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C Rosati

Publications and source records attributed to C Rosati.

At least 19 recordsLinked to original sources
PubMed1992

Cicletanine sulfate: inhibition of anion transport systems and natriuretic activity.

In contrast with cicletanine, its urinary sulfoconjugate metabolite (cicletanine sulfate) was active on membrane ion transport in human red blood cells. Cicletanine sulfate was a more potent inhibitor of the Na+ dependent [Cl-/HCO3-] exchanger (IC50 = 9 +/- 3 x 10(-5) mol/l; mean +/- SD of 4 experiments) than cicletanine (IC50 = 10(-3) mol/l). This inhibitory potency was intermediate between that of xipamide (IC50 = 2 x 10(-5) mol/l) and that of furosemide (IC50 = 2 x 10(-4) mol/l). Moreover, cicletanine sulfate exhibited modest inhibitory potency against the [Na+,K+,Cl-]-cotransport system (IC50 = 1 +/- 0.3 x 10(-3) mol/l; mean +/- SD of 4 experiments) and poor inhibitory activity against the [K+,Cl-]-cotransport system. Cicletanine sulfate was unable to modify the activity of Cl(-)-independent membrane carriers (Na+:H+ exchanger, Ca2+ pump, Na+:Li+ countertransport system and Na+,K+ pump). Following renal intraarterial administration in rats, cicletanine sulfate and not cicletanine, exhibited salidiuretic activity. In conclusion, the urinary sulfo-conjugate of cicletanine is an active anion transport inhibitor and natriuretic metabolite. In fact, this metabolite may be responsible for the salidiuretic action of cicletanine.

Animals↗
PubMed1992

Ultrastructural study of the choroid plexus of spontaneously hypertensive rats.

We previously gave an account of an increased ion transport activity in choroid plexus from spontaneously hypertensive rats. We have since examined this organ in scanning and transmission electronic microscopy. In the choroid plexus from young spontaneously hypertensive rats, the epithelial cells showed the following: a partial loss of the brush border and infoldings of basolateral membranes, an increased number of Golgi apparatus, vesicles, and mitochondria, and an activated nucleus. In adult hypertensive rats, the mitochondria had increased in number and tended to fill the cytoplasma while the nuclei had returned to a resting level. These ultrastructural changes furthermore suggest an increased secretory activity in the choroid plexus in spontaneously hypertensive rats.

Aging↗
PubMed1992

Primary colorectal anastomosis with the intracolonic bypass tube.

BACKGROUND: Intracolonic bypass with primary colocolonic or colorectal anastomosis may be an effective option in the operative management of complicated colonic disease when adequate bowel preparation is not possible. A pliable latex tube is anchored to mucosa and submucosa 3 centimeters proximal to a site of colocolonic anastomosis and later spontaneously evacuated by way of the rectum. METHODS: Twenty-nine consecutive patents who required urgent colorectal operations in the presence of unprepared bowel underwent left colon resection with intracolonic bypass and primary anastomosis. These patients would have otherwise undergone multistage procedures for the management of the colorectal disorders. Demographic data, APACHE II scores, and type and frequency of complications were recorded. RESULTS: Between July 1, 1990, and June 30, 1991, 31 patients were eligible for entry in the study. Two patients ultimately had contraindications for the use of intracolonic bypass. The causes encountered included complicated diverticular disease, colonic carcinoma, sigmoid volvulus, and iatrogenic colorectal injury. Complications included wound infection (7), myocardial infarction (2), prolonged ileus (1), deep vein thrombosis (2), and anastomotic leak (2). Postoperative myocardial infarction and subsequent multiorgan system failure were responsible for the only death in this study. CONCLUSIONS: Intracolonic bypass permits a safe primary anastomosis where multistage procedures would otherwise be required. Avoidance of colostomy and the attendant socioeconomic benefits warrants further study of this method.

Aged↗
PubMed1992

[Erythrocyte sodium-lithium countertransport in diabetic children: 12 months development and relationship with familial hypertension].

