Fruit-and-vegetable rich diet low in fat significantly reduced blood pressure.
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Journal Article↗
Biomedical subjects
A G Logan
Publications and source records attributed to A G Logan.
Cardiovascular, renal, and neurohumoral responses to single large-volume paracentesis in patients with cirrhosis and diuretic-resistant ascites.
OBJECTIVE: Large volume paracentesis is an effective treatment for refractory ascites, but the need for routine infusion of albumin or other volume expanders remains controversial. The aim of this study was to assess the short term effects of a single 5-L paracentesis without albumin replacement on total central blood volume, systemic and renal hemodynamics, sodium homeostasis, and neurohumoral factors. PATIENTS AND METHODS: Twelve patients with biopsy-proven cirrhosis and tense, diuretic-resistant ascites were studied before and 48 h after a single 5-L paracentesis without albumin infusion. Systemic hemodynamics and total central blood volume were assessed using radionuclide angiography. Glomerular filtration rate and effective renal plasma flow were measured by inulin and para-aminohippurate clearances, respectively. Lithium clearance was used as an index of proximal tubular reabsorption of sodium. In addition, plasma concentrations of neurohumoral factors were determined. RESULTS: Total central blood volume was 2.41 +/- 0.33 L/m2 (mean +/- SEM) before and 2.34 +/- 0.18 L/m2 48 h after large volume paracentesis (p = 0.76). Similarly, no differences were detected in the cardiac index, glomerular filtration rate, effective renal plasma flow, urinary sodium excretion, hematocrit, plasma renin activity, or concentrations of plasma aldosterone, norepinephrine, or atrial natriuretic factor. CONCLUSIONS: A single large volume paracentesis without albumin replacement causes no disturbances in systemic and renal hemodynamics 48 h after the procedure. These results suggest that a single 5-L paracentesis without albumin infusion is a safe and satisfactory short term option for the management of patients with cirrhosis and tense, diuretic-resistant ascites.
Aged↗
Dietary salt restriction increases vascular insulin resistance.
BACKGROUND: Recent studies have shown that insulin has a direct vasodilator effect and that vascular sensitivity to insulin is impaired in hypertension. How the vasodilator effect of insulin is regulated physiologically is unknown. It has been appreciated that salt restriction may have adverse effects on glucose and lipid metabolism--processes regulated by insulin. To determine whether dietary salt restriction might affect vascular sensitivity to insulin, we studied 13 subjects (including eight borderline hypertensive subjects and five normotensive subjects) after 1 week of a normal sodium diet (240 mEq/day) and after 1 week of a low-sodium diet (20 mEq/day) with a randomized, double-blind crossover design. METHODS AND RESULTS: Vascular sensitivity to insulin was assessed with the dorsal hand vein linear variable differential transformer technique. When the "normal" salt diet was given, vascular sensitivity for insulin was significantly less (i.e., dose that produced the half-maximal response [ED50] insulin was higher) in hypertensive subjects (ED50 insulin for hypertensive subjects, 5.75 milliunits (mU)/min; ED50 insulin for normotensive subjects, 0.23 mU/min; p < 0.05). Vascular sensitivity to insulin was inversely correlated with mean arterial pressure and plasma norepinephrine concentration. When the low salt diet was given, vascular sensitivity to insulin decreased in both the normotensive and hypertensive groups, paralleling an increase in plasma norepinephrine. Blood pressure was not significantly decreased by reducing salt intake. CONCLUSION: In these younger normotensive and hypertensive subjects, dietary salt restriction increases resistance to the vasodilating effects of insulin.
Adult↗
Accurate measurement of impaired glomerular filtration using single-dose oral cimetidine.
