[Adaptations of the heart and vessels in arterial hypertension].
Explore the source record for details and available documents.
Adaptation, Physiological↗
Biomedical subjects
A Borghetti
Publications and source records attributed to A Borghetti.
[The L-arginine-nitric oxide system: physiology, physiopathology and clinical relevance].
In this review we describe what is known about nitric oxide (NO), focusing on its clinical significance. It is now well appreciated that NO is a pivotal endogenous messenger molecule in a variety of physiological and pathophysiological processes. In the cardiovascular system NO participates in the paracrine regulation of vascular tone, body fluid homeostasis and platelet aggregation and adhesion. In the nervous system NO is a neurotransmitter that underpins several functions, including the formation of memory. In addition, NO is produced in large quantities during host defense and immunologic reactions. Perturbation in NO bioactivity has been shown to represent an important pathophysiologic mechanism underlying a number of disease states, such as atherosclerosis, hypertension, diabetes mellitus, and septic shock.
Animals↗
[The relationship between regional sympathetic activity and the onset of arterial hypertension in spontaneously hypertensive rats].
Several studies on spontaneously hypertensive rats (SHR) have demonstrated increased activity of the sympathetic nervous system (SNS). Using microdialysis, we have observed a greater release of norepinephrine (NE) into the interstitia of striated muscle, than that observed in control Wistar-Kyoto (WKY) rats in the prehypertensive phase. We confirmed these results in the subcutaneous adipose tissue where the sympathetic output controls metabolism. This study was carried out in order to evaluate SNS activity in two district tissue types conducted during both the prehypertensive phase (4-5 weeks of age) and the established hypertensive phase (15-16 weeks of age). Interstitial concentrations of NE were measured by microdialysis in striated muscle and subcutaneous adipose tissue. Two groups of rats were studied. Each group was made up of 8 subjects, SHR and WKY, males of 4-5 weeks of age with a mean body weight of 80 and 75 g respectively. Arterial systolic pressure (tail-cuff) values were 106 mmHg (standard deviation +/-8.2) in SHR and 101 mmHg (standard deviation +/-6.9) in WKY rats (NS). Two microdialysis probes were positioned in the subcutaneous fatty tissue and in the striated muscle of the parascapular region and perfused with Ringers' solution. The dialysate was collected every 30 min for 150 min and analyzed in high-performance liquid chromatography-every day. The content of NE and other catecholamines was determined. The same animals in both groups were reevaluated at 15-16 weeks of age. The mean body weight at this time was 246 g for the SHR and 289 g for the WKY rats. Arterial systolic pressure was 161 mmHg (standard deviation +/-13.3) and 108 mmHg (standard deviation +/-15.6) respectively (p < 0.01, Student's t test). Interstitial levels of NE were higher in SHR than in WKY rats in both tissues examined in the prehypertensive phase and in the established hypertensive phase. Mean NE values from subcutaneous adipose tissue in 4-5 week-old SHR were 1362.1 +/- 181.3 pg/ml compared to 479.0 +/- 162.3 pg/ml in WKY rats (p < 0.001, Student's t test). Muscle tissue NE levels in SHR were 1292.7 +/- 319.1 vs 536.3 +/- 146.7 pg/ml in WKY rats (p < 0.001, Student's t test). Values from the same rats at 15-16 weeks of age were 1405.0 +/- 148.3 pg/ml in SHR compared to 501.6 +/- 131.2 pg/ml in fatty tissue from WKY rats and 1893.7 +/- 214.6 vs 502.0 +/- 118.8 pg/ml in muscle tissue from the respective groups (p < 0.001, Student's t test). Significant differences (p < 0.01, Student's t test) were also observed in mean NE values in striated muscle tissue during the developing phase of hypertension. These findings document SNS hyperactivity in SHR when compared to WKY normotensive controls. This increase in SNS activity was observed in both the prehypertensive phase and in the established hypertensive phase indicating a complete disassociation from regional components of regulation (baroreceptor control and metabolic control), at least in the prehypertensive phase. These results may suggest as alteration in primitive sympathetic central outflow. Higher interstitial NE concentrations in the muscle tissue from SHR during the hypertensive phase compared to levels of young animals that are still normotensive, reveal an interesting pathophysiological aspect for the development of arterial hypertension.