It has been suggested that an increased erythrocyte Na-Li countertransport (Na-Li CNT) rate in patients with IDDM is associated to the risk of developing diabetic nephropathy. Little is known, however, about the possible influence of metabolic control on Na-Li activity. Aims of the study were to evaluate Na-Li CNT at the onset of IDDM and during the remission phase and its relationship with some clinical and metabolic parameters. Twelve insulin-dependent diabetic children (6 males, 6 females; mean age 10 +/- 0.6 years) were studied at the onset and 1, 4, 12 months after the diagnosis; 6 of them had a family history of hypertension. Twelve healthy children (6 males, 6 females; mean age 12 +/- 0.3 years) served as controls. As compared to control subjects (212 +/- 24 mumol/l RBC/h), red cell Na-Li countertransport activity of diabetic children was significantly higher at the onset (354 +/- 31 mumol/l RBC/h) of IDDM and at the first month (348 +/- 36 mumol/l RBC/h). Red cell Na-Li countertransport activity returned toward normal range at the fourth (239 +/- 33 mumol/l RBC/h) and twelfth month (162 +/- 34 mumol/l RBC/h). No correlation was found between the values of red cell Na-Li countertransport activity and those of clinical and biochemical parameters at any time. Patients with hypertensive relatives showed at baseline evaluation a significantly higher red cell Na-Li countertransport activity than those without (436 +/- 28 vs 273 +/- 34 mumol/l RBC/h; p < 0.002). This difference, although not statistically significant, was still evident at the late follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)

Antiporters↗
PubMed1991

Pneumonia complicating abdominal sepsis. An independent risk factor for mortality.

Nosocomial pneumonia (NP) is associated with a significant mortality, 66% in a previous retrospective study of NP complicating intra-abdominal sepsis (IAS). We prospectively compared the outcome of NP complicating IAS with that of recurrent IAS (R-IAS) in the absence of NP. Data were collected prospectively on 300 patients with IAS; 34 patients who presented with pneumonia were excluded from the analysis (44% mortality). One hundred seventy-one patients with no NP and no R-IAS (group 1) had a hospital mortality of 20% (34 patients); 36 without NP in whom R-IAS developed (group 2) had a 17% mortality (six patients); and 47 with NP but no R-IAS (group 3) had a 53% mortality (25 patients). Finally, 12 patients who had both NP and R-IAS suffered a 75% mortality (nine patients). We examined the relationships among the following putative risk factors and mortality: APACHE (acute physiology and chronic health evaluation) II score (at initial presentation with IAS), the need for mechanical ventilatory assistance following initial treatment for peritonitis, steroid requirement, generalized peritonitis vs abscess, and the need for surgical as opposed to percutaneous treatment. Using mortality as the dependent variable, group 2 vs 3 as the explanatory variable, and the risk factors as confounders, logistic regression analysis indicated that the group difference was significant after controlling for confounders. We conclude that NP complicating IAS is an independent risk factor associated with a significant mortality compared with R-IAS. These data challenge the notion that death in IAS is usually due to recurrent or persistent intra-abdominal infection.

Abdomen↗
PubMed1991

Flow-dependent stimulation of sodium and cholesterol uptake and cell growth in cultured vascular smooth muscle.

A10 vascular smooth muscle cells were placed in a flow chamber and exposed to the circulation of foetal calf serum at different rates and pressures. Under unidirectional laminar flow, physiological flow rates and pressures had almost no effect on internal sodium content. Indeed, pressure values greater than 150 mmHg were required to observe modest increases in sodium content. Conversely, a short exposure to turbulent flow (3 min) induced a strong increase in cell sodium content. At flow rates found in large human arteries, the onset of such ionic change required pressure levels of 50-85 mmHg. The restoration of laminar flow allowed the elimination of the excess cell sodium content, with a half-life of 3-4 h. Opening of calcium channels by the turbulent flow was suggested by the following observations: (1) nitrendipine fully prevented sodium uptake, with an inhibitory concentration of 50% of approximately 2 x 10(-7) mol/l; and (2) exposure to turbulent flow increased cytosolic free calcium content by approximately 80%. In addition to sodium uptake, turbulent flow stimulated cell uptake of exogenous cholesterol. Although the restoration of laminar flow allowed the rapid elimination of approximately two-thirds of the excess in cell cholesterol (with a half-life of 30-60 min), one-third of the excess cholesterol remained in the cells for more than 24 h. Finally, cell replication was faster in cells exposed to turbulent flow than in control cells subjected to laminar flow. The results show that turbulent flow provokes membrane ion transport changes in vascular smooth muscle cells, which are associated with enhanced cholesterol uptake and cell hyperplasia. Therefore, the departure from unidirectional laminar flow may be a pathogenic factor in primary hypertension and/or atherosclerosis.

