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Biomedical subjects

J Gaya

Publications and source records attributed to J Gaya.

At least 19 recordsLinked to original sources
PubMed1996

Acute phase is the only significantly reduced component of the injury response after laparoscopic cholecystectomy.

The objective demonstration of improved postoperative recovery suggests that the surgical injury response induced by the laparoscopic approach is less intensive than that after open surgery. Twenty-five patients diagnosed as having noncomplicated gallstones were studied prospectively. They were operated by laparoscopy (group I, n = 12) or open surgery (group II, n = 13). Analgesia requirements (p < 0.026) and postoperative stay (p < 0.001) were significantly less in group 1. Cholecystectomy performed by either technical options induced a significant increase over basal values of glucose, lactate, white blood cell count, prolactin, ACTH, cortisol, interleukin 6, C-reactive protein, and PCO2. Both surgical procedures induced a significant reduction of total proteins, albumin, prealbumin, free fatty acids hemoglobin, hematocrit, and pH. There were no differences between the levels of growth hormone, insulin, glucagon, or PO2 during any of the periods studied. Comparison of the results of the two cholecystectomy techniques showed that laparoscopic cholecystectomy induced a significantly less intensive acute-phase response (area under the curve) of interleukin 6 (17 +/- 17 versus 47 +/- 26 pg/ml x hr x 10(2); p < 0.003), C-reactive protein (16 +/- 12 versus 35 +/-16 mg/dl x hr x 10; p < 0.004), and prealbumin (16 +/- 2.7 versus 13.8 +/- 2.3 mg/dl x hr x 10(2); p < 0.05). The surgical injury response after laparoscopic cholecystectomy is similar to that after open cholecystectomy, but the aeute-phase response component is less intense. This finding may be a consequence of the reduced size of the operative wound with laparoscopic cholecystectomy.

Adrenocorticotropic Hormone↗
PubMed1995

Effect of antihypertensive treatment on the increased beta 2-adrenoceptor density in patients with essential hypertension.

The effect of different antihypertensive drugs on the increased surface beta 2-adrenoceptor density in essential hypertension was evaluated to elucidate whether the possible effect of the treatment on these receptors was secondary to blood pressure decreases or a specific effect of the drugs. Thirty-nine untreated essential hypertensive patients and 28 normotensive control subjects were studied in basal conditions. Hypertensive patients were randomly assigned to three treatment groups: bisoprolol (10 mg/day, n = 15), enalapril (20 mg/day, n = 12), and verapamil SR (240 mg/day, n = 12), and were studied before and after 1 month of treatment. Plasma catecholamines were determined by a radioenzymatic assay. Surface beta 2-adrenoceptors were measured in intact lymphocytes by radioligand binding assay using the hydrophilic ligand [3H]-CGP12177. beta 2-adrenoceptor density was increased in hypertensive patients (P < .01). After treatment, mean blood pressure decreased similarly in the three groups, while plasma catecholamines showed no significant changes in any group. beta 2-adrenoceptor number decreased only in bisoprolol-treated patients (P < .05). Mean blood pressure decreases correlated with beta 2-adrenoceptor decrements only in bisoprolol-treated patients (r = 0.65, P < .05). beta 2-adrenoceptor density correlated with plasma epinephrine levels in the control group (r = -0.50, P < .01), but not in hypertensive patients before treatment. This correlation was also observed in hypertensive patients treated with bisoprolol (r = -0.52, P < .05), but not in those treated with verapamil or enalapril. Our results suggest that bisoprolol treatment reduces the increased surface beta 2-adrenoceptor density and restores its regulation by epinephrine in essential hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Reversible decrease of surface beta 2-adrenoceptor number and response in lymphocytes of patients with pheochromocytoma.