Animals↗
[Continuous veno-venous hemofiltration in acute renal insufficiency and heart failure].
The application of intermittent renal replacement therapies in critically ill patients with both acute renal failure and heart failure is often associated with circulatory instability and refractory hypotension. We have evaluated the efficacy and safety of a continuous technique (continuous veno-venous hemofiltration-CVVH) in 7 patients (1 male, 6 females, mean age 77 +/- 4 years) referred to our intermediate care unit for oliguria, acute renal failure and NYHA functional class IV, CVVH was performed by a peristaltic pump with blood flow at 200 ml/min, controlled ultrafiltration production rate (25 ml/min), minute to minute microprocessor controlled fluid balance system, biocompatible filters, low-dose prostacyclin for the extracorporeal circuit maintenance. Non invasive evaluation of cardiac function was performed by Doppler echocardiography. A total of 673 hours of CVVH were performed, with a mean extracorporeal circuit duration of 96 +/- 26 hours/patient (range 15-134). Daily urea clearance was 32 +/- 21. A mean body weight decrease of 10% was obtained (body weight before-CVVH 64.5 +/- 6 kg vs end-CVVH 58.5 +/- 5 kg, p < 0.01, paired data Student's test) without any hemodynamic worsening; metabolic control was adequate (urea before-CVVH 251 +/- 73 mg% vs end-CVVH 117 +/- 18 mg%, p < 0.01). Hospital survival was 42% (3/7 patients). In patients with acute renal failure and severe heart failure, CVVH allows an easy control of both fluid balance and acid-base equilibrium, along with the maintenance of acceptable hemodynamic stability.
Acid-Base Equilibrium↗
Age-related changes in interstitial norepinephrine. A microdialysis study in spontaneously hypertensive rats.
This study was aimed at evaluating the time course of interstitial norepinephrine (NE) concentrations in the white adipose tissue and at assessing NE release after local perfusion with tyramine hydrochloride (TYR) in rats of different ages. Two groups of eight spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY) rats, aged 14 to 16 weeks, were studied. The same animals were reexamined at the age of 52 to 54 weeks. A soft microdialysis probe was implanted subcutaneously in the parascapular region and was perfused with Ringer solution (flow rate: 2.0 microL/min). After an equilibration period, NE levels were monitored for 120 min, following which, TYR (0.1 nmol/min) was perfused for 90 min. Dialysates from each 30 min collection period were analyzed by HPLC using electrochemical detection. At 14 to 16 weeks, SHR showed higher NE concentrations in dialysates as compared to WKY (1124.0 pg/mL v 541.4 pg/mL; P < .001) and a blunted response to TYR challenge. The net output, estimated by subtracting basal values, was 86.0 pg NE/h in SHR as compared to 212.5 pg NE/ h in WKY (P = .005). Differences in basal NE levels persisted in the same aged groups (P < .001) as well as a blunted response to TYR. The net NE output was still lower in SHR as compared to WKY (320.4 pg NE/h v 414.7 pg NE/h in WKY; P = .023). Basal levels of NE in SHR could be accounted for by either a higher amount of the neurotransmitter stored into and released from vescicles or by an increased firing rate of the sympathetic fibers. Since TYR is known to deplete axoplasmic but not vesicular NE available for neurotransmission, the response of SHR to TYR challenge is consistent with an increased turnover rate of NE. Aging was associated with an increased response to TYR in both strains, thus suggesting an age-dependent decline in turnover rates or changes in NE reuptake mechanisms.
Adipose Tissue↗
Renal effects of captopril, indomethacin and nifedipine in nephrotic patients after an oral protein load.