To improve the validity of a timed creatinine clearance as a measure of glomerular filtration rate (GFR), we investigated whether a single 800-mg dose of oral cimetidine was sufficient to inhibit tubular secretion of creatinine (TScr). Forty-five 3-hour timed creatinine clearances (Clcr) with single 800-mg dose oral cimetidine (TCC) in 17 renal transplant recipients with marked renal function impairment (creatinine 2.0 to 7.1 mg/dL) were compared with simultaneous [125I]-iothalamate GFR (Cliothal). For comparison, 13 timed Clcr without cimetidine (TC), and 36 24-hour Clcr were performed. The TCC was the most accurate: the ratio (mean +/- SD) of TCC:Cliothal was 1.12 +/- 0.02, compared with 1.33 +/- 0.08 for Clcr:Cliothal and 1.53 +/- 1.02 for TC:Cliothal. The difference between Cliothal and TCC was small over the range of GFRs tested (mean +/- 2 SD), 0.9 +/- 2.5 mL/min/1.73 m2. The intraclass correlation (R) for within-subject reproducibility of the TCC in five subjects was 0.8 (95 percent CI; 0.5, 0.9), and in 11 subjects who had at least three GFR determinations over 24 weeks, the TCC was as responsive to change in GFR as Cliothal. There was an inverse relationship between fractional excretion of cimetidine and GFR (r2 = -0.70), suggesting increased tubular secretion of cimetidine with decreasing GFR. In conclusion, a single 800-mg oral dose of cimetidine was effective in inhibiting TScr such that the TCC was an accurate, reproducible, and responsive test of GFR.
Administration, Oral↗
Effect of hyperglycaemia on arterial pressure, plasma renin activity and renal function in early diabetes.
1. In insulin-dependent diabetes mellitus, hyperglycaemia has a profound effect on renal and systemic haemodynamic function. The mechanism for this is unknown. 2. We conducted a study in 11 males with insulin-dependent diabetes mellitus, within 6 years of diagnosis. We examined the neurohumoral, haemodynamic and renal variables during euglycaemia (4.0-6.0 mmol/l) and after a 12 h period of hyperglycaemia (8.5-10.5 mmol/l). Subjects were examined in a sodium-replete state during supine rest and during simulated orthostatic stress induced by lower body negative pressure at -15 mmHg. 3. Variations in glycaemia markedly influenced plasma renin activity, which was increased at baseline during hyperglycaemia (3.82 +/- 0.66 pmol of angiotensin I h-1 ml-1 compared with 2.13 +/- 0.33 pmol of angiotensin I h-1 ml-1 during euglycaemia, P = 0.009), and rose further during simulated orthostatic stress. Mean arterial pressure was also elevated during hyperglycaemia (89 +/- 2 mmHg compared with 81 +/- 3 mmHg during euglycaemia, P = 0.03), both at rest and during orthostatic stress. 4. The renal haemodynamic effects of hyperglycaemia included maintenance of glomerular filtration rate in the face of significant declines in renal blood flow, and a probable increase in filtration fraction (0.21 +/- 0.01 compared with 0.18 +/- 0.01 during euglycaemia, P = 0.06). The responses of mean arterial pressure and renal blood flow to simulated orthostatic stress were not affected by hyperglycaemia, but the forearm vascular response was significantly augmented. 5. These data suggest that sustained hyperglycaemia activates the renin-angiotensin system, thereby increasing systemic and renal vasomotor tone. Over time such changes may have deleterious microvascular consequences.
Adult↗
Is knowing your cholesterol number harmful?
To examine the potential adverse psychological effects of screening for hypercholesterolemia, 287 men working at a motor-car assembly or steel-making plant who were ultimately diagnosed as having hypercholesterolemia and 236 randomly selected normal cholesterol controls from the same plants completed psychological questionnaires at the initial screen and 1-year later. At baseline and before diagnosis, hypercholesterolemic men scored higher on mental health and lower on negative affect than controls (p values < 0.05). One year later no adverse changes on the psychological measures were found irrespective of the type of follow-up care that they were randomly assigned to receive. Surprisingly only about half of the hypercholesterolemic men believed they had hypercholesterolemia at follow-up despite being told otherwise. Baseline scores of those who did not accept the label (n = 122) [classified as deniers] were higher on measures of positive affect and lower on measures of negative effect than those of hypercholesterolemic men who accepted the disease label (n = 73) (p values < 0.05). Moreover they held more negative attitudes towards dietary change at baseline (p < 0.03), made fewer dietary changes (p values < 0.05), and had a lesser change in total cholesterol. We conclude that a hypercholesterolemia detection and treatment program conducted in a working adult population had no adverse psychological consequences. It did, however, reveal a large subset of hypercholesterolemic men who did not accept the label despite being told they had this problem. Denial was a significant barrier to health behaviour change and may represent a maladaptive coping style for men at risk of cardiovascular disease. High cholesterol appears to be associated with better mental health and those who deny having hypercholesterolemia have the best mental health. The multifarious relationship between cholesterol, mental health, and denial deserves further study.