To study the effect of chronic exposure to elevated plasma catecholamines on surface beta 2-adrenoceptor density, we measured these receptors in the lymphocytes of 9 patients with pheochromocytoma as well as in 27 healthy control subjects. Binding experiments were performed on intact lymphocytes using the hydrophilic ligand [3H]-CGP12177. Lymphocyte beta 2-adrenergic response was also measured in three patients. beta 2-adrenoceptor density (p < 0.01), and isoproterenol-stimulated increase in cAMP were reduced in patients with pheochromocytoma. Both parameters normalized (p < 0.05) when patients were reevaluated 4 weeks after tumor removal, coinciding with normalization of plasma epinephrine (r = -0.95, p < 0.01) and to log of plasma norepinephrine (r = -0.58, p < 0.05) in patients. We conclude that chronic catecholamine excess induces a decrease of lymphocyte beta 2-adrenoceptor surface number and response that is reversible upon normalization of plasma catecholamine levels. This regulation is mainly dependent on plasma levels of the hormone epinephrine, but norepinephrine may also play a regulatory role at supraphysiological levels.

Adrenal Gland Neoplasms↗
PubMed1995

Parathyroid hormone and platelet cytosolic calcium concentration in essential hypertension.

To investigate the possible relationships between blood pressure, parathyroid hormone (PTH) and platelet cytosolic Ca2+ concentration ([Ca2+]i) in patients with essential hypertension, we studied 17 patients with this disease aged 48 +/- 2 years and 17 normotensive controls aged 44 +/- 3 years. Platelet [Ca2+]i was measured by spectrofluorimetry using the dye Fura-2 acetoxymethylester. Patients with essential hypertension displayed lower levels of serum ionized Ca2+ (0.99 +/- 0.03 versus 1.1 +/- 0.01 mmol/l, P < 0.05) and higher serum intact PTH levels (37 +/- 3 versus 26 +/- pg/ml, (P < 0.01) than the normotensive controls. Although serum levels of intact PTH were significantly correlated with mean arterial pressure (MAP) in the combined group of subjects (r = 0.42, P < 0.05), there was no correlation when each group was considered separately. Resting platelet [Ca2+]i was also higher in patients than in controls (57 +/- 3 versus 48 +/- 2 nmol/l, P < 0.005). When platelets were stimulated in vitro with thrombin, the increment in [Ca2+]i was also greater in patients than in controls in the presence of extracellular Ca2+ (264 +/- 24 versus 194 +/- 19 nmol/l, P < 0.05) but not in its absence (123 +/- 12 versus 112 +/- 10 nmol/l). The thrombin-induced increment in [Ca2+]i was correlated with MAP in the hypertensive patients (r = 0.64, P < 0.01) and in the combined group of subjects (r = 0.42, P < 0.05). There was no relationship between resting or thrombin-induced [Ca2+]i and serum PTH in either group of patients or in the combined group of subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Thyroid testing using the Cobas Core immunoassay system. A multicentre study.

The random access immunoanalyzer Cobas Core and the Cobas Core Thyroid Assays were assessed as to their clinical usefulness in the analysis of different thyroid diseases. Four centres participated in this study measuring the following five thyroid tests per sample on the instrument: thyrotropin, free thyroxine, thyroxine, triiodothyronine and free triiodothyronine. The assessment was based on studies of precision and clinical samples. Within- and between-series precisions showed a mean CV over all assays of 4.3 and 6.1%, respectively. Comparison of the test results with clinical data demonstrated that the Cobas Core results are in accordance with diagnosed thyroid diseases. A good discrimination between normal and disease status and between untreated and treated status was found. Furthermore, 370 sera measured with Technicon Immuno-1 TSH and FT4 assays were compared to the respective Cobas Core EIAs). A good correlation between the assays was demonstrated.

Evaluation Studies as Topic↗
PubMed1994

Blunted natriuretic response to human urine extracts with Na+,K(+)-ATPase inhibiting activity in experimental cirrhosis.

