Biomedical subjects
Publications and source records attributed to L Campanacci.
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The effect of chronic treatment with indapamide on blood pressure (BP), baroreceptor sensitivity (BRS) and vascular reactivity (VR) were investigated in 10 patients with essential hypertension. After 3 months of therapy with indapamide 2.5 mg/d the mean arterial pressure (MAP) had decreased from 135 +/- 6 to 112 +/- 2 mmHg (p less than 0.001); the heart rate (HR) had not changed, VR had decreased from 6.1 +/- 1.2 to 4.8 +/- 1.8 (pg . min . kg)-1 (p less than 0.05), and BRS had increased from 8.3 +/- 3.7 to 12.2 +/- 5.3 ms/mmHg (p less than 0.005), with a leftshift of the relationship between BP and heart period. An inverse correlation was found between the pre-treatment systolic blood pressure and the change in baroreceptor sensitivity after indapamide (r = 0.59; p less than 0.05). In conclusion, chronic treatment with indapamide enhances BRS and resets the reflex. The resetting may account for the lack of tachycardia at rest observed after treatment with indapamide. The mechanism by which indapamide interferes with the baroreceptor reflex requires further investigations.
1. Baroreceptor sensitivity and vascular reactivity to noradrenaline were assessed in patients with essential hypertension chronically treated with diuretics during treatment and 6-8 weeks after its withdrawal. 2. Stopping diuretics was followed by an increase in mean arterial blood pressure and vascular reactivity, while baroreceptor sensitivity decreased. 3. Baroreceptor sensitivity during treatment correlated directly with the time during which patients remained normotensive after stopping diuretics. 4. An inverse correlation was found between vascular reactivity and baroreceptor sensitivity after diuretic withdrawal and between the patients' age and baroreceptor sensitivity during diuretic therapy. 5. We conclude that the impairment of baroreceptor sensitivity after stopping diuretic therapy could result in an enhanced vascular response to noradrenaline, and a sensitive baroreflex could contribute to the control of blood pressure during diuretic treatment and buffers the return of high blood pressure when diuretics are stopped.
Evidence for muscle protein wasting and abnormal muscle metabolism is common in uremia. Muscle DNA content is considered a reliable reference standard in normal and undernourished adults. Muscle RNA content rapidly changes during starvation and refeeding. The ratio of noncollagen alkali-soluble proteins (ASP) to DNA is considered to be an estimate of the cytoplasmic volume of a single cell, and the RNA: DNA ratio is an index of the ribosomal capacity for protein synthesis. Muscle DNA, RNA, ASP, water, and fat content were determined in muscle biopsy specimens from chronically uremic patients receiving conservative treatment (CT), maintenance hemodialysis (two centers), or CAPD. Nutrient intake was low and the anthropometric indices were decreased in all groups of patients, except in the hemodialysis patients from one center. Serum proteins and muscle ASP: DNA and RNA: DNA ratios were decreased. The nutritional status was reassessed in some malnourished CAPD patients after about one year of careful nutritional advice and was unchanged. These results suggest that chronically uremic patients on CT are often malnourished, primarily because of an inadequate protein and/or energy intake. Muscle nucleic acid and protein content are useful tools for nutritional assessment at a cellular level in humans with chronic renal failure and can be used to monitor the response to nutritional therapy.
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Hypertriglyceridemia is often present in chronically uremic patients treated with maintenance hemodialysis and has been considered a risk factor in the accelerated development of atheroma. Muscle carnitine content is low in hemodialyzed patients. This abnormality may help to explain the myopathy and cardiomyopathy often observed in these subjects. In addition, carnitine might play a role in the hypertriglyceridemia in renal failure. Carnitine, which is necessary for fatty acid oxidation, has been recently reported to lower serum triglycerides in patients with type IV hyperlipoproteinemia. Carnitine was administered intravenously three times weekly at the end of hemodialysis in eight patients. Carnitine was given in 0.5 g doses for 8 weeks and then in 1.0 g doses for 6 additional weeks. There was a significant decrease in serum triglycerides at the end of treatment. In contrast, serum lipids in eight hemodialysis patients receiving placebo did not change significantly. Carnitine administration does not cause any side effect except some euphoria. These results suggest that carnitine may be effective in the treatment of hypertriglyceridemia in dialysis patients.
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The metabolic effects of an acute acetate load have been investigated in chronic uremic patients and in controls. The decay rate of blood acetate levels was significantly lower in patients than in controls. Higher levels of blood acetoacetate and 2-oxoglutarate and plasma triglycerides were observed in the patients after the load. No difference was detectable in plasma levels of unesterified fatty acids and cholesterol between the two groups of subjects. Acetate oxidation in citric acid cycle may be reduced in uremia owing to a lack of coenzyme A. These observations raise the possibility that chronic acetate administration with the dialysate induces hypertriglyceridemia and accelerates the development of atherosclerosis in hemodialysis patients.
High plasma concentrations of triglycerides and low plasma concentrations of esterified cholesterol and lysolecithin, with an impaired rate of VLDL and LDL catabolism, have been reported in chronic uremic patients. An important contribution to these abnormalitites might be an impaired activity of the (LCAT). Serum LCAT activity and cholesteryl ester clearance were determined in 11 patients with chronic renal failure and in 10 controls. LCAT activity was determined by using the serum of each patient both as a source of enzyme and as a substrate ("intrinsic" activity) and was compared with the activity determined on a standard substrate ("extrinsic activity), so as to ascertain the presence of inhibitory factors in the patients' sera. Both activityes have been found to be significantly (P less than 0.01) lower in chronic uremic patients than in controls. The cholesteryl ester clearance apparently did not respond to the stimulatory effect of hypertriglyceridemia, as observed in other cases of dislipoproteinemias. The parallel decrease of both enzyme activities makes it unlikely that it is due to the presence of "uremic toxins" inhibiting the enzyme activity. LCAT synthesis in the liver is probably reduced in chronic uremia. These results suggest that in chronic uremia the VLDL fail to cooperate in their own catabolism.
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Following a brief outline of the history of haemodialytic technique, the most relevant recent progress is illustrated. Advances include the success of the internal artero-venous fistula for access to the vessels, of "less than" single "greater than" haemodialytic units, of three-times-a-week dialysis, and the creation of new disposable dialyzers of high efficiency and low priming volume. Some of the problems posed by the patient in periodic haemodialysis are then examined (the problem involved in the risk of hepatitis, that of persistent severe anemia even after haemodialysis has been begun and that of osteopathy) and the most suitable measures for preventing or limiting these situations are presented. Finally, survival indices of patients undergoing periodic haemodialysis are examined and it is concluded that, although various clinical problems have as yet failed to find a complete solution, the patient under haemodialysis can enjoy a satisfactory state of rehabilitation to family and working life and survive even for more than ten years after the terminal phase of uraemia.
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