Renal disease. II. The treatment of minimal change nephropathy and focal segmental glomerulosclerosis

Pressure garments are the mainstay of burn scar management despite limited scientific evidence. This study demonstrates a simple method of directly measuring the cutaneous pressures generated by a pressure garment. The results show pressure garments generate an increase in subdermal pressures in the range 9-90 mmHg depending on the anatomical site. Garments over soft sites generate pressures ranging from 9 to 33 mmHg. Over bony prominences the pressures range from 47 to 90 mmHg. This method is believed to be more representative of the pressures generated than the interpositional techniques that measure garment-skin interface pressure, as it avoids garment distortion, the interference effect of the measurement device (size, conformation, area) and directly measures subdermal pressures. The method should be useful for larger research projects on pressure therapy and also for clinical management of pressure garments in the treatment of hypertrophic scar.     

Effects of alpha1-blockade on the forearm vascular resistance responses to lower body negative pressure in young borderline hypertensives

To determine whether alpha1-blockade affects the forearm vascular resistance responses to lower body negative pressure (LBNP) in borderline hypertensives, six hypertensives (HTN; mean arterial pressure [MAP] = 109.9 +/- 1.7 mm Hg, mean +/- SE) and seven normotensives (NTN; MAP = 81.5 +/- 1.4 mm Hg) underwent exposures of LBNP at pressures of -10, -20, and -40 mm Hg during systemic alpha1-receptor blockade (BLK) and during placebo (PLA). Resting forearm vascular resistance (FVR) was greater in HTN than in NTN during PLA (34.8 +/- 5.4 v 17.5 +/- 3.1 units; P < .05), but not during BLK (28.1 +/- 5.2 v 25.3 +/- 9.9 units). When expressed as a percentage of resting FVR, LBNP evoked an increased FVR (P < .001) that did not differ significantly between BLK and PLA in either group. FVR was higher (P < .001) in HTN than in NTN throughout both trials; at -40 mm Hg of LBNP during BLK, the increase in FVR was greater (P < .05) in HTN than in NTN (131 +/- 42 v 48 +/- 15%). MAP (relative to resting) was maintained throughout LBNP during PLA but, at -40 mm Hg, was lower (P < .01) during BLK for both groups. HR was elevated in BLK and was increased at -40 mm Hg (P < .01) for each group in each trial. This increase was greater during BLK (P < .05). These data suggest that borderline hypertensives have a greater vasoconstrictor response to LBNP than do normotensives and alpha1-blockade does not appear to attenuate this response.     

Right atrial and right ventricular transmural pressures in dogs and humans. Effects of the pericardium

BACKGROUND: To determine the transmural pressure-dimension relations of the right atrium (RA) and right ventricle (RV) before and after pericardiectomy, six open-chest dogs were instrumented with pericardial balloons placed over the RA and RV free walls. METHODS AND RESULTS: PA appendage dimensions and RV free-wall segment lengths were measured using sonomicrometry. Intact-pericardium RA and RV transmural pressures were calculated by subtracting the pericardial pressures (measured using balloons) from the cavitary pressures. Pooled data from six animals with pericardium intact indicate that at RA and RV cavitary pressures of 5, 10, and 15 mm Hg, RV pericardial pressure was 4.3 +/- 0.3, 8.6 +/- 1.0, and 13.3 +/- 1.5 mm Hg, respectively, and RA pericardial pressure was 4.8 +/- 0.3, 9.6 +/- 0.6, and 14.6 +/- 0.6 mm Hg, respectively (mean +/- SD). With calculated unstressed dimensions, the cavity dimension data were normalized to strain (in percent). We determined that in the dog, RV strain would increase by 14% and RA by 68% to maintain cavitary pressure at 10 mm Hg on pericardiectomy. To compare these results with clinical data, RV (n = 7) and RA (n = 6) transmural pressures were measured using balloons in patients (age, 19 to 76 years) undergoing cardiac surgery. RA transmural pressure of six patients was 1.0 +/- 1.5 mm Hg when central venous pressures (CVPs) ranged from 3 to 16 mm Hg. RV transmural pressure equaled 1.2 +/- 1.9, 2.3 +/- 1.9, and 3.4 +/- 2.0 mm Hg when CVP was 5, 10, and 15 mm Hg, respectively. CONCLUSIONS: Pericardial constraint (as evaluated by the ratio of pericardial to intracavitary pressures when CVP is 10 mm Hg) accounted for 96% of RA cavitary pressure in the dog and 89% in humans and at least 86% of RV cavitary pressure in the dog and 77% in humans.     

