High-dose angiotensin-converting enzyme inhibition restores body fluid homeostasis in heart-transplant recipients.
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OBJECTIVES: We tested the hypothesis that salt and fluid retention in heart-transplant recipients (HTRs) is caused by a failure to reflexively suppress the renin-angiotensin-aldosterone system (RAAS). BACKGROUND: It is known that extracellular fluid volume is expanded (12% to 15%) in HTRs who develop hypertension. METHODS: Responses to volume expansion were measured in eight HTRs (ages 57 +/- 6 years) and six liver-transplant recipients (LTRs) (ages 52 +/- 2 years) both before and after treatment with captopril (225 mg/day). After three days of a standardized diet, 0.154 mol/l saline was infused at 8 ml/kg/h for 4 h. Blood pressure, hormones, and renal function were monitored for 48 h. After four months, the same subjects received captopril (225 mg/day), and the protocol was repeated. RESULTS: Before captopril, saline infusion suppressed the RAAS in LTRs but not in HTRs, resulting in elimination of 86 +/- 12% versus 50 +/- 11% of the sodium load by 48-h postinfusion. Blood pressure increased only in the HTRs (+16 +/- 5/9 +/- 3 mm Hg) and remained elevated for 48 h (p < or = 0.05). After captopril, sodium elimination was comparable in the liver (87 +/- 13%) and heart groups (86 +/- 12%) and blood pressure did not change in either group. CONCLUSIONS; Heart transplant recipients have blunted diuretic and natriuretic responses to volume expansion that is mediated by their inability to suppress the RAAS. Pharmacologic suppression of the RAAS normalized defects in blood pressure and fluid homeostasis. These findings indicate that hypertension in HTRs is caused, in part, by a failure to reflexively suppress the RAAS when these patients become hypervolemic. (+info)
Fluid status in CAPD patients is related to peritoneal transport and residual renal function: evidence from a longitudinal study.
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BACKGROUND: Both peritoneal transport characteristics as well as residual renal function are related to outcome in patients treated with continuous ambulatory peritoneal dialysis (CAPD). It has been suggested that part of this relationship might be explained by an effect of both parameters on the fluid state in CAPD patients or by the relationship between inflammation and peritoneal transport. METHODS: In the present study, the relationship between fluid state [extracellular water (ECW) (sodium bromide); total body water (TBW) (deuterium oxide)] with peritoneal transport characteristics (2.27% glucose dialysate/plasma creatinine [D/P (creat)] ratio), residual renal function (residual glomerular filtration rate [rGFR] by urine collection) and C-reactive protein (CRP) was assessed in 37 CAPD patients in a cross-sectional and longitudinal design, with 25 patients completing the study. RESULTS: In the cross-sectional part ECW, corrected for height (ECW:height), was inversely related to rGFR (r=-0.40, P=0.016), whereas during the longitudinal part, D/P[creat] was related to the change in ECW (r=0.40, P=0.05). Neither D/P[creat] nor rGFR were related to CRP, whereas a significant relationship was observed between ECW:height and CRP (r=0.58, P=0.0001). Patients were dichotomized according to rGFR (<2 or >2 ml/min). Despite a higher daily peritoneal glucose prescription (216.3+/-60.0 vs 156.5+/-53.0 g/24 h; P=0.004) and peritoneal ultrafiltration volume (1856+/-644 vs 658+/-781 ml/24 h, respectively; P=0.0001), the patients with a rGFR <2 ml/min showed a higher ECW:height compared with the group with rGFR >2 ml/min (12.5+/-3.8 vs 9.2+/-2.2 l/m, respectively; P=0.003). Results for TBW were comparable. CONCLUSION: Fluid state was significantly related to peritoneal transport characteristics and rGFR. The larger ECW:height in CAPD patients with a negligible rGFR existed despite a higher peritoneal ultrafiltration volume and higher peritoneal glucose prescription. These findings raise doubts as to whether fluid state in CAPD patients with a diminished rGFR can be adequately controlled on standard glucose solutions without an additional sodium and fluid restriction. The preliminary finding of a relationship between CRP and fluid state might suggest a relationship between overhydration and inflammation. (+info)
Diagnosis and treatment of diabetic ketoacidosis and the hyperglycemic hyperosmolar state.