Human urine and plasma extracts contain a material that inhibits the enzyme Na+,K(+)-ATPase (the endogenous sodium pump) and produces natriuresis in the bioassay animal. This endogenous sodium pump inhibitor(s), also known as digitalis-like factor, is thought to be involved in sodium and extracellular fluid volume homeostasis. Increased urine and plasma sodium pump inhibiting activity have been reported in patients with cirrhosis and sodium retention. The aim of the study was to assess the renal response to i.v. administration (0.2 ml/min per kg bw for 10 min) of a human urine extract containing sodium pump inhibiting activity (28.5 nmol equivalent ouabain/ml) in eight conscious rats with cirrhosis and ascites and eight control rats. Baseline urinary excretion of Na+,K(+)-ATPase inhibiting activity was significantly higher in cirrhotic rats with ascites than in control rats (235 +/- 40 vs 91 +/- 16; p < 0.01). Human urine extract induced a significant (p < 0.05) increase in glomerular filtration rate in control (3.2 +/- 0.4 to 4.2 +/- 0.5 ml/min) and cirrhotic rats (3.0 +/- 0.3 to 4.0 +/- 0.5 ml/min). In control rats it also increased urinary sodium excretion (1.47 +/- 0.22 to 2.43 +/- 0.5 microEq/min, p < 0.01) and fractional sodium excretion (0.29 +/- 0.01 to 0.43 +/- 0.04%, p < 0.025). In contrast, in cirrhotic rats with ascites neither sodium excretion nor fractional sodium excretion was significantly affected. No changes were observed in plasma aldosterone and atrial natriuretic peptide concentrations in either group. These data suggest that in cirrhosis there is a renal resistance to the natriuretic effect of endogenous sodium pump inhibitor(s).

Animals↗
PubMed1994

Intracellular calcium concentration and activation of the Na+/H+ exchanger in essential hypertension.

To investigate the relationship between changes in intracellular calcium concentration ([Ca2+]i) and agonist-induced activation of the Na+/H+ exchanger in essential hypertension (EH), platelet [Ca2+]i and pHi were measured in 24 patients with EH (14 males) aged 48 +/- 2 years and 23 matched normotensive controls (NT) (12 males) aged 45 +/- 3 years. Measurements were done with spectrofluorimetry using the dyes Fura-2 for [Ca2+]i and BCECF for pHi. [Ca2+]i and pHi were measured in the resting condition and after stimulation in vitro with 0.1 U/ml human thrombin. The thrombin-induced rise in pHi was Na+ dependent and amiloride sensitive, indicating that it was mediated by the Na+/H+ exchanger. Unstimulated [Ca2+]i was higher in patients with EH than in NT (60 +/- 3 vs. 48 +/- 1 nmol/liter, P < 0.005), but there were no differences in resting pHi between both groups (7.16 +/- 0.01 vs. 7.16 +/- 0.008). In the presence of 1 mmol/liter external calcium (Ca2+o), thrombin-induced increment in [Ca2+]i was significantly greater in patients with EH than in NT (281 +/- 21 vs. 206 +/- 19; P < 0.05) as was the pHi increment (EH: 0.137 +/- 0.01; NT: 0.095 +/- 0.01; P < 0.05). Both agonist-induced increments in [Ca2+]i and in pHi were correlated with mean arterial pressure (MAP) only in the EH group (r = 0.58, P < 0.005 and r = 0.59, P < 0.005, respectively). The agonist-induced rise in pHi was positively correlated with the rise in [Ca2+]i both in the EH group (r = 0.65, P < 0.001) and in the NT (r = 0.55, P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Platelets↗
PubMed1994

Effect of antihypertensive treatment on intracellular calcium concentration and intracellular pH in essential hypertension.

The platelet intracellular calcium concentration ([Ca2+]i) and intracellular pH (pHi) were measured by spectrofluorimetry with the dyes Fura-2 and BCECF, respectively, in 19 patients with essential hypertension (10 males), aged 48 +/- 2 years, before and after 12 weeks of antihypertensive treatment and in 19 normotensive controls (11 males), aged 46 +/- 3 years. [Ca2+]i and pHi were measured in the resting state and after stimulation in vitro with 0.1 U/ml human thrombin. In patients with essential hypertension, both resting [Ca2+]i (61 +/- 4 nmol/l) and thrombin-induced maximal increase in [Ca2]i (291 +/- 26 nmol/l) were significantly (P < 0.01) greater than in the normotensive controls (resting 49 +/- 2 nmol/l and thrombin-induced 199 +/- 21 nmol/l). With respect to pHi, no difference in resting pHi between both groups was found (7.16 +/- 0.01 vs. 7.16 +/- 0.01). However, pHi increment at 300 seconds in response to thrombin was higher in the patients with essential hypertension than in the controls (0.131 +/- 0.02 vs. 0.083 +/- 0.01 pH units, P < 0.05). The increment in pHi was blunted by the amiloride derivative EIPA, indicating that it was mediated by the Na+/H+ exchanger. After antihypertensive therapy in the essential hypertensive patients, basal [Ca2+]i was significantly reduced (52 +/- 2 nmol/l, P < 0.01) and was not statistically different to the value found in the normotensive controls. Resting pHi suffered no significant modification after treatment (7.17 +/- 0.01, P = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Intracellular calcium mobilization and activation of the Na+/H+ exchanger in platelets.

