine subjects. Compared to low Na, high Na intake produced an 80% increase in the angiotensin II-binding capacity (P less than 0.01) with no significant change in binding affinity. We conclude that human platelets possess angiotensin receptors whose binding characteristics and modulation by dietary sodium resemble the properties of the receptors on "classical" animal angiotensin target tissues. The platelet may provide an accessible source of angiotensin receptors for a detailed study of angiotensin-receptor interaction in human tissue.

Angiotensin II↗
PubMed1982

Abnormal renin short feedback loop in essential hypertension is reversible with converting enzyme inhibition.

The suppression of renin release by angiotensin II (AII) (the so-called short feedback loop) is blunted in essential hypertension. To determine whether this abnormality is reversible, renin release was assessed in sodium-restricted essential hypertensives and normal controls: (a) during the administration of captopril for varying intervals and (b) following the infusion of graded doses of AII (0.3-3 ng/kg per min) before and after plasma levels of AII had been chronically reduced with captopril (25-50 mg every 6 h) for 70 h. In control subjects, the maximal increment above control in plasma renin activity (PRA) after a single dose of captopril (11.9+/-3 ng/ml per h) was significantly (P < 0.02) greater than in hypertensives (8.1+/-1.7 ng/ml per h) despite similar reductions in AII levels and significantly greater decrements in diastolic blood pressure in the hypertensives. When captopril was continued for 70 h, the PRA increments above base line in hypertensive subjects (11.4+/-2.9 ng/ml per h) rose to levels seen in the controls (11+/-2.6 ng/ml per h); there were no significant differences in the AII or diastolic blood pressure decrements between the two groups. Compared with normotensive subjects, AII failed to suppress renin release in hypertensive subjects despite significantly greater diastolic blood increments and comparable AII levels achieved at each AII dose. After captopril treatment, AII now produced significant declines in PRA in the hypertensives; moreover, comparing declines pre- and postcaptopril, greater PRA decrements were seen either at comparable rises in levels of AII or diastolic blood pressure. Finally, the suppression of PRA by AII postcaptopril in hypertensives was now indistinguishable from that seen in normal controls. Thus, the impaired regulation of renin by AII is reversible with prolonged captopril treatment, suggesting that this abnormality is not due to a fixed structural defect but to a reversible lesion.

Angiotensin II↗
PubMed1982

Communicating health information to urban Mexican Americans: sources of health information.

Data from a six-week hypertension campaign aimed at urban Mexican Americans were analyzed to document how they receive their health information and to identify the communication channels most likely to reach different segments of the Mexican-American community. The nine sources of information examined were doctor, nurse, pharmacist, family, friends, radio, newspaper, television, and magazine. The most common source of health information reported was doctor, followed by television, newspapers, magazines, family, and radio. Interview language (Spanish or English) was a significant predictor of the amount of health information received from all nine sources. Sex, family income, education, and age also were shown to affect the amount of health information received from various sources. Profiles of respondents most likely to use each source of health information are presented and implications for health educators are discussed.

Adolescent↗
PubMed1982

Impact on retention: comparison of two CPR training programs.

CPR trainees who completed 8-hour, 3 session and 4-hour single session courses were studied for skill and cognitive retention one year after certification. Knowledge and performance scores were significantly higher for trainees from the long course, but performance skills for both groups were below certification level when compared to American Heart Association standards. The findings suggest the need for further evaluation of course components which could improve retention levels for all trainees.

Adolescent↗