The cardiovascular interaction between caffeine and nicotine in humans

In a placebo-controlled, double-blind randomized design, we investigated the cardiovascular interaction between caffeine (250 mg intravenously) and nicotine (4 mg chewing gum) in 10 healthy volunteers, both under baseline conditions and during physical and mental stress (standing up and mental arithmetic). Caffeine alone induced a significant increase in blood pressure associated with a decrease in heart rate, whereas nicotine alone increased both blood pressure and heart rate. The combination of caffeine and nicotine increased systolic and diastolic blood pressure by 10.8 +/- 2.0 and 12.4 +/- 1.9 mm Hg, respectively. This pressor response did not differ significantly from the calculated additive effects of caffeine and nicotine on blood pressure, measuring 12.9 +/- 2.0 and 14.2 +/- 2.1 mm Hg, respectively. Heart rate and forearm blood flow also showed a similar response when the combination of caffeine and nicotine was compared with the calculated sum. During physical stress (standing up), blood pressure, heart rate, and plasma catecholamines increased in the placebo test. The pressor response to standing up was less pronounced after the combination of caffeine and nicotine compared with the sum of the separate effects (combination versus sum: delta diastolic blood pressure, 24.7 +/- 1.9 versus 35.2 +/- 2.6 mm Hg [p < 0.01]; delta mean arterial pressure, 22.1 +/- 2.0 mm Hg versus 28.6 +/- 1.6 mm Hg [p < 0.05]). The plasma catecholamine response did not differ between the combination and the sum of both drugs. During mental arithmetic, blood pressure, heart rate, and forearm blood flow increased in the placebo test. The forearm vasodilator response to mental stress was attenuated by the combination of caffeine and nicotine compared with the sum of both drugs (combination versus sum: delta forearm blood flow, -0.1 +/- 0.3 versus 1.4 +/- 0.5 ml/100 ml/min [p < 0.05]). We conclude that the combined administration of caffeine and nicotine shows additive effects on cardiovascular parameters during baseline conditions but less than additive effects during sympathoadrenal stimulation.     

Lycra garments designed for patients with upper limb spasticity: mechanical effects in normal subjects

OBJECTIVE: To assess the stretch of pronator muscles produced by a specifically designed upper-limb Lycra garment that could have a better acceptability than rigid splints in treating upper-limb spasticity. DESIGN: Double-blind comparison among three garments. They were designed to produce a supinating, a pronating, and no torsional force, and were individually manufactured and tested in 10 healthy volunteers. MAIN OUTCOME MEASURE: Angular position and passive rotational stiffness of the forearm were measured with and without each of the garments immediately after the garment was fitted and every hour for 6 hours. RESULTS: When put on by a trained person, the supinator garment supinated the forearm in all subjects (mean, 17 degrees; p < .01; range, 5 degrees to 44 degrees) while the pronator garment pronated the forearm in 8 of 10 subjects (mean, 5 degrees; p < .01). These effects gradually decayed over 6 hours, as garment position was not readjusted. Passive rotational stiffness of the forearm increased by about 30% with each type of garment. The garments designed to produce no torsional force exerted no intrinsic rotational effect. CONCLUSION: Individually made Lycra garments can produce continuous stretch of muscles for several hours and may be useful in the treatment of spasticity. The garments, however, must be put on by a trained person and their position adjusted when necessary.     

Transdiaphragmatic pressure gradients and the lower esophageal sphincter after tight abdominal wall plication in the rat

