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Biomedical subjects

A Stella

Publications and source records attributed to A Stella.

At least 91 records · Page 5Linked to original sources

Analysis of the dynamics of renal vascular resistance and urine flow rate in the cat following electrical stimulation of the renal nerves.

In ten sino aortic denervated, vagotomized and aneasthetized cats, renal efferent nerves were stimulated for 30 s with trains of constant current pulses at frequencies in the range 5-30 Hz. The arterial pressure, heart rate, urine flow rate (electronic drop counter) and renal blood flow (electromagnetic technique) were recorded. Subsequent computer processing gave the true means of renal artery pressure (MRAP) and renal blood flow (MRBF) and hence the renal vascular resistance (MRVR), over each cardiac cycle. Recovery of MRVR after the end of stimulation exhibited two distinct time constants. The fast component had a time constant of 2.03 +/- 0.26 s and represented 60.2 +/- 1.71% of the recovery. The time constant of the slower component was 14.1 +/- 1.9 s and represented 36.0 +/- 1.6% of the recovery. The relationship between MRVR and stimulus frequency was sigmoidal with maximum sensitivity at stimulus frequencies of 12.6 +/- 0.76 Hz. Changes in urine flow rate, in contrast, followed a hyperbolic function with maximum response sensitivity occurring at very low stimulus frequencies. Changes in urine flow rate were 50% complete at stimulus frequencies of 5 Hz. Identification of two distinct components in the relaxation phase of renal vascular resistance leads to a reasonable hypothesis that 60% of total renal vascular resistance may lie proximal to the glomerulus, whereas 36% may be accounted for by the efferent arterioles.

Anesthesia↗

Excretory responses to renal nerve stimulation during inhibition of neutral metalloendopeptidase and angiotensin-converting enzyme in the rat.

To evaluate the interaction between renal nerves, the atrial natriuretic peptide (ANP), and the renin-angiotensin system (RAS), electrical stimulation of renal nerves was performed in spontaneously hypertensive rats (SHR) and in their normotensive controls, Wistar Kyoto rats (WKY), before and after pharmacologic treatment with (a) a neutral endopeptidase inhibitor (NEP-i) to enhance the intrarenal ANP activity; (b) an ACE inhibitor (ACE-i) to block RAS; (c) both NEP-i and ACE-i; and (d) the vehicle of the drugs. Renal nerve stimulation did not change arterial pressure (AP) but reduced renal blood flow (RBF), glomerular filtration rate (GFR), and urinary sodium excretion (UNa+V) in both WKY and SHR. NEP-i treatment in WKY and SHR had no systemic or renal hemodynamic effects but increased GFR and urinary cyclic guanosine monophosphate (GMP) excretion; UNa+V increased (+2.78 +/- 0.31 microEq/min) in WKY, whereas it did not change in SHR (+0.83 +/- 0.79 microEq/min). In both strains, ACE-i treatment reduced AP, increased RBF, and did not change GFR and UNa+V. The combined treatment with NEP-i and ACE-i did not modify the natriuretic effect observed in NEP-i treated WKY (+4.29 +/- 1.25 microEq/min), but it elicited a natriuretic effect in SHR (+3.98 +/- 1.29 microEq/min). Pharmacologic treatment did not change the hemodynamic and excretory responses to renal nerve stimulation in both WKY and SHR. In conclusion, NEP-i treatment increased UNa+V in normotensive rats without changing AP. In hypertensive rats, the natriuretic effect of NEP-i became evident only after block of RAS by ACE-i. Neither NEP-i nor ACE-i, even in combination, could modify the renal responses to sympathetic stimulation.

Angiotensin-Converting Enzyme Inhibitors↗

Clinical findings in a family with familial adenomatous polyposis and a missense mutation of the adenomatous polyposis coli gene.

BACKGROUND: More than 100 different mutations in the adenomatous polyposis coli (APC) gene have been identified; virtually all lead to the production of a truncated protein. Clinical details of patients with missense mutations undoubtedly cosegregating with the disease have not been reported and may be relevant in understanding the APC protein function. METHODS: In one family with familial adenomatous polyposis (FAP) the APC gene was analyzed by SSCP and sequencing of the aberrant SSCP band. RESULTS: A missense mutation in exon 15 at nucleotide 4921 segregating with the disease was observed. This predicts a tryptophan instead of an arginine at amino acid 1641 of the APC protein. No such mutation was present in 100 control subjects. CONCLUSIONS: In this family the colonic manifestations are as expected for classical FAP. However, the occurrence of congenital hypertrophy of the retinal pigment epithelium is unusual, owing to the inconsistency of this manifestation between family members and because congenital hypertrophy of the retinal pigment epithelium is generally absent when mutations are after codon 1387.

