Plasma levels of atrial natriuretic peptide (ANP) in valve replacements under fentanyl anaesthesia.
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Biomedical subjects
Publications and source records attributed to M Minieri.
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In order to verify the hypothesis that possible interactions with the autonomic nervous system may contribute to the cardiovascular effects of atrial natriuretic factor (ANF), 9 rabbits were anesthetized to study the effect of the infusion of synthetic human ANP (2 mcg/kg in bolus followed by 0.2 mcg/kg/min for 20 min iv) on the reflex responses induced by intra-arterially injected BK (250 ng) and hypertonic NaCl (10%) or glucose (40%). The infusion of ANP provoked a decrease in systolic (SBP, 14%) and diastolic (DBP, 8%) pressure without any significant changes in heart rate (HR). The injection of BK and hypertonic NaCl into femoral arteries carried out during ANP infusion produced cardiorespiratory response patterns similar to those observed in control conditions. After injecting BK, a fall in SBP (25%), DBP (50%) and HR (16%), and an increase in breathing frequency were observed. After injecting NaCl, an increase occurred in SBP (20%), DBP (25%), HR (10%) and in depth of breathing. In the present experimental conditions, ANP has not been found to be capable of significantly interfering with the reflex pattern of cardiorespiratory responses either from the inhibition or activation of the sympathetic nervous system induced by chemical stimulation of muscle receptors.
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In this prospective, multicenter trial, 140 cirrhotic patients with no previous upper gastrointestinal bleeding and with esophageal varices endoscopically judged to be at high risk of hemorrhage were randomized to receive either sclerotherapy or conservative treatment for the prevention of first variceal bleeding. The end-points of the study were bleeding and death. Life table curves showed that prophylactic sclerotherapy significantly diminished the incidence of variceal hemorrhage (p less than 0.001) and overall mortality (p less than 0.01). Two-year cumulative bleeding rate was 18% in the sclerosis group (95% confidence interval = 10 and 31) and 57% (95% confidence interval = 40 and 72) in the control group. Two-year cumulative mortality rate was 30% (95% confidence interval = 19 and 45) in the sclerotherapy group and 56% (95% confidence interval = 39 and 72) in the controls. One patient died after hemorrhage from an ulcer secondary to sclerotherapy. Analysis by the Cox model of the factors potentially confounding or interacting with the effect of sclerotherapy suggested that sclerotherapy was more efficient in preventing first bleeding in patients with decompensated disease (Child B and C) than in those in good condition (Child A). However, the 2-year cumulative bleeding rate of untreated Child A patients was only 19%, showing how in this group the endoscopic findings were unreliable in selecting high-risk varices and explaining why after a 2-year follow-up prophylactic sclerosis did not show any benefit in such patients. We conclude that sclerotherapy can decrease the incidence of first variceal bleeding and death for a period of 2 years in cirrhotic patients with high-risk varices.
The lipid composition of different anatomic regions of 150 day-old UM-X7.1 cardiomyopathic hamster and age-matched controls (Syrian golden hamsters) was examined. Cardiomyopathic hamsters exhibit a phospholipid to protein ratio higher than healthy animals in atria, whereas the contrary is true in the other anatomic regions examined. In all tissues the cholesterol to phospholipid ratio is higher in cardiomyopathic hamster than in controls. Healthy and UM-X7.1 hamsters differ substantially as far as the percent distribution of fatty acids in total lipids is concerned, the lipids from cardiomyopathic animals accumulating fatty acids of the omega-6 series and being relatively poor in monoenoic fatty acids. The different fatty acid composition of heart lipids appears to be a consequence of a generalized disturbance of the lipid metabolism in cardiomyopathic hamsters during congestive heart failure.
The aim of this review is to provide a critical and concise discussion of present knowledge on the role of atrial natriuretic factor (ANF) in physiological as well as pathological pulmonary conditions. The lung contributes only to a small extent to the production of circulating ANF; on the other hand, the lung represents the major degrading site of the protein. Plasmatic ANF concentration increment during lung disease may therefore be due to a reduction in ANF plasma removal enzyme rather than to increased ANF production. Lung tissue shows more ANF receptor sites than any other organ. The effect of ANF on bronchial and pulmonary artery muscle lining is particularly evident. In fact ANF administration in asthmatic patients leads to bronchodilation comparable to dilation induced by salbutamol. Furthermore, elevated levels of circulating ANF seem to influence fluid redistribution through alveolar-capillary membrane leading to protein mobilization through the alveolar space. On the contrary, in the cardiomyopathic hamster ANF induces relevant guanylate cyclase activation before the animal has developed hemodynamic changes. Guanylate-cyclase activation may protect the lung through counteracting pulmonary edema formation, as shown by fluid reduction in alveolar spaces following pneumotoxic agents administration. This effect seems independent of natriuretic and hypotensive ANF effects.