BACKGROUND: Gastroesophageal reflux (GER) is increasingly recognized as a complication of surgical closure of gastroschisis and omphalocele. AIM: This study tests the hypothesis that forceful abdominal wall closure reinforces the transdiaphragmatic pressure gradients that constitute the main GER-driving force and challenges the antireflux barrier. MATERIALS AND METHODS: Abdominal and esophageal pressures as well as lower esophageal sphincter pressures (LESP) and length (LESL) were measured in 17 adult rats before tight abdominal wall plication, after it, and 1 week later. RESULTS: This maneuver increased the transdiaphragmatic expiratory gradient from 0.67 +/- 1.31 to 6.97 +/- 2.68 mm Hg (P < .01) and the inspiratory gradient from 4.36 +/- 1.13 to 10.79 +/- 2.31 mm Hg (P < .01) by markedly increasing both the expiratory (from 1.47 +/- 0.74 to 9.44 +/- 1.85 mm Hg; P < .01) and inspiratory (from 0.98 +/- 0.69 to 6.83 +/- 1.55 mm Hg; P < .01) intraabdominal pressures. These changes were transient, and all pressures became normal after 1 week. The antireflux barrier functioned properly under these new conditions because both LESP and the diaphragmatic pinch-cock pressure (DPP) increased, from 20.3 +/- 3.63 to 26.5 +/- 4.31 mm Hg (P < .01) and from 16.4 +/- 7.25 to 22.5 +/- 4.36 mm Hg (P < .01), respectively, while LESL remained unchanged. CONCLUSION: Tight abdominal wall plication in the rat generates high intraabdominal pressures and thus reinforces the transdiaphragmatic pressure gradients, but these conditions elicit a healthy barrier response with sphincteric reinforcement. In addition, these changes are transient and fade out some time after operation. These facts should be taken into account for understanding the pathogenesis of GER after repair of abdominal wall defects in human babies.     

Toe pressure determination by audiophotoplethysmography

PURPOSE: The purpose of this study was to evaluate the performance of audiophotoplethysmography as a modality to measure toe pressure without the requirement of a recorder. METHOD: A portable photoplethysmograph with an audio output was used to determine toe pressures, and the results were compared with those obtained by a commercial photoplethysmograph with a recorder. RESULTS: Thirty-one measurements in control subjects and 62 measurements in patients with arterial occlusive disease were performed. The average toe pressure recorded with oscillography with standard photoplethysmography was 103.5 mm Hg +/- 14.7 SD and 95.9 mm Hg +/- 13.4 SD with audio-photoplethysmography. In the patient group the pressure recorded with a commercial photoplethysmograph was 65.3 mm Hg +/- 34.9 SD compared with 61.6 mm Hg +/- 34.8 SD obtained with audio-photoplethysmography. The difference in both groups was insignificant, and the correlation between both methods was very good. CONCLUSION: A portable hand-held photoplethysmograph equipped with an audio output was used to measure toe pressure in control subjects and in patients with arterial occlusive disease. The results have been compared with the oscillometric method by a standard commercial photoplethysmograph connected to a recorder. The correlation was very good in the control and patient groups, and the difference between both methods was below the level of statistical significance. The fact that no recorder is needed may help in introducing toe pressure measurement into everyday office diagnostic practice.     

Comparative accuracy of three automated techniques in the noninvasive estimation of central blood pressure in men

Automated devices have regularly replaced manual sphygmomanometry for the determination of blood pressure not only in homes and clinics, but also in emergency and critical care settings. Few studies exist that correctly assess the accuracy of these devices, and even fewer that specifically compare commercially available units that rely on different physiologic events for measurement. Six hundred pressure measurements were obtained from 120 subjects using 1 of 3 randomly selected blood pressure monitors. In addition, central arterial pressure measurements were obtained simultaneously and directly from the ascending aorta of each subject. Overall, these devices tended to overestimate diastolic (+2.5 mm Hg, p < 0.0001) and mean (+3.8 mm Hg, p < 0.0001) pressures, but not systolic (+0.7 mm Hg, p = NS) pressure. Compared with the other 2 devices, device I, relying on oscillometric detection, demonstrated a significantly smaller mean absolute error for diastolic pressure (4.9 +/- 3.0 vs 7.0 +/- 4.8 and 6.2 +/- 5.3 mm Hg, p < 0.0001) and mean pressure (4.0 +/- 3.2 vs 7.8 +/- 5.9 and 8.6 +/- 7.5 mm Hg, p < 0.0001), and a trend toward smaller error with systolic pressure (6.8 +/- 6.5 vs 7.3 +/- 6.8 and 8.0 +/-5.6 mm Hg, p = 0.19). Clinically significant (+/-10 mm Hg) errors were common with each device (24.8% overall), but serious (+/-20 mm Hg) errors were unusual (3.2%) and did not occur at all with device I during diastolic and mean pressure measurement. All of the devices tested could be expected to perform satisfactorily in most clinical settings provided that an average error of 4.0 to 8.6 mm Hg is tolerable. This level of accuracy typically extended throughout the range of pressures anticipated in most noncritical clinical situations. As implemented in the devices tested, noninvasive measurement by oscillometry with stepped deflation is more accurate than automated auscultation.     