Adenomatous Polyposis Coli↗

Functional evidence of inhibitory reno-renal reflexes in spontaneously hypertensive rats.

The experiments were performed to study the role of the renal nerves and the reno-renal reflexes in the control of water and sodium excretion in spontaneously hypertensive rats (SHR) compared to their normotensive controls, Wistar Kyoto (WKY) rats. Unilateral renal denervation in anaesthetized animals produced a slight, progressive decrease in arterial pressure in both WKY and SHR rats. The glomerular filtration rate temporarily increased in the kidney that underwent the denervation in the SHR group only. After unilateral renal denervation a sharp increase in water and sodium excretion from the ipsilateral kidney was observed in both WKY and SHR. One hour after the denervation, the percent changes in water and sodium excretion were smaller in WKY (+32 +/- 19% and +24 +/- 17%) than in SHR rats (+84 +/- 15% and +93 +/- 20%). In the kidney contralateral to the denervation a reduction in water and sodium excretion was observed and this reduction was prompter in SHR than in WKY rats. One hour after the denervation, the percent changes in water and sodium excretion were similar in WKY (-21 +/- 8% and -18 +/- 7%) and SHR (-19 +/- 6% and -19 +/- 7%). In control groups, sham denervation did not cause significant changes in glomerular filtration rate, and urinary water and sodium excretion. Arterial pressure slightly and progressively decreased in both control groups. Electrical stimulation of the efferent renal nerves performed in WKY and SHR produced similar decreases in renal blood flow, glomerular filtration rate, and water and sodium excretion in the two groups for the same frequencies of stimulation. As this finding indicates that renal targets in hypertensive rats are normally responsive to the neural drive, our data demonstrate that renal responses to unilateral renal denervation in hypertensive rats are equal to the responses observed in normotensive rats. Our results indicate that tonically active inhibitory renorenal reflexes normally operate in spontaneously hypertensive rats.

Animals↗

Coagulation and plasma fibronectin parameters in HELLP syndrome.

OBJECTIVES: HELLP syndrome (hemolysis, elevated liver enzymes and low platelets) has a high fetal mortality and maternal morbidity, partly due to its late diagnosis. In order to facilitate earlier diagnosis, we studied the changes occurring in natural coagulation inhibitors, fibronectin and haptoglobin as potential early markers of endothelial damage, coagulation cascade activation and intravascular hemolysis. METHODS: The study compared antithrombin (AT-III), protein C and S activity, plasma fibronectin, 'prothrombin time' and 'partial prothrombin time' (AST, ALT), lactate dehydrogenase (LDH), bilirubin and serum haptoglobin in 17 asymptomatic controls, 19 preeclampsia patients and 11 HELLP syndrome patients. RESULTS: HELLP syndrome patients had higher fibronectin and D-dimer values, lower AT-III and protein C activity, a lower platelet count and higher LDH than healthy controls; only 25% had raised bilirubin. Serum haptoglobin was lower in HELLP syndrome. CONCLUSIONS: Early on in HELLP syndrome, there is probably a pro-coagulatory imbalance in the placental microcirculation. Endothelial damage causes tissue thromboplastin release and coagulation cascade activation due to collagen exposure; the vascular lesion increases thromboplastin in the bloodstream and triggers distant coagulation processes, suggesting compensated disseminated intravascular coagulopathy. Measuring plasma fibronectin and coagulation inhibitors should be supported by testing haptoglobin as a marker of intravessel hemolysis to differentiate conventional preeclampsia from HELLP.

Adult↗

The morphology of elastin in non-specific and inflammatory abdominal aortic aneurysms. A comparative transmission, scanning and immunoelectronmicroscopy study.

The maintenance of the mechanical properties of the vessels results from the correct arrangement of smooth muscle cells and extracellular fibrous proteins (elastin and collagen) in their wall. The morphology of extracellular matrix modifications, particularly of elastin, was investigated in inflammatory (IA) and non specific (NSA) abdominal aortic aneurysms by scanning (SEM), transmission (TEM) and immunoelectron microscopy. Both NSAs and IAs were significantly characterized by extensive extracellular matrix remodelling, including different patterns of elastin degradation. Elastic and collagen fibres distribution appeared to be extensively altered in IAs, while it conformed more to a normal pattern in NSAs. With respect to NSAs, the morphology of elastic fibres in IAs was modified to such an extent that their identification by TEM had a rely on immunocytochemical methods and by SEM on back-scattered electron analysis. The observed ultrastructural changes are indicative of the central role of extracellular matrix modifications in the pathogenesis of IAs and NSAs.