Adult↗
Effect of insulin on the venoconstrictive response to norepinephrine in normal human subjects: the influence of sodium status.
Hyperinsulinemia and insulin resistance have been implicated in the pathogenesis of essential hypertension, with alterations in insulin-induced vasodilatation as one possible mechanism. The aims of this study were to assess the local vasodilatory action of insulin on a dorsal hand vein and the influence of sodium status on the insulin effect in healthy human subjects. Distensibility of a superficial hand vein and response to norepinephrine, insulin, and nitroglycerine were measured by the linear variable differential technique. Fourteen healthy subjects were studied after a low (20 mmol) and high (200 mmol) sodium diet for 7 days. All subjects gained weight (P < .005) and had higher central venous pressure (P = .003) on a high sodium intake. Baseline mean arterial pressure, heart rate, and fasting plasma glucose levels were not significantly different between the two diets. High sodium diet, however, resulted in a higher calculated insulin/glucose ratio (P = .029) implying reduced tissue sensitivity to insulin. Baseline plasma norepinephrine was significantly higher on the low (1.29 +/- 0.13 nmol/L) compared with the high sodium diet (0.79 +/- 0.11 nmol/L) (P < .005). The dorsal hand vein was significantly more dilated at the baseline level on a low sodium (2.60 +/- 0.12 mm) than on a high sodium diet (2.20 +/- 0.12 mm) (P = .034). However, the maximal constriction achieved with norepinephrine was not significantly different between the two diets. Only an insulin dose of 0.8 mU/min on a low sodium diet was able to significantly dilate the norepinephrine preconstricted vein (77 +/- 9% of baseline diameter versus ED50) (P = .002).(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Small, blue collar work site hypertension screening: a cost-effectiveness study.
This study determined the cost-effectiveness of one- versus two-stage hypertension screening at small to medium-sized blue collar, multicultural work sites using voluntary health organization and public health unit personnel. Workers with diastolic blood pressure (DBP) > or = 90 mm Hg were randomly allocated to one- or two-stage screening with differing physician referral protocols based on blood pressure level and treatment status. At first screening of 7856 workers, 12.5% had DBP > or = 90 mm Hg or < 90 and on medication with 64% aware of having hypertension, 42% on medication and 30% controlled (DBP < 90 mm Hg). One year later, there were no significant differences in effects or cost-effectiveness between groups. Both had significant DBP decrease (8.5 mm Hg), 54% had seen a physician within the recommended time, and 50% were controlled on medication or any treatment. One-stage screening, being easier to implement, is the preferred option.
Adult↗
Abnormalities in the renal and vascular responses to LBNP in humans with early diabetes.
Plasma atrial natriuretic factor (ANF) concentrations are increased in subjects with insulin-dependent diabetes mellitus (IDDM). A potential contribution of ANF to the maintenance of abnormalities in renal hemodynamic function has been considered but not proven in human diabetic subjects. The aim of these experiments was to determine the response of renal blood flow (RBF), glomerular filtration rate (GFR), filtration fraction (FF), and urinary sodium excretion (UNaV) to a reduction of plasma ANF concentrations induced by application of nonhypotensive lower body negative pressure (LBNP) in a group of subjects with early, uncomplicated, well-controlled IDDM compared with control subjects. Baseline supine measurements before LBNP revealed the diabetic subjects to have a significantly higher plasma ANF (31 +/- 2 vs. 24 +/- 2 pg/ml, P = 0.05). GFR tended to be higher (118 +/- 11 vs. 104 +/- 9 ml/min) and UNaV tended to be depressed (188 +/- 25 vs. 240 +/- 25 mumol/min) despite equal sodium intake, but not significantly so. In addition IDDM subjects exhibited significantly lower baseline plasma norepinephrine (PNE) concentrations (0.91 +/- 0.20 vs. 1.60 +/- 0.2 nmol/l, P = 0.03). Forearm vascular resistance (FVR) was not significantly different between the two groups (29 +/- 5 vs. 33 +/- 5 units). LBNP induced comparable decreases in ANF and central venous pressure (CVP) in both groups. The anticipated renal response to ANF reduction (declines in GFR, FF, and UNaV) occurred only in the normal control group. The percent decline in GFR (11% vs. 34.5%, P = 0.01) was markedly attenuated in IDDM subjects. The expected reflexive increase in PNE and FVR also did not occur in IDDM subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Insulin blunts the natriuretic action of atrial natriuretic peptide in hypertension.