A hereditary chiasmal optic neuropathy

The purpose of this study was to examine hand sensibility of surgeons wearing single and double latex gloves. Evaluation of hand sensibility, including cutaneous pressure thresholds, moving two-point discrimination, and static two-point discrimination, was performed on 25 surgeons (mean age 45 years). The dominant hand index finger was assessed with no glove, single glove, and double glove. The majority of surgeons had a moving and static two-point discrimination of 2 or 3 mm. The lowest cutaneous pressure thresholds were found when measured with no gloves and increased with single and double gloves. Statistically significant differences in cutaneous pressure thresholds using Semmes-Weinstein monofilaments were found for gloves versus no gloves (p < 0.0003) and single versus double gloves (p = 0.0003). Statistically significant differences in moving two-point discrimination were found for no gloves versus double gloves (p = 0.05) and single versus double gloves (p = 0.02). In conclusion, we found significant differences in hand sensation when measured with single and double gloves.     

Telomerase activity and microsatellite instability in colorectal cancer and adenoma

BACKGROUND AND PURPOSE: We investigated the role of actin polymerization in regulating arterial diameter in response to increasing pressure and modulating forced dilatation of cerebral arteries at pressures above the upper limit of autoregulation. METHODS: Posterior cerebral arteries (n = 12) were isolated and pressurized in a special arteriograph that allowed control of intravascular pressure and measurement of lumen diameter. Intact arteries in the absence (control) or presence of 3.0 mumol/L cytochalasin B (CB), an inhibitor of actin polymerization, were subjected to stepwise increases in pressure from 75 to 200 mm Hg. Lumen diameter was continuously recorded, as was the pressure at which forced dilatation (loss of tone) occurred. After a period of time at 200 mm Hg, pressure was returned to 75 mm Hg and the extent of tone recovery was evaluated. RESULTS: Arteries with and without CB developed a similar amount of tone during equilibration at 75 mm Hg: percent tone = 27 +/- 3% for control versus 29 +/- 4% for CB arteries (P > 0.05). However, arteries in the presence of CB could not withstand pressure as well and underwent FD at significantly lower pressures: 168 +/- 5 mm Hg for control versus 142 +/- 5 mm Hg for CB arteries (P < 0.01). The amount of tone that arteries regained after FD when pressure was returned to 75 mm Hg was also less in CB arteries: percent tone = 34 +/- 3% for control versus 11 +/- 2% for CB arteries (P < 0.01). CONCLUSIONS: Cytoskeletal integrity appears important for maintaining cerebral arterial diameter during changing intravascular pressure. In addition, the process of actin polymerization may be a significant contributor to development of myogenic tone after forced dilatation.     

Fetoplacental vascular tone during fetal circuit acidosis and acidosis with hypoxia in the ex vivo perfused human placental cotyledon

OBJECTIVES: Our purpose was to determine the effects of acidosis and acidosis-hypoxia on fetoplacental perfusion pressure and its response to angiotensin II. STUDY DESIGN: Perfused cotyledons from 14 placentas were studied with either an acidotic fetal circuit perfusate (n = 7) or an acidotic-hypoxic fetal circuit perfusate (n = 7). Each cotyledon's fetal vasculature was initially perfused under standard conditions and bolus injected with 1 x 10(-10) moles of angiotensin II. Fetoplacental perfusate was then replaced with either an acidotic medium (pH 6.90 to 7.00 and Po2 516 to 613 mm Hg) or an acidotic-hypoxic medium (pH 6.90 to 7.00 and Po2 20 to 25 mm Hg) followed by an angiotensin II injection. The vasculature was subsequently recovered with standard perfusate and again injected with angiotensin II. Perfusion pressures within each group were compared by one-way analysis of variance, and results were expressed as mean pressure +/- SEM. RESULTS: Resting fetoplacental perfusion pressure did not change when the fetal circuit perfusate was made acidotic (28 +/- 1 mm Hg vs 25 +/- 2 mm Hg) or acidotic-hypoxic (26 +/- 2 mm Hg vs 25 +/- 2 mm Hg). The maximal fetoplacental perfusion pressure achieved in response to angiotensin II did not differ with an acidotic perfusate (41 +/- 2 mm Hg vs 38 +/- 1 mm Hg) or with an acidotic-hypoxic perfusate (39 +/- 2 mm Hg vs 36 +/- 2 mm Hg). CONCLUSIONS: In the perfused placental cotyledon fetoplacental perfusion pressure and pressor response to angiotensin II are not affected by fetal circuit acidosis or acidosis-hypoxia. This suggests that neither fetal acidosis nor fetal acidosis combined with hypoxia has a direct effect on fetoplacental vascular tone.     