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Diabetic ketoacidosis and the hyperglycemic hyperosmolar state are the most serious complications of diabetic decompensation and remain associated with excess mortality. Insulin deficiency is the main underlying abnormality. Associated with elevated levels of counterregulatory hormones, insulin deficiency can trigger hepatic glucose production and reduced glucose uptake, resulting in hyperglycemia, and can also stimulate lipolysis and ketogenesis, resulting in ketoacidosis. Both hyperglycemia and hyperketonemia will induce osmotic diuresis, which leads to dehydration. Clinical diagnosis is based on the finding of dehydration along with high capillary glucose levels with or without ketones in the urine or plasma. The diagnosis is confirmed by the blood pH, serum bicarbonate level and serum osmolality. Treatment consists of adequate correction of the dehydration, hyperglycemia, ketoacidosis and electrolyte deficits. (+info)
Abnormal ion and water composition of veins and normotensive arteries in coarctation hypertension in rats.
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We examined the water, sodium, and potassium composition of the thoracic aorta, abdominal aorta (plus iliac arteries), and veins (vena cava and portal vein) from rats with aortic coarctation. The aortas of 10 rats (group A) were coarcted above the renal arteries to produce hypertension. Control groups consisted of 10 rats sham-coarcted above and 10 rats coarcted below the renal arteries. In group A rats heart weights and carotid artery pressures were elevated over controls (P less than 0.01), whereas there were no significant differences in femoral arterial pressures. In group A rats both the hypertensive thoracic aorta and the normotensive abdominal aorta contained about 20% more water per unit of wet weight, and about 35% and 60% more sodium and potassium, respectively, per unit of dry weight than did the corresponding portions of aorta from control rats (P less than 0.01). In group A rats water (P less than 0.01), sodium (P less than 0.02), and potassium (P less than 0.05) contents of veins also were increased. There were no significant correlations between level of carotid arterial pressure and magnitude of changes in arterial and venous composition, nor were there significant differences between the magnitude of changes in the normotensive and hypertensive portions of the aorta. These results indicate that in rats abnormalities in vascular wall salt and water content are not necessarily a direct effect of the elevated pressure in hypertension. (+info)
Changes in renal medullary transport proteins during uncontrolled diabetes mellitus in rats.
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We tested whether the abundance of transport proteins involved in the urinary concentrating mechanism was altered in rats with uncontrolled diabetes mellitus (DM). Rats were injected with streptozotocin and killed 5, 10, 14, or 20 days later. Blood glucose in DM rats was 300-450 mg/dl (control: 70-130 mg/dl). Urine volume increased in DM rats from 41 +/- 7 ml/100 g body wt (BW) at 5 days to 69 +/- 3 ml/100 g BW at 20 days (control: 9 +/- 1). Urine osmolality of DM rats decreased at 5 days DM and remained low at 20 days. UT-A1 urea transporter protein in the inner medullary (IM) tip was 55% of control in 5-day DM rats but increased to 170, 220, and 280% at 10, 14, and 20 days DM, respectively, due to an increase in the 117-kDa glycoprotein form. UT-A1 in the IM base was increased to 325% of control at 5 days DM with no further increase at 20 days. Aquaporin-2 (AQP2) increased to 290% in the IM base at 5 days DM and 150% in the IM tip at 10 days; both showed no further increase at 20 days. NKCC2/BSC1 increased to 240% in outer medulla at 20 days DM, but not at 5 or 10 days. UT-B and ROMK were unchanged at any time point. The increases in UT-A1, AQP2, and NKCC2/BSC1 proteins during uncontrolled DM would tend to limit the loss of fluid and solute during uncontrolled diabetes. (+info)
Influence of fluid status on techniques used to assess body composition in peritoneal dialysis patients.