Hyperinsulinemia and insulin resistance are implicated in the etiology of hypertension, but the mechanisms involved have not been established. The objectives of this study were to determine whether untreated essential hypertensive patients are more sensitive to the antinatriuretic action of insulin and more resistant to the counteracting natriuretic effect of atrial natriuretic peptide in contrast to age- and sex-matched normotensive control subjects. Urinary sodium excretion was measured at baseline, during hyperinsulinemic euglycemic clamp, and during coadministration of insulin and atrial natriuretic peptide. Baseline urinary sodium excretion was not significantly different in the normotensive subjects (415 +/- 47 mumol/min, n = 12) and hypertensive patients (381 +/- 18 mumol/min, n = 10); with the institution of insulin infusion, there was a similar and significant decline from baseline (P < .001) to 289 +/- 35 mumol/min in normotensive subjects and 235 +/- 17 mumol/min in hypertensive patients. Atrial natriuretic peptide was able to oppose the antinatriuretic action of insulin in normotensive subjects, increasing urinary sodium excretion significantly to a mean level of 352 +/- 31 mumol/min (P < .05), which did not differ significantly from baseline. In the hypertensive group, atrial natriuretic peptide infusion had no effect on urinary sodium excretion (238 +/- 18 mumol/min), and the difference from baseline remained highly significant (P < .001). The hypertensive patients were significantly less insulin sensitive than their normotensive counterparts, as reflected by a lower glucose utilization rate and higher mean baseline plasma insulin level (P < .05 for each).(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Report of the Canadian Hypertension Society Consensus Conference: 2. Diagnosis of hypertension in adults.
OBJECTIVE: To update recommendations for the diagnosis of mild hypertension in adults and to assess the role of echocardiography, self-measurement of blood pressure and ambulatory blood pressure monitoring. DATA SOURCES: Literature reviews of previous consensus conferences were updated with searches of MEDLINE for the period Jan. 1, 1988, to Nov. 15, 1991, and supplemented by reference lists and personal files. STUDY SELECTION: Panel members selected relevant articles and rated them according to methodologic criteria. DATA EXTRACTION: The data extracted concerned the measurement of blood pressure, the diagnosis of hypertension, the treatment of mild hypertension, and the reliability and validity of echocardiography, self-measurement of blood pressure and ambulatory blood pressure monitoring in the diagnosis of mild hypertension. The recommendations made were graded according to the level of evidence available, circulated to many experts and approved at a consensus conference. MAIN RESULTS: Previous recommendations for the accurate measurement of blood pressure remain mostly unchanged. Antihypertensive treatment should be prescribed for patients (including the elderly) with an average diastolic blood pressure of at least 100 mm Hg, for those with isolated systolic hypertension (systolic blood pressure of at least 160 mm Hg and diastolic blood pressure of less than 90 mm Hg) and for patients with a diastolic blood pressure of 90 to 99 mm Hg and target-organ damage. Clinical judgement is required in treating patients with a diastolic blood pressure of 90 to 99 mm Hg without target-organ damage, and individual risk for cardiovascular disease must be taken into account. There is insufficient evidence to warrant the routine use of echocardiography, self-measurement of blood pressure or ambulatory blood pressure monitoring in diagnosis. CONCLUSIONS: Recent high-quality evidence supports several new recommendations for the diagnosis of mild hypertension in adults. Additional research is needed to determine the role of echocardiography, self-measurement of blood pressure and ambulatory blood pressure monitoring.
Adult↗
Angiotensin II modulates atrial natriuretic factor-induced natriuresis in cirrhosis with ascites.