Blood pressure survey in a population of newborn infants

Systolic blood pressure in the arm was measured in infants at the ages of 4 to 6 days and 5 to 7 weeks by the Doppler ultrasound technique. At the age of 4 to 6 days the mean blood pressure (+/- SE of mean) in 469 sleeping infants was 70-7 +/- 0-3 mm Hg, rising at 5 to 7 weeks to 89-7 +/- 0-9 mm Hg (in 144 infants). In 252 infants awake at 5 to 7 weeks blood pressure was 96-8 +/- 0-6 mm Hg. In 391 infants in whom measurements were made on both occasions blood pressure at 4 to 6 days was significantly related to blood pressure at 5 to 7 weeks. Thus those infants with relatively high blood pressures at 4 to 6 days showed a weak tendency to have relatively high blood pressures at 5 to 7 weeks. In this trend continues with age it would suggest that the tendency to develop hypertension may already be demonstrable at the age of 4 to 6 days.     

Cytochrome P-450 inhibition blocks bone resorption in vitro and in vivo

BACKGROUND AND METHODS: To find an intra-abdominal pressure (IAP) range for laparoscopic procedures that elicits only moderate splanchnic and pulmonary hemodynamic and metabolic changes, including hepatic and intestinal tissue pH and superficial hepatic blood flow, we installed an IAP of 7 and 14 mm Hg each for 30 minutes in 10 healthy pigs (30 +/- 4 kg). RESULTS: In parallel with the increase of IAP, the mean transmural pulmonary artery pressure increased (from 25 +/- 3 to 27 +/- 4 at 7 mm Hg IAP and 30 +/- 6 mm Hg at 14 mm Hg IAP, p < 0.05); the pulmonary artery-to-pulmonary capillary wedge pressure gradient also increased (from 17 +/- 2.7 to 21 +/- 3 mm Hg at 7 mm Hg IAP and 24 +/- 4.2 mm Hg at 14 mm Hg IAP, p < 0.01), and the arterial oxygenation decreased (p < 0.005). Relevant changes at an IAP of 14 mm Hg were observed in right atrial pressure during inspiration (from 7 +/- 2 to 12 +/- 3 mm Hg, p < 0. 0001) and in abdominal aortic flow (from 1.43 +/- 0.4 to 1.19 +/- 0. 3 L/min, p < 0.01). However, transmural right atrial pressure and cardiac output remained essentially unchanged. Portal and hepatic venous pressure increased in parallel with the IAP (portal: from 12 +/- 3 to 17 +/- 3 at 7 mm Hg IAP and 22 +/- 3 mm Hg at 14 mm Hg IAP, p < 0.01; hepatic venous: from 8 +/- 3 to 14 +/- 6 at 7 mm Hg IAP and 19 +/- 6 mm Hg at 14 mm Hg IAP, p < 0.005), but the transmural portal and hepatic venous pressures decreased (p < 0.01), indicating decreased venous filling. Portal flow was maintained at 7 mm Hg but decreased at 14 mm Hg from 474 +/- 199 to 395 +/- 175 mL/min (p < 0. 01), whereas hepatic arterial flow remained stable. Hepatic superficial blood flow decreased during insufflation and increased after desufflation. Tissue pH fell together with portal and hepatic venous pH (intestinal: from 7.323 +/- 0.05 to 7.217 +/- 0.04; hepatic: from 7.259 +/- 0.04 to 7.125 +/- 0.06, both p < 0.01) at 14 mm Hg. CONCLUSION: The hemodynamic and metabolic derangement in the pulmonary and splanchnic compartments are dependent on the extent of carbon dioxide pneumoperitoneum. The effect of low IAP (7 mm Hg) on splanchnic perfusion is minimal. However, higher IAPs (14 mm Hg) decrease portal and superficial hepatic blood flow and hepatic and intestinal tissue pH.     