Animals↗
PubMed1991

Appendicular abscess presenting as neoplastic ileocecal obstruction.

Most complications after appendectomy occur within weeks of the operation. The authors present a case in which an appendicular abscess presented more than 18 years after appendectomy for acute appendicitis. The abscess simulated a neoplastic obstructive process, and a communication was demonstrated between the cecum and the abscess cavity through the appendiceal stump.

Abscess↗
PubMed1991

[Pseudotumor cerebri due to the cessation of corticosteroids. A case report].

Cerebral pseudotumour is an endocranial hypertensive syndrome marked by the absence of focal neurological signs, the integrity of neuroradiological tests and an increased liquor pressure with normal composition of the liquor itself. It is normally self-limiting but if endocranial hypertension persists it may severely affect sight. It may be idiopathic or secondary to a number of conditions. The authors report a case of cerebral pseudotumour following the suspension of corticosteroid treatment. The pathology resolved rapidly following lumbar puncture. The paper focuses on the pathogenetic mechanisms and the still undefined therapeutic possibilities.

Adrenal Cortex Hormones↗
PubMed1990

The beneficial effect of atrial natriuretic peptide on cyclosporine nephrotoxicity.

Nephrotoxicity is the most common and important side effect of cyclosporine (CyA) therapy. It is characterized by a fall in glomerular filtration rate (GFR) and by a decrease in sodium and water excretion. Since atrial natriuretic peptide (ANP) has been shown to increase GFR and to cause a potent diuretic and natriuretic effect, we have investigated the potential beneficial action of ANP on CyA induced renal injury. To this end two groups of animals were studied: 1) rats that received an intravenous infusion of CyA (20 mg/kg body weight) (acute studies) and 2) rats that have been treated with daily intraperitoneal injections of CyA (20 mg/kg body weight) for a total of seven days (chronic studies). To both groups of rats synthetic ANP was administered intravenously as a bolus (10 micrograms/kg) and then as a constant infusion (1 microgram/kg/min). In group 1 the CyA administration resulted in a decrease in GFR, urine output, urinary sodium and potassium excretion. After ANP infusion there was a prompt restoration of GFR, with a large rise in urine, sodium and potassium excretion rates. Similar effects on renal hemodynamics and electrolyte excretion rates were detected after ANP administration in chronic CyA treatment. These data show that the administration of ANP to rats that have been exposed to acute or chronic CyA treatment is able to reverse the harmful effect of CyA on renal function.

Acute Kidney Injury↗
PubMed1990

Stimulatory action of endothelin-1 on membrane Na+ transport in vascular smooth muscle cells in culture.

Endothelin-1 was able to induce an immediate and transient increase in cytosolic free Ca2+ concentrations in the A10 cell line of vascular smooth muscle. This was associated with a strong stimulation of the Na+:H+ exchange, the Na+, K+ pump and the [Na+,K+,Cl-]-cotransport system. Pump stimulation appeared to be secondary to sodium entry through Na+:H+ exchange because it was absent in Na+ loaded cells and in the presence of ethyl-isopropyl-amiloride. Cotransport stimulation was blocked by indomethacin, suggesting the involvement of a cyclooxygenase product. In conclusion, the monovalent ionic perturbations associated to the vasoconstrictor and mitogenic actions of endothelin-1 are counterbalanced by activation of the Na+,K+ pump and the [Na+,K+,Cl-]-cotransport system.