BACKGROUND: In this study we investigated whether the increase in proteinuria induced by an oral protein load may be prevented by the angiotensin-converting enzyme inhibitor (ACEI) captopril in patients with nephrotic syndrome, and whether the effects of captopril on renal haemodynamics and/or glomerular selectivity are comparable to those obtained with the nonsteroidal anti-inflammatory drug (NSAID) indomethacin and the calcium-channel blocker (CaCB) nifedipine. METHODS: Twelve subjects underwent the following treatments: (1) low-protein meal (0.2 g protein/kg body wt), (2) high-protein meal (1.3 g protein/kg body wt), (3) high-protein meal plus oral captopril (50 mg), (4) high-protein meal plus oral nifedipine (10 mg), (5) high-protein meal plus oral indomethacin (50 mg). Urine and blood samples were obtained after meals and tested for total protein, immunoglobulin G and albumin. GFR and renal plasma flow (RPF) were calculated from iothalamate and p-aminohippuric acid clearances respectively. RESULTS: Mean arterial pressure decreased significantly after both captopril (-4%, P = 0.001) and nifedipine (-5%, P = 0.0019). Compared with the low-protein meal, mean values of GFR and RPF increased significantly after the high-protein meal alone (+21%, P = 0.0002; +10%, P = 0.0491 respectively), and after captopril (+18%, P = 0.0025; +24%, P = 0.0034 respectively) or nifedipine administration (+30%, P = 0.0001; +21%, P = 0.0036 respectively), whereas they remained unchanged after the high-protein meal plus indomethacin administration. FF did not change significantly under the five experimental conditions. The increase in urinary protein excretion induced by the meat load (total protein +18%, P = 0.0102; albumin +26%, P = 0.0316; IgG +28%, P = 0.0203) was entirely blocked by both captopril and indomethacin, whereas it was further increased by nifedipine administration. CONCLUSIONS: Both captopril and indomethacin, but not nifedipine, are able to prevent the increase in urinary protein excretion rate following a meat meal. The antiproteinuric effect of captopril is comparable to that of indomethacin, but the renal haemodynamic changes induced by these drugs differ considerably, because the filtration capacity and the renal functional reserve were preserved by captopril and decreased by indomethacin. The reduction in systemic blood pressure following administration of both captopril and nifedipine does not account for changes in proteinuria, since, with a similar degree of blood pressure lowering, urinary protein excretion is reduced by captopril and increased by nifedipine.
Adolescent↗
Effectiveness of dietary protein augmentation associated with angiotensin-converting enzyme inhibition in the management of the nephrotic syndrome.
To determine whether the increase in proteinuria resulting from high dietary protein intake could be prevented by angiotensin-converting enzyme inhibition (ACEI), we performed paired studies on 8 nephrotic patients with normal GFR. They were fed sequential diets with a protein content of 0.8 (LPD) and 1.6 g/kg BW (HPD) each for 8 weeks. Patients on HPD received enalapril (ENAL) 10 mg/day. Despite the significant difference in protein intake, urinary protein excretion, at the end of the two dietary periods, was not statistically different. However, total serum protein and serum albumin increased significantly with HPD + ENAL treatment. The capability of ACEI to prevent the increase in proteinuria induced by HPD may be due to changes in glomerular hemodynamics, possibly mediated by changes in the activity of angiotensin II. Our study indicates that protein metabolism in nephrotic patients is better maintained with HPD + ENAL than with LPD alone.
Adolescent↗
Effect of aging on left ventricular filling in untreated hypertensive patients.
The aim of this study was to evaluate the influence of age and other clinical and echocardiographic parameters on left ventricular filling in a group of 174 untreated patients with mild to moderate hypertension (aged 20-82 years; mean 51.2 years) and in 189 age-matched normotensive subjects. All subjects underwent an echocardiographic study with pulsed Doppler evaluation of left ventricular filling. Left ventricular dimensions and indexes of systolic function were similar and within normal limits in both groups. Left ventricular filling was altered in hypertensive subjects < 65 years with a decrease of peak early velocity (peak E), an increase of peak atrial velocity (peak A) and a reduced E/A ratio. However in subjects > or = 65 years, we did not observe any differences in transmitral flow velocity pattern between hypertensive and normotensive subjects. The stepwise regression analysis showed that age alone explains up to 8% of peak E variance, 14% of peak A and 26% of E/A ratio in hypertensives, while in normotensives it explains up to 18% of peak E variance, 50% of peak A and 61% of E/A ratio. The other variables entered into the regression slightly improved the predictive power. In conclusion, age is the major independent factor affecting left ventricular filling in both groups, even if its predictive power was smaller in the hypertensive group. The similarity of diastolic filling pattern in elderly hypertensive and normotensive subjects suggests that the 'aging factor' plays an important role in influencing left ventricular filling pattern so as to mask the effect of hypertension in the elderly patients.