Porous-coated total hip arthroplasty in the young

OBJECTIVE: To evaluate whether thromboxane A2 participates in the ischemia-reperfusion injury associated with acute compartmental syndrome (ACS) and if by using a cyclooxygenase inhibitor this can be either reduced or abolished. DESIGN: To assess the role of thromboxane A2 in ACS, a tourniquet was applied for 2 hours to the hind limb of 12 dogs. Group 1 (n = 6) served as controls while group 2 (n = 6) was pretreated with lysine-acetyl-salicylate (Lysoprim). Blood thromboxane B2 levels and intracompartmental pressures were assayed prior to inflation of the tourniquet and at 5 minutes, 90 minutes, and 24, 72, and 144 hours after deflation. RESULTS: Five minutes after deflation, the compartmental pressure increased from 11.2 +/- 2.2 mm Hg to 16.1 +/- 3.3 mm Hg and 17 +/- 2.2 mm Hg (mean +/- SD) in groups 2 and 1, respectively. At 90 minutes and 24 hours, pressures were 17.1 +/- 3.3 mm Hg and 23.2 +/- 3.3 mm Hg (P<.01) and 15.3 +/- 2.6 mm Hg and 25.2 +/- 1.8 mm Hg (mean +/- SD) (P<.001), respectively, in groups 2 and 1. A similar effect, although of a lesser magnitude, was observed in the counterlateral limb. Thromboxane B2 levels increased from a mean (+/- SD) of 46 +/- 5.5 pg/0.1 mL to 132 +/- 7.5 pg/0.1 mL at 90 minutes in group 1, while remaining unchanged in group 2. CONCLUSIONS: Thromboxane A2 plays a major role in the ischemia-reperfusion injury of acute compartmental syndrome. By using a cyclooxygenase inhibitor both the levels of thromboxane and the compartmental pressures can be reduced.     

Evaluation of a pulsatile pediatric ventricular assist device in an acute right heart failure model

BACKGROUND: The development of pulsatile ventricular assist devices for children has been limited mainly by size constraints. The purpose of this study was to evaluate the MEDOS trileaflet-valved, pulsatile, pediatric right ventricular assist device (stroke volume = 9 mL) in a neonatal lamb model of acute right ventricular failure. METHODS: Right ventricular failure was induced in ten 3-week-old lambs (8.6 kg) by right ventriculotomy and disruption of the tricuspid valve. Control group 1 (n = 5) had no mechanical support whereas experimental group 2 (n = 5) had right ventricular assist device support for 6 hours. The following hemodynamic parameters were measured in all animals: heart rate and right atrial, pulmonary arterial, left atrial, and systemic arterial pressures. Cardiac output was measured by an electromagnetic flow probe placed on the pulmonary artery. RESULTS: All results are expressed as mean +/- standard deviation and analyzed by Student's t test. A p value less than 0.05 was considered statistically significant. Base-line measurements were not significantly different between groups and included systemic arterial pressure, 80.6 +/- 12.7 mm Hg; right atrial pressure, 4.6 +/- 1.6 mm Hg; mean pulmonary arterial pressure, 15.6 +/- 4.2 mm Hg; left atrial pressure, 4.8 +/- 0.8 mm Hg; and cardiac output, 1.4 +/- 0.2 L/min. Right ventricular injury produced hemodynamics compatible with right ventricular failure in both groups: mean systemic arterial pressure, 38.8 +/- 10.4 mm Hg; right atrial pressure, 16.8 +/- 2.3 mm Hg; left atrial pressure, 1.4 +/- 0.5 mm Hg; and cardiac output, 0.6 +/- 0.1 L/min. All group 1 animals died at a mean of 71.4 +/- 9.4 minutes after the operation. All group 2 animals survived the duration of study. Hemodynamic parameters were recorded at 2, 4, and 6 hours on and off pump, and were significantly improved at all time points: mean systemic arterial pressure, 68.0 +/- 13.0 mm Hg; right atrial pressure, 8.2 +/- 2.3 mm Hg; left atrial pressure, 6.4 +/- 2.1 mm Hg; and cardiac output, 1.0 +/- 0.2 L/min. CONCLUSIONS: The results demonstrate the successful creation of a right ventricular failure model and its salvage by a miniaturized, pulsatile right ventricular assist device. The small size of this device makes its use possible even in small neonates.     