Resistance to the natriuretic action of atrial natriuretic factor (ANF) in cirrhosis with ascites has been correlated with rising levels of antinatriuretic factors, such as renin, angiotensin II (AII), and aldosterone, as well as increased sympathetic nerve activity. To determine whether AII can serve as a mediator rather than only as a marker of the antinatriuresis, a nonpressor dose of AII (5 ng/kg/min) was given during an ANF infusion in eight patients with cirrhosis and ascites who responded to ANF infusion with a natriuresis. Patients were maintained in metabolic balance and measurements of para-aminohippuric acid, inulin, and lithium clearance were taken before and during infusion of ANF with or without AII. Atrial natriuretic factor infusion was associated with a natriuretic response accompanied by an increase in glomerular filtration rate, filtration fraction, and lithium clearance compared with baseline. The addition of AII was associated with a return of the glomerular filtration rate to baseline, with no change in filtration fraction. This was reversible on withdrawal of AII infusion. Natriuresis induced by ANF occurred despite baseline elevations of the renin angiotensin aldosterone system and was associated with an increase in distal delivery of sodium and a decrease in fractional reabsorption of distally delivered sodium as estimated by lithium clearance parameters. Angiotensin II infusion exerted effects on both proximal and distal nephron sites to abrogate ANF-induced natriuresis. These results suggest that AII may serve as a mediator as well as a marker of resistance to the natriuretic effect of ANF in patients with cirrhosis and ascites.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Atrial natriuretic peptide during acute and prolonged exercise in well-trained men.
In this study, cardiac performance and circulating immunoreactive atrial natriuretic peptide (Ir-ANP) were measured during sustained exercise to examine the relationship between cardiac filling, heart rate and circulating ANP. Fifteen well-trained male subjects (mean age = 27.6 +/- 1 years) were studied during two exercise sessions. Initially, graded exercise to maximum was performed to determine maximal oxygen consumption (VO2max). On a separate occasion subjects performed 150 minutes of continuous exercise at 70-74% of the maximal heart rate, with radionuclide angiography performed at rest and every 50 minutes, in conjunction with Ir-ANP, blood pressure and heart rate measurements. During maximal exercise subjects reached a VO2max of 47.9 +/- 2.1 ml/kg/min. Ir-ANP increased from 9.8 +/- 1.1 pg/ml at rest to 45.2 +/- 6.6 pg/ml at maximal exercise. Ir-ANP remained elevated (28.9 +/- 3.4 pg/ml) 3 minutes after exercise (p < 0.05). During prolonged exercise, left ventricular end-diastolic filling decreased significantly between 50 and 150 minutes (p < 0.05), with progressive rise in heart rate observed between 50 (141 +/- 8 beats/minute) and 150 minutes (154 +/- 3 beats/min; p < 0.05). No change in left ventricular end-systolic counts, or arterial blood pressure were observed throughout the exercise period. Ir-ANP was elevated significantly during prolonged exercise, increasing from 9.4 +/- 1.7 at rest, to 19.2 +/- 3.4 after 50 minutes, 17.8 +/- 4.3 pg/ml after 100 minutes of exercise (p < 0.05), and 23.5 +/- 2.1 pg/ml by 150 minutes of exercise. A weak correlation (r = 0.33) was observed between heart rate and Ir-ANP throughout the exercise session.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Assessment of atrial natriuretic peptide resistance in cirrhosis with head-out water immersion and atrial natriuretic peptide infusion.
The nature of sodium retention in cirrhosis complicated by ascites has been studied for the last 30 years. Resistance to the natriuretic action of atrial natriuretic peptide (ANP) may play a potential role in this sodium retention. To further evaluate this possibility, we studied 12 patients with biopsy-proven cirrhosis and ascites on 2 consecutive days after a 7-day period off diuretics while receiving a 20 mmol/day sodium restricted diet. Following a crossover design, patients underwent head-out water immersion (HWI) for 3 h and were infused with a alpha-human ANP for 2 h on 2 consecutive days. Blood and urine samples were collected hourly. Five patients displayed a natriuretic response to HWI, sufficient to achieve negative sodium balance, and these patients were termed responders. Each of these five patients also displayed a natriuretic response to ANP infusion. In contrast, the other seven patients (nonresponders) consistently failed to develop a natriuretic response to either maneuver. The two groups had similar elevations in plasma ANP concentrations, but at baseline differed in terms of plasma sodium, plasma renin activity, and serum aldosterone. Despite higher serum aldosterone concentrations, nonresponders excreted less potassium than responders during the peak effect of the interventions, suggesting greater sodium delivery to the aldosterone-sensitive nephron segment in responders. We conclude that the inability to mount an adequate sodium excretory response to HWI in patients with cirrhosis may be conveyed through increased antinatriuretic factors that decrease the sodium delivery to the medullary collecting duct and inhibit the natriuretic effect of ANP at that site.