Adult↗
Monitoring norepinephrine levels by microdialysis in the white adipose tissue of spontaneously hypertensive rats.
1. To investigate whether microdialysis is suitable to monitor catecholamine in white adipose tissue of conscious rat and to assess eventual differences in norepinephrine (NE) interstitial levels, two groups of 12 male spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats, 14-16 weeks old, were compared. 2. A flexible microdialysis probe was implanted subcutaneously in the parascapular region, and perfused with Ringer solution (flow rate: 2.0 mu L/min). After a 20 min equilibration period, NE levels were monitored over a 120 min period; then, tyramine hydrochloride (0.1 nmol/min) was perfused for 80 min. Dialysates from each 20 min collection period were analysed by HPLC with electrochemical detection for NE. 3. Basal levels of NE (adjusted for the recovery) were higher in SHR compared to WKY (1210.0 +/- 140.5 pg/mL dialysate vs 573.3 +/- 75.8 pg/mL dialysate; P < 0.001, ANOVA). In both strains tyramine perfusion increased NE concentration in dialysates; the net (i.e. baseline subtracted) NE output was lower (76.3 pg/h, s.e.m. 22.3) in SHR compared with that shown by WKY rats (201.0 pg/h, s.e.m 18.4, P < 0.01). 4. The increased basal levels of NE observed in SHR are associated with a blunted response to tyramine challenge. Since tyramine is known to cause NE release from the cytosol but not from vesicle stores, such a blunted response is consistent with an increased turnover rate of NE or with an accelerated uptake in pre-synaptic vesicles which, together with the higher basal levels, would suggest increased noradrenergic activity.
Adipose Tissue↗
Microdialysis as a tool to assess interstitial norepinephrine levels in adipose tissue of spontaneously hypertensive rats.
The microdialysis technique was applied to the study of norepinephrine (NE) metabolism in white adipose tissue of spontaneously hypertensive (SHR, n = 6) and normotensive Wistar-Kyoto (WKY, n = 6) rats. Mean concentrations of interstitial NE were much higher in SHR as compared to WKY (mean +/- SEM: 980.9 +/- 125.6 pg/ml vs 520.7 +/- 96.1 pg/ml; p = 0.01) over the 180 min experimental period. These results are consistent with the hypothesis that sustained outflow from nerve endings of the peripheral sympathetic system may play a role in the maintenance of arterial hypertension. Owing to its low invasiveness, the microdialysis technique allows to continuously monitor NE extracellular levels in conscious and freely-moving animals.
Adipose Tissue↗
Renal effects of nifedipine and captopril in patients with essential hypertension and reduced renal reserve.
In this study we investigated the short-term effects of calcium channel blockers and angiotensin-converting enzyme inhibitors on renal hemodynamics and the urinary excretion of proteins with different relative mass in subjects with mild to moderate essential hypertension and apparently normal glomerular filtration rate but reduced renal functional reserve. Sixteen subjects underwent the following four treatments: (1) low-protein meal (0.2 g protein/kg body wt), (2) high-protein meal (1.3 g protein/kg body wt), (3) high-protein meal plus oral nifedipine (20 mg), and (4) high-protein meal plus oral captopril (50 mg). Two urine samples were obtained after meals. Blood samples were drawn at the midpoint of each 120-minute urine collection period. Urine and serum were tested for total protein, immunoglobulin G, albumin, alpha 1-microglobulin, retinol binding protein, and beta 2-microglobulin. Glomerular filtration rate and renal plasma flow were assessed by iothalamate and p-aminohippuric clearance, respectively. Compared with the high-protein meal alone, nifedipine elicited a clear-cut increase in the urinary excretion of total protein (+60%, P < .01), immunoglobulin G (+58%, P < .01), albumin (+25%, P < .05), retinol binding protein (+47%, P < .05), and beta 2-microglobulin (+52%, P < .05); captopril decreased the urinary excretion rate of immunoglobulin G (-26%, P < .05), albumin (-22%, P < .05), and beta 2-microglobulin (-34%, P < .05). The ratio between the clearances of immunoglobulin G and albumin was higher after nifedipine (+21%, P < .01) and unchanged after captopril (-9%, P = NS) compared with the high-protein meal alone.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Hypophosphatemia and phosphorus depletion in respiratory and peripheral muscles of patients with respiratory failure due to COPD.