Mineralocorticoid induced hypertension and noradrenaline spillover in man

This study examined haemodynamics and noradrenaline spillover in five normal men before and on day 7 of oral fludrocortisone treatment, 0.3 mg/day. Resting systolic (105 to 115 mm Hg, standard error of the difference +/- 2.0, p < 0.01) and diastolic (65 to 73 mm Hg, +/- 3.0, p < 0.05) blood pressure increased, as did cardiac output, from 5.0 to 5.7 L/min (+/- 0.1, p < 0.01). Calculated total peripheral resistance fell from 21.2 to 20.0 mm Hg/L/min (+/- 0.4, p < 0.05). Fludrocortisone produced a fall in plasma potassium, renin and aldosterone concentrations and haematocrit and a rise in body weight. Cold pressor responses were increased by fludrocortisone, from 7.5 to 20 mm Hg (+/- 3.0, p < 0.01), and forearm vascular resistance rose 12 arbitrary resistance units (R) before and 36 R units after treatment (+/- 5.0, p < 0.01). Total body spillover of noradrenaline was decreased from 9.48 to 7.36 ng/kg/min (+/- 0.86, p < 0.05). There were no changes in forearm noradrenaline spillover at rest or during cold pressor stimulation. It appears unlikely that the sympathetic nervous system plays a major role in the pathogenesis of mineralocorticoid hypertension in man.     

Effects of hypervolemia on interdialytic hemodynamics and blood pressure control in hemodialysis patients

The influence of hypervolemia on hemodynamics and interdialytic blood pressure, as well as in relation to vascular compliance, was investigated in 10 hemodialysis patients who were not receiving vasoactive medication. All subjects were studied during a relative normovolemic interdialytic period (from 1 kg below dry weight postdialytic until dry weight predialytic) and a hypervolemic interdialytic period (from 1 kg above dry weight postdialytic until 3 kg above dry weight predialytic). Interdialytic blood pressure was measured with an ambulatory blood pressure monitor. Cardiac output was echographically measured and total peripheral resistance calculated postdialytic, mid-interdialytic, and predialytic. At the same time, a blood sample was drawn for analyzing vasoactive hormones, sodium, and hematocrit. In all patients, ideal dry weight was estimated by echography of the caval vein. Arterial and venous compliance were measured with an ultrasound vessel wall movement detector system and a strain-gauge plethysmograph. After fluid load, an increase in intravascular volume, an increase in caval vein diameter and cardiac output, and a decrease in peripheral resistance was observed. No significant influence of a 3-L fluid load was found on interdialytic blood pressure course (153+/-24 mm Hg/90+/-19 mm Hg in the hypervolemic period and 146+/-27 mm Hg/89+/-22 mm Hg in the normovolemic period). Sodium and osmolality were similar in the hypervolemic and normovolemic interdialytic periods. After fluid load, a decrease in arginine vasopressin and angiotensin II was observed, which probably contributed to the decreased systemic vascular resistance. Catecholamines were not influenced by fluid load, but increased during the interdialytic period, suggesting accumulation after dialysis. Three of the 10 patients had higher systolic but not diastolic blood pressures after fluid load (159+/-13 mm Hg/81+/-22 mm Hg in the hypervolemic period and 135+/-16 mm Hg/81+/-22 mm Hg in the normovolemic period). No correlation could be found between arterial or venous compliance and blood pressure changes. We concluded that a 3-L interdialytic fluid load does not result in higher blood pressure in most hemodialysis patients.     

Propranolol in mitral stenosis during sinus rhythm

Patients with early symptomatic mitral stenosis usually suffer from pulmonary congestion on the basis of left atrial and pulmonary venous hypertension. They are often in sinus rhythm, and cardiac output is usually well maintained. Symptoms occur most often when heart rate, cardiac output, or both are increased. In this study, intravenous propranolol administered to patients with pure mitral stenosis in sinus rhythm resulted in significant reductions in mitral diastolic gradient (-7.1 mm. Hg +/- 1.6 SED), mean pulmonary wedge pressure (--6.9 mm. Hg +/- 1.2) and mean pulmonary artery pressures (--9.0 mm. Hg +/- 1.2). This was due to simultaneous reduction of heart rate (--13.0 beats/minute +/- 2.6 and cardiac output (--0.5 L./minute +/- 0.2). A small associated reduction of left ventricular systolic pressure (--5.1 mm. Hg +/- 2.6) was not accompanied by adverse clinical effects. A potential role for propranolol in medical management of pure mitral stenosis in the presence of sinus rhythm is suggested.     