Aortic Aneurysm, Abdominal↗

Effects of adenosine-receptor agonists on renin release in anaesthetized rats.

OBJECTIVE: To investigate the effects of the interaction between adenosine receptors and renal nerves on renin release. MATERIALS AND METHODS: The effects on renin secretion of A1 (2-chloro-N6-cyclopentiladenosine) and A2 (2-hexynil-5'-N-ethyl-carboxamido-adenosine) adenosine-receptor agonists were studied in two groups of anaesthetized rats, each with one kidney surgically denervated. Arterial blood pressure and the renal blood flow of innervated and denervated kidneys were continuously recorded. Cannulae were inserted into both renal veins through femoral veins. After 1h of rest, A1 and A2 agonists were intravenously infused for 30 min in the two groups of rats. Plasma renin activity was measured by radioimmunoassay in blood samples drawn simultaneously from both renal veins and the femoral artery before and after the drug infusion. RESULTS: Infusions of A1 and A2 agonists produced comparable hypotensive effects. During A1 agonist administration, the heart rate decreased significantly, but it did not change after A2 agonist treatment. Renal blood flow was reduced by administration of the A1 agonist in both kidneys, while A2 agonist administration significantly reduced the renal blood flow of the innervated kidney only. The veno-arterial difference in plasma renin activity decreased after the A1 agonist infusion in both kidneys, but after the A2 agonist infusion it increased significantly in the innervated kidney only. CONCLUSIONS: Renal nerves do not influence the inhibition of renin release mediated by A1 adenosine receptors. In vivo, A2-receptor agonist administration can stimulate renin release only in the presence of intact renal nerves.

Adenosine↗

Clotting inhibitors and fibronectin as potential markers in preeclampsia.

OBJECTIVES: As conventional laboratory tests fail to identify early preeclampsia, the aim of this study was to seek a marker of endothelial injury and select more sensitive tests for monitoring the activation of the coagulation cascade. METHODS: Using routine blood sampling methods, PT, PTT, AT-III, proteins C and S, platelets, fibrinogen and fibronectin were measured in 18 preeclamptic patients and 17 controls with a normal pregnancy. RESULTS: Preeclampsia was associated with higher fibronectin and lower AT-III, protein C and protein S. The platelet count, fibrinogen and PT were similar. PTT was longer in preeclampsia. CONCLUSION: As AT-III revealed compensated coagulopathy and fibronectin demonstrated preeclamptic vascular lesions before these were apparent from routine tests, measuring these elements could contribute to the earlier diagnosis and better treatment of chronically-altered coagulation in preeclampsia.

Antithrombin III↗

Morphology of small aneurysms: definition and impact on risk of rupture.

BACKGROUND: Parietal characteristics of small aortic aneurysms predictive of increased risk of rupture are unknown. METHODS: Prospective morphologic evaluation was performed in 135 consecutive cases of small (< 5 cm) abdominal aortic aneurysm. Twelve cases (9%) were found to be ruptured and sent for emergency surgery. The remaining 123 patients were evaluated with ultrasonography, angiography, and intraoperatively during elective surgery. Ninety-six (78%) also underwent computerized tomography (CT) scanning. The evaluation assessed the thickness of the endoluminal thrombus and arterial wall as well as the presence of saccular outpouchings ("blisters"). Also noted were any areas of impending rupture, defined as discontinuity of the arterial wall with only a thrombus preventing rupture. RESULTS: Blisters were discovered intraoperatively in 12 aneurysms. Digital subtraction angiography (DSA) revealed 3 (25%) of these preoperatively. Eleven of the patients with blisters were examined preoperatively with CT scanning, which detected 3 blisters (27%). Both endoluminal thrombus and wall thickness were measurable by CT scan but not ultrasonography. The incidence of impending rupture was significantly greater in patients with blisters than in those without (71% versus 29%, P = 0.0001). The incidence of impending rupture was similar whether the amount of endoluminal thrombus was more or less than 2 cm (57% versus 40%, P = 0.386). Rupture was no more frequent when aneurysmal walls were thicker or thinner than 0.3 cm (14% versus 20%, P = 0.719). In an analysis using logistic regression, the presence of a blister was the only independent morphologic predictor of impending rupture (P = 0.001, Wald = 15). CONCLUSION: In patients with small aneurysms, increased attention should be directed to the preoperative detection of blisters.