Aldosterone↗
Atrial natriuretic factor counteracts sodium-retaining actions of insulin in normal men.
It has been hypothesized that hyperinsulinemia is causally related to hypertension by its effect on renal sodium transport. To examine the relationship between the sodium-retaining actions of insulin and atrial natriuretic factor (ANF), 16 healthy subjects were studied on three occasions, approximately 1 wk apart, using standard clearance techniques to evaluate responses during the acute administration of insulin, low-dose ANF, or both. In study 1, the euglycemic clamp was used to increase plasma insulin 10-fold to an average of 320 +/- 14 (SE) pM. This maneuver produced an immediate and persistent fall in sodium excretion from 0.315 +/- 0.02 to 0.207 +/- 0.02 mmol/min (P < 0.001) independent of change in renal hemodynamics, lithium clearance, and catecholamines. The decline in sodium excretion was associated with a marked increase in fractional distal sodium reabsorption. Systolic and diastolic pressure did not change significantly. In study 2, low-dose ANF (0.3 pmol.kg-1.min-1) designed to raise plasma levels to twice baseline was administered simultaneously in a repeat of study 1. This maneuver abolished insulin-mediated sodium reabsorption. In study 3, low-dose ANF infusion alone produced no changes in tubular handling of sodium. Our findings indicate that insulin at levels found in hyperinsulinemic states caused sodium retention and that physiological increases in plasma ANF concentration abolished the sodium-retaining action of insulin. Our findings suggest that if hypertension is causally related to hyperinsulinemia, mechanisms besides renal sodium retention are responsible for the hypertensive properties of insulin.
Adult↗
Refractory ascites in cirrhosis: roles of volume expansion and plasma atrial natriuretic factor level elevation.
Cirrhotic patients with ascites refractory to diuretics also have blunted response to marked elevations of plasma atrial natriuretic factor levels alone or to moderate intravascular volume expansion by head-out water immersion. However, these patients usually undergo natriuresis after peritoneovenous shunting. To dissect the factors responsible for this response, we studied the effects on separate days of moderate intravascular volume expansion and highly elevated plasma atrial natriuretic factor levels (head-out water immersion and atrial natriuretic factor infusion) or marked volume expansion and moderate plasma atrial natriuretic factor level elevation (head-out water immersion and albumin infusion) in 13 alcoholic cirrhotic patients with massive ascites. Three of these patients, who responded to initial head-out water immersion with a negative sodium balance, served as controls. Unresponsiveness to head-out water immersion was confirmed in the remaining 10 patients on both days on the basis of blunted natriuretic response (urinary sodium excretion < 0.8 mmol/hr after 2 hr). In contrast, these 10 refractory patients were able to achieve negative sodium balance with both combinations. Mean urinary sodium excretion increased from a baseline level of 0.13 +/- 0.10 mmol/hr to a peak level of 2.29 +/- 0.61 mmol/hr after head-out water immersion and atrial natriuretic factor infusion and from 0.10 +/- 0.3 mmol/hr to 1.61 +/- 0.62 mmol/hr after head-out water immersion and albumin infusion. Both maneuvers were associated with suppression of plasma renin activity and serum aldosterone levels. With head-out water immersion and atrial natriuretic factor infusion, we noted a significant increase in 5' cyclic GMP levels, a second messenger of atrial natriuretic factor, indicating possible activation of atrial natriuretic factor receptors at the inner medullary collecting ducts. In contrast, with head-out water immersion and albumin infusion no such increase in levels occurred, indicating that the increase in urinary sodium excretion was mainly due to increased delivery of sodium to the cortical distal nephron, as indicated by a disproportionate increase in urinary potassium excretion. In conclusion, massive (as opposed to moderate) volume expansion or greatly elevated levels of plasma atrial natriuretic factor associated with moderate volume expansion can improve blunted atrial natriuretic factor responsiveness in cirrhotic patients with refractory ascites. This appears to be achieved by way of a marked increase in distal delivery of filtrate in the kidney, with or without activation of distal atrial natriuretic factor receptors in the inner medullary collecting ducts.