Animals↗
PubMed1989

Atrial natriuretic peptide has no direct effect on proximal tubule sodium and water reabsorption.

Infusion of ANP has been shown to increase the urinary excretion of sodium and water. However it is still controversial in which tubular segment sodium reabsorption is inhibited. To clarify this problem we have performed in vivo and in vitro studies to examine the direct effect of ANP on rat proximal tubules. The in vivo effect of ANP has been tested by using the micropuncture technique and in particular the shrinking droplet method that allows each investigated tubule to serve as its own control. Addition of either low (10(-9) M) or high (2 x 10(-6) M) concentrations of ANP to the luminal perfusate resulted in no significant change in isotonic fluid reabsorption (Jv). The same holds when the proximal tubules were perfused on both the tubular and peritubular side, with modified Ringer solution containing 10(-9) M ANP. To examine possible in vitro effects of ANP we prepared highly purified proximal tubule suspension derived from rat renal cortex and monitored oxygen consumption (QO2) that is tightly coupled to sodium transport in this segment. Synthetic ANP, either at low (10(-9) M) or at high (10(-6) M) concentrations, did not affect basal rate of tubular respiration. Moreover the peptide hormone (10(-9) M) did not inhibit nystatin stimulated and ouabain sensitive QO2. These results indicate that the enhancement of renal sodium excretion induced by ANP is not related to a direct inhibition of sodium transport in the proximal tubule.

Amphotericin B↗
PubMed1989

Erythrocyte Na+, K+ pump inhibition after saline infusion in essentially hypertensive subjects: effects of canrenone administration.

The effects of a 2-litre isotonic saline infusion, with and without prior oral canrenone (150 mg) administration, on erythrocyte Na+, K+ pump, urinary sodium excretion and arterial pressure were evaluated in nine patients with essential hypertension. Ouabain-sensitive Na+ efflux in fresh erythrocytes was used as an index of Na+, K+ pump activity, and the inhibitory effect on this ion efflux of preincubation of erythrocytes in plasma was used to test the presence of a circulating ouabain-like substance. Erythrocyte Na+, K+ pump activity decreased significantly (P less than 0.01) after saline infusion; canrenone administration was able to prevent this inhibition. Plasma from hypertensive patients obtained before saline infusion significantly (P less than 0.01) inhibited the Na+, K+ pump of erythrocytes from normal subjects, while plasma taken after the saline infusion plus canrenone was unable to produce any significant inhibition. Both systolic and diastolic arterial pressure fell significantly (P less than 0.05) only at the end of saline infusion with prior canrenone administration. This study supports the hypothesis that protection of Na+, K+ pump against endogenous inhibitors, other than exogenous, seems to be a pharmacological effect of canrenone, and may partly explain its antihypertensive activity.

Adult↗
PubMed1989

Stimulation of Na(+)-H+ exchange, the Na(+)-K+ pump and Na+,K+,Cl- cotransport by endothelin-1 in cultured vascular smooth muscle cells.

Endothelin-1 concentrations higher than 10(-10) mol/l were able to strongly stimulate Na(+)-H+ exchange, the Na(+)-K+ pump and the Na+,K+Cl- cotransport system in A10 vascular smooth muscle cells. The stimulation of Na(+)-H+ exchange was more marked in fresh than in H(+)-loaded cells, suggesting an increase in the apparent affinity for internal H+. Pump stimulation appeared to be secondary to sodium entry through Na(+)-H+ exchange because it was absent in (1) Na(+)-loaded cells and (2) in the presence of ethyl-isopropylamiloride (EIPA). Stimulation of cotransport was blocked by indomethacin, suggesting the involvement of a cyclo-oxygenase product. In conclusion, the action of endothelin-1 in vascular smooth muscle induces the onset of negative feedback mechanisms which enhance the ability of the vascular cells to regulate disturbances in Na+,K+ and Cl- contents.