In 22 patients (19 men, 3 women; mean [+/- SD] age, 63 +/- 6 years) with chronic obstructive pulmonary disease (COPD), phosphorus content was measured by spectrophotometric methods on muscle fragments of both peripheral (quadriceps femoris needle biopsy in 22 patients) and respiratory muscles (external intercostal muscle surgical biopsy in 14 patients). Thirty age- and sex-matched subjects were used as controls (19 for quadriceps femoris muscle biopsy and 11 for intercostal muscle biopsy). Serum phosphorus levels, as well as the main determinants of overall phosphorus metabolism (dietary intake of phosphorus and renal phosphate handling), were also obtained in all patients and control subjects. Muscle phosphorus content of both respiratory and peripheral muscles was significantly reduced in the COPD patient group, no matter what reference index was used (fat-free dry muscle weight or muscle fragment DNA content); muscle phosphorus depletion was present in about 50 percent of patients with COPD. In the same patient group, a significant relationship between muscle and serum phosphorus levels was demonstrable in the case of peripheral muscles only. No relationship was found between phosphorus content of both types of skeletal muscles and dietary phosphorus intake levels or with nutritional status, even though patients with COPD had significantly reduced anthropometric, biochemical, and immunologic indices as compared with controls. Renal phosphorus handling indices of the COPD patient group were compatible with a condition of inadequacy of the renal compensatory mechanism to hypophosphatemia and phosphorus depletion (low percent tubular reabsorption of phosphorus, low renal threshold concentration values). Our study suggests that phosphorus depletion occurs frequently in COPD, but in this clinical condition serum phosphorus levels are not representative of cellular phosphorus levels. Phosphorus depletion, which is equally severe in respiratory and peripheral muscles, could depend, at least in part, on malnutrition and a condition of renal phosphorus wasting possibly linked to some drugs commonly used in patients with COPD (xanthine derivatives, diuretics, etc).
Aged↗
Controlled clinical evaluation of the subpedicle connective tissue graft for the coverage of gingival recession.
The purpose of this study was to clinically evaluate the 1-year coverage of gingival recessions by a subpedicle connective tissue graft according to the original technique compared to untreated recessions by measuring probing sulcus depth (PSD), height of keratinized tissue (HKT), and mucogingival junction location changes. Paired gingival recessions were selected in 15 patients. In each patient, one recession was randomly assigned for treatment (test group) and the other recession was left untreated (control group) for 1 year. Surgery consisted of a connective tissue graft covered by a double papilla full thickness flap. Height of recession (HR), PSD, HKT, and cemento-enamel junction to mucogingival junction distance (CEJ-MGJ) were recorded with a calibrated probe before surgery and 1 year postoperatively. The control group showed no statistically significant differences in any of the parameters. In the test group, HR mean decreased significantly (P < 0.0006) from 3.66 mm to 1.09 mm, representing a mean root coverage of 70.5%. HKT mean increased significantly (P < 0.0006) from 1.60 mm to 4.30 mm, and PSD mean showed no statistical difference. CEJ-MGJ remained statistically unchanged. The subpedicle connective tissue graft may provide a good amount of root coverage and a substantial increase of keratinized tissue. Connective tissue grafted beneath the alveolar mucosa does not induce its transformation into keratinized gingival tissue.
Adult↗
Cryopreserved cancellous bone allograft in periodontal intraosseous defects.