Adult↗
Impaired cardiopulmonary response to exercise in moderate hypertension.
OBJECTIVE: To identify the limiting factors of exercise performance in subjects with hypertension associated with left ventricular hypertrophy. The secondary objective was to establish relationship between peripheral function and exercise capacity. DESIGN: Cardiopulmonary exercise testing was conducted using two protocols: a graded exercise test to maximal effort established maximal exercise capacity, followed by a step-incremental test combining gas-exchange measures and radionuclide angiography. The exercise responses were compared within and between groups. SETTING: All hypertensive subjects were selected from the Toronto Tri-Hospital Hypertension Clinic. Normal subjects were recruited from the surrounding community. PATIENTS: Twelve patients with established hypertension and left ventricular hypertrophy (determined by echocardiography) were studied as a referred/volunteer sample. All had no evidence of coincident diseases and were unmedicated at time of testing. A volunteer sample of normal, healthy subjects acted as a control. INTERVENTIONS: Graded exercise to maximum and step-incremental (submaximal and steady-state) exercise was used to quantify cardiopulmonary function during exercise stress. MAIN OUTCOME MEASURES: These included (for exercise performance) maximal oxygen intake (VO2max), the ventilatory anaerobic threshold, total peripheral resistance and blood lactate. Cardiac function measures included ejection fraction and ventricular volumes. RESULTS: Cardiac function data obtained during exercise in hypertensive subjects included an increase in the pressure to volume ratio, but a blunted ejection fraction response at peak exercise (P less than 0.05). Although end-diastolic volume increased during exercise (P less than 0.05), values were lower during both levels of exercise compared with normal subjects. Mean +/- SD end-systolic volume increased from 39 +/- 22 at rest to 42 +/- 23 mL during peak exercise. Hypertensive subjects had a lower VO2 max (mean 27.4 +/- 4.8 mL/kg/min) compared with normals (40.0 +/- 8.5 mL/kg/min) and a lower ventilatory anaerobic threshold (14.4 +/- 2.9 versus 27.6 +/- 5.8 mL/kg/min, P less than 0.005). Furthermore, hypertensive patients had a significantly elevated total peripheral resistance at rest (2.5 +/- 1.0 versus 1.8 +/- 0.4 peripheral resistance units) and at peak exercise (1.6 +/- 0.7 versus 0.8 +/- 0.2, P less than 0.01) compared with normal subjects (P less than 0.05). A correlation coefficient of 0.92 was found between total peripheral resistance and VO2 max in hypertensive subjects (P less than 0.01). CONCLUSIONS: These data suggest that peripheral factors, specifically a failure to reduce significantly total peripheral resistance, limits exercise performance despite a maintenance of left ventricular function during exercise in patients with moderate hypertension. The use of cardiopulmonary exercise testing can help in identifying the underlying cause of exercise intolerance in this population and limited left ventricular reserve at peak exercise, and may offer a sensitive measure of therapeutic end-points.
Adult↗
Varicella-zoster virus retinitis in patients with the acquired immunodeficiency syndrome.
We examined five patients infected with the human immunodeficiency virus who developed a rapidly progressive necrotizing retinitis characterized by early patchy choroidal and deep retinal lesions and late diffuse thickening of the retina. In all but one case, the retinitis began in the posterior pole with little or no clinical evidence of vasculitis. All five patients had relentless progression of disease and were left with atrophic and necrotic retinae, pale optic-nerve heads, and narrowed vasculature. None of the patients developed aqueous or vitreal inflammation or retinal detachment. Clinical and laboratory evidence suggested that varicella-zoster virus was the causal agent in all five cases. First, the onset of retinitis in four cases either succeeded or was coincident with an eruption of dermatomal zoster. Second, varicella-zoster virus was cultured from the two chorioretinal specimens and varicella-zoster virus antigen was detected in the vitreal aspirate from one case. Third, by means of immunocytochemistry, varicella-zoster virus antigen was found in the outer retinae of both enucleation specimens. Fourth, viral capsids with the size and shape of herpesviridae were found in the outer retinae of both enucleation specimens. The clinical features observed in this study are distinct from those described for the acute retinal necrosis syndrome and appear to constitute a new and highly characteristic pattern of varicella-zoster virus-induced disease.
Acquired Immunodeficiency Syndrome↗