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OBJECTIVE: A reliable assessment of nutritional state in peritoneal dialysis (PD) patients is of great importance. Nevertheless, techniques used to assess body composition in patients on PD may be affected by abnormalities in fluid status. The primary aim of the present study was to compare different techniques used to evaluate body composition and to assess the influence of fluid status on the assessment of body composition. The secondary aim was to assess the relevance of handgrip muscle strength in the nutritional evaluation of the patient. METHODS: In 40 PD patients, dual-energy x-ray absorptiometry (DEXA), multifrequency bioimpedance analysis (MF-BIA), and anthropometry were compared with respect to the evaluation of body composition [fat mass and lean body mass (LBM; by DEXA), and fat-free mass (FFM; by MF-BIA, anthropometry]. The influence of fluid status on the measurement of LBM/FFM by the various techniques was assessed by their relation to left ventricular end-diastolic diameter (LVEDD), assessed by echocardiography, and by estimating the ratio between extracellular water (ECW) and total body water (TBW), assessed by bromide and deuterium dilution, with LBM (DEXA). The relevance of handgrip muscle strength as a nutritional parameter was assessed by its relation to LBM and other nutritional parameters. RESULTS: Despite highly significant correlations, wide limits of agreement between the various techniques were present with respect to assessment of body composition (expressed as % body weight) and were most pronounced for anthropometry: LBM (DEXA) - FFM (MF-BIA) = 3.4% +/- 12.2%; LBM (DEXA) - FFM (anthropometry) = -5.7% +/- 7.8%; fat mass (DEXA - MF-BIA) = -4.2% +/- 7.9%; fat mass (DEXA - anthropometry) = 2.9% +/- 7.2%. The ratio between ECW and LBM (DEXA) was 0.36 +/- 0.08 L/kg (range 0.25 - 0.67 L/kg), and the ratio between TBW and LBM was 0.75 +/- 0.06 L/kg (range 0.63 - 0.86 L/kg), which shows the variability in hydration state of LBM/FFM between individual patients. LBM/FFM measured by all three techniques was significantly related to LVEDD, suggesting an important influence of hydration state on this parameter. Handgrip muscle strength was significantly related to LBM/FFM, as measured by all three techniques, but not to other nutritional parameters. CONCLUSION: Wide limits of agreement were found between various techniques used to assess body composition in PD patients. The assessment of body composition was strongly influenced by hydration state. The handgrip test is related to body composition, but not to other nutritional parameters. (+info)
Osmotic regulation of estrogen receptor-beta in rat vasopressin and oxytocin neurons.
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The vasopressin (VP) magnocellular neurosecretory cells (MNCs) in the supraoptic and paraventricular (PVN) nuclei are regulated by estrogen and exhibit robust expression of estrogen receptor (ER)-beta. In contrast, only approximately 7.5% of oxytocin (OT) MNCs express ER-beta. We examined the osmotic regulation of ER-beta mRNA expression in MNCs using quantitative in situ hybridization histochemistry. Hyper-osmolality induced via 2% hypertonic saline ingestion significantly decreased, whereas sustained hypo-osmolality induced via d-d-arginine VP and liquid diet increased ER-beta mRNA expression in MNCs (p < 0.05). Thus, the expression of ER-beta mRNA correlated inversely with changes in plasma osmolality. Because hyper-osmolality is a potent stimulus for VP and OT release, this suggests an inhibitory role for ER-beta in MNCs. Immunocytochemistry demonstrated that the decrease in ER-beta mRNA was translated into depletion of receptor protein content in hyper-osmotic animals. Numerous MNCs were positive for ER-beta in control animals, but they were virtually devoid of ER-beta-immunoreactivity (IR) in hyper-osmotic animals. The osmotically induced decrease in ER-beta expression was selective for MNCs because ER-beta-IR remained unaltered in PVN parvocellular neurons. Plasma estradiol and testosterone were not correlated with ER-beta mRNA expression after osmotic manipulation, suggesting that ER-beta expression was not driven by ligand availability. Expression of FOS-IR in MNCs with attenuated ER-beta-IR, and the absence of FOS-IR in parvocellular neurons that retain ER-beta-IR suggest a role for neuronal activation in the regulation of ER-beta expression in MNCs. Thus, osmotic modulation of ER-beta expression in MNCs may augment or attenuate an inhibitory effect of gonadal steroids on VP release. (+info)
Life threatening ventricular arrhythmias with transient or correctable causes.
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Traditionally, myocardial ischemia, electrolyte disorders, and proarrhythmic drug reactions have been considered transient and correctable causes of life threatening ventricular tachyarrhythmias. Recent evidence suggests that patients whose ventricular tachyarrhythmias are attributed to these "causes" have a poor outcome. This overview reviews the available literature examining ischemia, electrolyte disorders and pro-arrhythmic drug reactions as potentially reversible causes of ventricular tachycardia (VT) and ventricular fibrillation (VF). While all 3 are undoubtedly involved in the genesis of these tachyarrhythmias, and all 3 deserve particular clinical attention (outlined in the text), difficulties in the identification and/or reversal of their influences exist. Proarrhythmic drug reaction may be a reversible cause of VT/VF, hypokalemia and hypomagnesemia should be considered risk factors for VT/VF, and the role of ischemia is complex. Accordingly, physicians should use extreme caution in attributing life-threatening ventricular tachyarrhythmias to these 3 conditions. Further research is required to identify "truly reversible" causes of VT/VF. (+info)