The purpose of this study was to evaluate the potential of cryopreserved cancellous bone allograft (CCBA) in the treatment of intraosseous periodontal defects compared to surgical debridement alone (DEBR). Cancellous bone was procured from femur heads that had been extracted for hip prosthesis procedures and cryopreserved in liquid nitrogen (-196 degrees C) in a tissue bank. Ten patients without systemic disorders and advanced periodontal disease (at least 2 intraosseous defects) participated in this investigation. Measurements from the cemento-enamel junction were made after initial therapy for clinical attachment level; also gingival recession, probing pocket depth, plaque index, and gingival index and, at the time of surgery, alveolar crest height and osseous defect depth were measured. All measurements were repeated at 1 year-reentry. Sixteen defects were debrided and grafted (test sites) and 13 defects were debrided only (control sites). Soft tissue measurements showed no statistical differences between the 2 groups. Defect fill was significantly greater with CCBA (1.75 mm) than with DEBR (0.56 mm). Defect depth reduction was 2.06 mm for CCBA and 0.78 mm for DEBR. These values correspond to a percent-defect resolution of 60% for CCBA and 29% for DEBR. Hard tissue measurements showed significant differences between the 2 groups. CCBA seems to be effective in the short-term treatment of intraosseous periodontal defects.
Adult↗
Effects of water immersion on forearm vascular resistance in normotensive subjects.
Explore the source record for details and available documents.
Adult↗
[Pediatric oncology: results and future therapeutic perspectives].
Explore the source record for details and available documents.
Adolescent↗
Glomerular hyperfiltration in essential hypertension: hormonal aspects.
Glomerular hyperfiltration is thought to play a pivotal role in causing renal damage in essential hypertension. An increase in glomerular filtration rate can be experimentally induced by an acute oral protein load through still unclarified mechanisms, although hormonal factors have been postulated; in already hyperfiltering nephrons, the capacity to further increase glomerular filtration rate upon stimulation with an acute protein load (i.e. renal functional reserve) would conceivably be reduced, even in the presence of apparently normal renal function. The present study aimed at assessing whether renal functional reserve is preserved and/or is affected by different antihypertensive drugs in essential hypertensive patients without signs of renal function impairment; moreover, we tried to highlight changes in the plasma levels of natriuretic and antinatriuretic hormones potentially involved in the modulation of renal hemodynamics under the chosen experimental conditions. Renal hemodynamic parameters, plasma renin activity, aldosterone and atrial natriuretic factor were measured in fourteen essential hypertensives submitted to an acute oral protein load, alone or with a concomitant administration of either nifedipine or enalapril, as compared with a control carbohydrate meal. Glomerula filtration rate and renal plasma flow rose slightly but not significantly following an acute oral protein load as compared with a carbohydrate meal; no changes were noted in plasma atrial natriuretic factor levels, whereas plasma renin activity decreased. When nifedipine was administered together with the protein meal, both glomerular filtration rate and renal plasma flow increased significantly; there were also, parallel increases in plasma renin activity and atrial natriuretic factor. Administration of enalapril was associated with a decrease in both glomerular filtration rate and renal plasma flow; plasma renin activity showed an expected marked rise, whereas the plasma levels of atrial natriuretic factor were only slightly but not significantly reduced and plasma aldosterone fell. In conclusion, our data suggest that in our patients renal functional reserve was blunted. Clear-cut hyperfiltration was brought about by administration of nifedipine together with a protein meal, whereas enalapril completely abolished even the small increase in glomerular filtration rate seen after protein meal alone. The concomitant alterations in plasma renin activity, aldosterone and atrial natriuretic factor seemed to play no major role in the determinism of the observed renal hemodynamic changes.
Adult↗
Histologic case reports of coralline hydroxyapatite grafts placed in human intraosseous lesions: results 6 to 36 months postimplantation.
Four intrabony lesions from four patients were studied. Presurgical measurements included clinical attachment level, degree of recession, probing pocket depth, Plaque Index, Gingival Index, and Sulcular Bleeding Index. These measurements were also taken at 6-month intervals after surgery. Surgery involved exposing the intrabony defects by a papillary preservation technique, planing, and placing blocks of coralline hydroxyapatite. Three biopsy specimens and one block section were removed from the treated lesions at various periods ranging from 6 to 36 months. Clinical and histologic observation provided evidence of osteogenesis around and through the coralline hydroxyapatite.
Adult↗