Aged↗

Left-side inferior vena cava and inflammatory abdominal aortic aneurysms: a case report.

The incidence of isolated left-side inferior vena cava ranges from 0.2-0.5%. This anomaly is associated infrequently with an abdominal aortic aneurysm. A case is reported of left-side inferior vena cava associated with a symptomatic, 5-cm inflammatory abdominal aortic aneurysm. Preoperative computed tomography showed a perianeurysmal mantle strongly adherent to a left-side inferior vena cava. This report is the first of an infrarenal inferior vena cava anomaly associated with an inflammatory abdominal aortic aneurysm. The technical details required to perform the aortic reconstruction via a transperitoneal approach are described and discussed.

Aortic Aneurysm, Abdominal↗

Long-term cryopreservation of autologous veins in rabbits.

This study was undertaken to determine the effect of long-term cryopreservation on graft ultrastructure and endothelial cell viability in an animal model. The jugular veins from 12 New Zealand White rabbits were excised with a 'no-touch' technique and divided into four groups: control group (fresh veins); group 1, veins cryopreserved for 1 month; group 2, veins cryopreserved for 2 months; and group 3, veins cryopreserved for 3 months. Cryopreservation was accomplished by rapid freezing (-5 degrees C s-1 to -196 degrees C) in a solution of 17.5% dimethylsulphoxide and 20% fetal bovine serum and by storage in liquid nitrogen. Veins were then implanted as a carotid autograft (three grafts/group). At the time of graft implantation a segment of the paired matched vein was perfusion-fixed and evaluated by scanning and transmission electron microscopy, whereas the remainder were subjected to endothelial cell culture techniques to determine cell viability. Autografts were removed 1 month after implantation and subjected to similar evaluations. Histological changes seen in cryopreserved veins were dependent on preservation time and included focal endothelial cell blebbing, cytoplasmic vacuolization and disruption of cell-to-cell contacts. Smooth muscle cells showed mitochondrial swelling. Patency was identical in all groups (66.6%). Explants at 1 month were similar in histological appearance to fresh veins with a smooth endothelial cell lining arranged longitudinally and intact cell junctions. Endothelial cells could be cultured from fresh veins and 1-month-old explants but not from the cryopreserved graft surface before implantation. the present technique of cryopreservation leads to some damage of graft architecture and loss of endothelial cell viability.(ABSTRACT TRUNCATED AT 250 WORDS)

Anastomosis, Surgical↗

Linkage studies in Italian families with familial adenomatous polyposis.

Linkage analysis was performed on 188 subjects belonging to 18 Italian families segregating for familial adenomatous polyposis (FAP) using 7 polymorphic markers (5 restriction fragment length and 2 dinucleotide repeat polymorphisms) mapping in 5q21. A two-point linkage analysis performed with the LINKAGE program gave significant lod scores (> 3) between the Pi227, C11p11, YN5.64, YN5.48 probes and the disease, whereas the ECB27, CB83 and EF5.44 markers showed lower lod scores. Some 11 recombination events were identified from the analysis of 101 meioses. The best map that we could determine confirmed that reported in previous studies. The location of the new marker, CB83, lying between YN5.64 and YN5.48, remains imprecise. No genetic heterogeneity was detected, with all the families showing linkage for at least one of the probes. One 34-year-old individual having an affected haplotype was however classified as healthy after clinical examinations. The results confirm the applicability of the linkage approach for presymptomatic diagnosis of FAP.

Adenomatous Polyposis Coli↗

Postoperative course of inflammatory abdominal aortic aneurysms.

Of 779 patients undergoing repair of abdominal aortic aneurysms over a 7-year period (1984-1990), 40 (5.1%) had gross features of inflammatory abdominal aortic aneurysms (IAAAs). Twenty IAAAs were assessed by CT scan preoperatively and postoperatively to evaluate the outcome of the inflammatory layer of the aneurysm in 19 cases. Complete postoperative regression was observed in nine cases (47.3%), partial regression in four (21%), and stable lesions in six (31.7%). No roentgenographic progression was found. The comparison between the roentgenologic outcome and preoperative clinical features (age, sex, erythrocyte sedimentation rate, and abdominal lumbar pain), pathologic findings, and follow-up time revealed a significant correlation (p < 0.05) between the postoperative outcome and the histologic findings in the wall (cell density and cell/fibrosis ratio). Complete regression of inflammation was observed when high cell density (16 +/- 0.7 cells/2116 microns 2) and a cell/fibrosis ratio > 1 were found. On the contrary, little or no regression of inflammation occurred when a low cell density (3.4 +/- 0.3 cells/2116 microns 2) and a cell/fibrosis ratio < 1 were found. Although it is generally thought that inflammation in IAAAs regresses after surgical repair, in our study, 31.7% of the postoperative CT scans showed no change. Histologically, the variability of morphologic aspects seemed to correlate with the relative proportions of cellular infiltrate and interstitial fibrosis in the aneurysmal wall. These proportions determine the postoperative course of the inflammation layer and, most likely, the response of the latter to steroid therapy as well.