Biological Transport↗
PubMed1989

A mechanical stress increases sodium ion content in vascular smooth muscle cells through a calcium-dependent pathway: prevention by cicletanine via a cyclo-oxygenase product.

The non-laminar (rather turbulent) flow induced by cell washings was able to reversibly increase the sodium ion (Na+) content in cultured A10 aortic smooth muscle cells. Similar changes, although to a lesser extent, were observed in cardiocytes but not in fibroblasts, erythrocytes, thymocytes or macrophages, suggesting that the changes are specific to excitable cells. The increase in vascular sodium content had the following properties: (1) It was inhibited by nitrendipine; (2) it was accompanied by an increase in the free cytosolic Ca2+ content; (3) it was unable to stimulate the sodium pump; and (4) it reflected the qualitative and quantitative composition of the incubation media. These observations suggested that a non-laminar flow is able to open potential-dependent calcium channels, with secondary internalization of high amounts of extracellular ions. These ionic perturbations were blocked by low concentrations of cicletanine; the half-maximal inhibitory concentration (IC50) was about 10(-9) mol/l on internal sodium. The protective effects of cicletanine were inhibited by indomethacin, suggesting that they are mediated by a cyclooxygenase metabolite, perhaps prostacyclin. Captopril and diuretic drugs such as hydrochlorothiazide, furosemide, spironolactone or acetazolamide were unable to protect vascular cells against the harmful effects of cell washings.

Animals↗
PubMed1989

Stimulation of the Na+, K+ pump and the (Na+, K+, Cl-) cotransport system by endothelin-1 in cultured vascular smooth muscle cells: involvement of cyclo-oxygenase products.

The effect of endothelin (ET-1) on vascular smooth muscle cell Na+ and K+ regulation was studied in the A10 cultured cell line. In contrast with other vasoconstrictors, ET-1 was able to strongly stimulate both the Na+, K+ pump and the (Na+, K+, Cl-) cotransport system at concentrations higher than 10(-10) M. This did not appear to reflect a direct interaction with the transport proteins because ET-1 was without effect on the same transport systems in human red cells. Indomethacin, at concentrations of 10(-5) M, was able to counteract the pump and cotransport stimulation by ET-1. These results suggest that the potent vasoconstrictive action of ET-1 induces a negative feedback mechanism via a cyclo-oxygenase product, which enhances the ability of vascular smooth muscle cells to regulate Na+ and K+ contents.

Biological Transport, Active↗
PubMed1989

[Ionic perturbations produced by a non-laminar flow in vascular smooth muscle cells in culture. Protection by cicletanine via a cyclo-oxygenase metabolite].

The non-laminar (rather turbulent) flow, induced by cell washings was able to reversibly increase internal Na+ contents in cultured aortic smooth muscle (A10 cells). Similar changes (although to a lesser extent) were observed in cardiocytes but not in fibroblasts, erythrocytes, thymocytes or macrophages, suggesting that they are specific for excitable cells. The increased vascular sodium content had the following properties: it was inhibited by nitrendipine; it was accompanied by an increase in free cytosolic Ca2 contents; it was unable to stimulate the sodium pump and (iv) it reflected the qualitative and quantitative composition of the incubation media. These observations suggested to us that the increased vascular sodium content results from the opening of potential-dependent calcium channels with secondary internalisation of high amounts of extracellular ions. The ionic perturbations were blocked by low concentrations of cicletanine (IC50 of about 10(-9) M on intracellular sodium). Moreover, the protective effects of cicletanine were inhibited by indomethacin, suggesting that they are mediated by a cyclo-oxygenase metabolite, perhaps prostacyclin. Sodium nitroprusside, a compound able to stimulate calcium entry in the sarcoplasmic reticulum via cyclic GMP, was also able to protect vascular cells (although it acted at higher concentrations than cicletanine). Conversely, captopril and diuretic drugs such as hydrochlorothiazide, furosemide, spironolactone and acetazolamide were unable to protect vascular cells against the deleterious effects of cell washings.

Antihypertensive Agents↗