Diminished venous vascular capacitance in patients with univentricular hearts after the Fontan operation

Patients who have undergone Fontan's operation are known to have impaired cardiac output response to dynamic exercise. This may be due to either poor cardiac function or a limited ability to mobilize blood from capacitance vessels due to increased resting venous tone. We tested the latter hypothesis by determining venous vascular capacitance at rest and during orthostatic stress produced by lower body negative pressure (LBNP) in 6 subjects who had undergone the Fontan operation and 6 healthy age-, sex-, height-, and weight-matched controls. Resting blood volume was similar for Fontan and control subjects (79 +/- 6 vs 70 +/- 3 ml/kg body weight, respectively), while central venous pressure (CVP) was elevated in Fontan subjects (18.4 +/- 1.0 vs 3.5 +/- 0.9 mm Hg, p < 0.05). Forearm venous capacitance at a distending pressure of 40 mm Hg was less in Fontan subjects than in controls (2.6 +/- 0.1 vs 3.9 +/- 0.5 ml/100 ml), while resting plasma norepinephrine level was elevated in Fontan subjects (255 +/- 28 vs 144 +/- 9 pg/ml, p < 0.05). The increase in calf volume (1.6 +/- 0.2 vs 2.3 +/- 0.2 ml) and decrease in CVP (-5.0 +/- 0.5 vs -6.7 +/- 1.1 mm Hg) during -30 mm Hg LBNP were smaller for Fontan than control subjects (p < 0.05). Reduced forearm venous capacitance and diminished pooling of blood into capacitance vessels of the leg during orthostatic stress indicated higher venous tone in Fontan than control subjects.(ABSTRACT TRUNCATED AT 250 WORDS)     

Oncotic pressure and edema formation in hypoalbuminemic HIV-infected patients with proteinuria

Human immunodeficiency virus nephropathy (HIVN) continues to challenge nephrologic consultative services at major urban institutions. Although noted in the literature, the decreased incidence of peripheral edema in HIVN has been unexplained to date. In HIV patients, total proteins frequently are found to be elevated due to an elevated globulin fraction. The impact that plasma proteins, specifically globulins, have on the total oncotic pressure has not been reported in HIVN, but may play a role in the paucity of edema noted in this proteinuric population. To evaluate the contributions of serum globulin to the total oncotic pressure and the presence or absence of edema in HIVN, we randomly selected 27 patients with proteinuria greater than 2.5 g/24 hr and serum albumin less than 3.1 g/dL from patients presenting to the nephrology outpatient clinic at the University of Miami/Jackson Memorial Hospital. Seventeen of the patients (63%) had a known diagnosis of HIV infection (group 1). These patients were subdivided into two subgroups: those presenting with clinically evident edema on physical examination (n = 7 [41%]; group 1A) and those who had an absence of edema (n = 10 [59%]; group 1B). Conversely, group 2 comprised 10 patients without known HIV infection, of whom six (60%) had edema (group 2A) and four (40%) did not (group 2B). Blood pressures were noted, and mean arterial pressure was calculated using standard formulas. Serum albumin, serum total proteins, and urine total proteins were measured using standard laboratory methods. Oncotic pressures for albumin (alpha), globulin (beta), and total protein (c) were calculated using the following formula: COPpl = alpha(2.8c + 0.18c2 + 0.012c3) + beta(0.9c + 0.12c2 + 0.004c3). We used Student's t-test to analyze the data. There is no significant difference between the albumin concentrations of HIV patients without edema (group 1B) and non-HIV patients with edema (group 2A), with mean concentrations of 2.3 +/- 0.1 g/dL versus 2.3 +/- 0.15 g/dL, respectively (P = NS). Group 1B, however, has a total oncotic pressure of 17.1 +/- 1.5 mm Hg, whereas both groups with edema (groups 1A and 2A) have statistically significant lower total oncotic pressures (12.1 +/- 2.3 mm Hg and 12.9 +/- 1.1 mm Hg, respectively; P < 0.05). The globulin oncotic pressures may account for some of the differences in total oncotic pressures, being significantly higher for those patients without edema in group 1B compared with group 2A (7.1 +/- 0.9 mm Hg v 3.9 +/- 0.4 mm Hg, respectively; P < 0.05). In patients with HIV, however, the presence or absence of edema is mandated by albumin concentration because both groups have similar globulin concentrations (group 1A 3.1 +/- 0.1 g/dL v group 1B 3.8 +/- 0.3 g/dL; P = NS). Mean arterial pressure does not play a role in edema formation in this study because the HIV patients without edema had the higher blood pressures (group 1B 97.8 +/- 4.7 mm Hg v group 2A 84.7 +/- 5.5 mm Hg; P < 0.05). We conclude that globulins play an important role in maintaining oncotic pressure in low albumin states. HIVN patients with increased serum immune globulin may benefit from higher globulin oncotic pressure, delaying the onset of clinical edema in the setting of proteinuria.