Adult↗

Content and turnover of extracellular matrix protein in human "nonspecific" and inflammatory abdominal aortic aneurysms.

Inflammatory aneurysms (IAs) have peculiar macroscopic and histological aspects which make them very different from nonspecific aneurysms (NSAs). These morphological differences seem to be determined by significant modifications of the extracellular matrix. Extracellular matrix protein component concentrations were determined biochemically in infrarenal aortic biopsies from 10 NSAs, five IAs and five non-aneurysmal aortic controls. The concentration of each wall component was expressed in % w/w (relative concentration) and in mg/wall longitudinal cm (absolute concentration) with reference to total protein recovered after hydrolysis and amino acid analysis. The biochemical results were correlated with the histological and ultrastructural features of the specimens. A significant increase in total collagen was observed in the two groups of aneurysms, with respect to the controls (NSA = 285%, IA = 382%). In contrast the 80-90% decrease in the relative concentration of elastin observed in both types of aneurysm was less marked (NSA = 55%, IA = 39%). This fall was not significant when expressed in mg/cm, although elastin derived peptide (EDP) levels in the plasma of these patients was significantly higher than in age-matched controls. The concentration of the soluble collagen fraction appeared significantly higher (Mann-Whitney, p < 0.05) in the IAs with respect to the NSAs, whilst no differences were observed between the two groups regarding the concentration of insoluble elastin and of wall and plasma EDPs. As well as providing evidence of increased elastin turnover, this study emphasises the conspicuous modifications of collagen deposition in the wall of abdominal aortic aneurysms which appeared more marked in the inflammatory group.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

Infertility in carriers of two bisatellited marker chromosomes.

Two unrelated sterile patients, a male and a female, with karyotypes characterized by the presence of two supernumerary bisatellited marker chromosomes, were studied with the aid of fluorescence in situ hybridization (FISH). Using alphoid centromeric specific probes, the markers were identified as an idic (15) (pter-q11) and a mar (14). In both cases a single accessory bisatellited marker was present in the karyotype of one of the parents. A possible correlation between the excess of constitutive heterochromatin and meiotic disturbances in the two patients is discussed.

Adult↗

Renal afferents signaling diuretic activity in the cat.

Mechanoreceptors and chemoreceptors have been identified inside the kidney, but their functional role is still largely unclear. The aim of this study was to investigate whether changes in urine output could modify the discharge rate of renal afferent fibers. Experiments were performed in anesthetized cats in which afferent renal nerve activity (ARNA) was recorded by standard electrophysiological techniques from a centrally cut renal nerve. Arterial pressure, renal blood flow velocity, urine flow rate, and renal pelvic pressure were also measured. Three diuretic maneuvers were tested in the same cat: intravenous administration of physiological saline (8 to 13 mL/min for 2 minutes), furosemide (1 mg/kg), and atrial natriuretic peptide (ANP, 1 microgram/kg). The three maneuvers increased urine flow rate and pelvic pressure, respectively, 137.0 +/- 20.6% and 136.8 +/- 21.1% (saline), 148.6 +/- 31.7% and 139.6 +/- 43.5% (furosemide), and 75.9 +/- 7.9% and 62.1 +/- 21.2% (ANP) at the time of the maximum response. Arterial pressure slightly increased after saline, did not change after furosemide, and slightly decreased after ANP. Renal blood flow increased after saline and did not change after furosemide and ANP. The three maneuvers increased ARNA by 98.4 +/- 15.2% (saline), 270.7 +/- 100.8% (furosemide), and 59.6 +/- 23.4% (ANP). Changes in ARNA significantly correlate with changes in both pelvic pressure and urine flow rate. Our data demonstrate that increments in urine flow rate increase the firing rate of renal afferent fibers and suggest that (1) pelvic pressure is the major determinant of the neural response, and (2) this increased afferent discharge is due to activation of renal mechanoreceptors.

Animals↗