The aim of the present study was to evaluate the regulatory relationship between the cytosolic free calcium concentration ([Ca2+]i and cytosolic pH (pHi). [Ca2+]i and pHi were measured using the fluorescent dyes fura-2 and BCECF [2',7'-bis-(carboxyethyl)-5,6-carboxyfluorescein] respectively. In a medium with 1 mmol/l extracellular calcium, thrombin (2.5 units/ml) induced an increment in [Ca2+]i of 638 +/- 31 nmol/l (n = 5) and an intracellular alkalinization of 0.14 +/- 0.01 pH units (n = 8). Both responses were dependent on the concentration of thrombin, displaying a sigmoidal dose-response pattern. The intracellular alkalinization was dependent upon extracellular Na+ and was amiloride-sensitive, indicating that it was mediated by activation of the Na+/H+ exchanger. When extracellular calcium was chelated with EGTA prior to the addition of thrombin, the intracellular alkalinization was not affected (0.15 +/- 0.02 at 2.5 units/ml thrombin, n = 8). Under these circumstances, the [Ca2+]i increment represents mobilization from internal stores, reaching 157 +/- 42 nmol/l at 2.5 units/ml thrombin. When platelets were preloaded with the intracellular calcium chelator MAPTAM (1,2-bis-5-methylaminophenoxylethane-NNN'-tetraacetoxymethyl acetate) to block the increase in [Ca2+]i induced by thrombin, no increment in pHi was observed. Moreover, MAPTAM-loaded calcium-depleted platelets had a basal pHi that was more acidic than in the presence of 1 mmol/l extracellular calcium (6.93 +/- 0.09 versus 7.14 +/- 0.01, n = 26, P < 0.001). Ionomycin induced an elevation of [Ca2+]i that was accompanied by a concomitant increase in pHi, which was Na(+)-dependent and amiloride-sensitive. [Ca2+]i and pHi increases induced by ionomycin were both dependent on the concentration of ionomycin. In conclusion, an increase in [Ca2+]i is necessary for the agonist-induced activation of the Na+/H+ exchanger in platelets. Non-agonist-induced increases in [Ca2+]i seems to prompt activation of the exchanger. In addition, Ca(2+)-depleted platelets have a more acidic basal pHi, indicating that the basal level of [Ca2+]i is also important for maintaining the basal pHi.

Blood Platelets↗
PubMed1993

Vasopressin in cerebrospinal fluid of newborns with hypoxic-ischemic encephalopathy. Preliminary report.

Vasopressin in cerebrospinal fluid has been measured in 27 fullterm newborns with hypoxic-ischemic encephalopathy. These newborns were divided into three groups according to the degree of neurological involvement, and they have been compared with a control group of 10 newborns. Determinations of vasopressin in cerebrospinal fluid and plasma were done by RIA. The cerebrospinal fluid vasopressin in asphyxiated newborns was higher than in the control group (p < 0.001); the mean concentration in the group of newborns classified as moderate or severe hypoxic-ischemic encephalopathy was higher than in the control group (18.7 pg/ml vs 4.66 pg/ml), and also higher than in the group classified as mild (14.2 pg/ml). Cerebrospinal fluid vasopressin values have a direct relationship to the plasmatic values at 12 hours of life (r = 0.76; p < 0.001). We concluded that vasopressin values in cerebrospinal fluid at 12 hours increase according to the clinical severity of the neonatal hypoxic-ischemic encephalopathy and that they have a strong relationship with plasmatic vasopressin.

Asphyxia Neonatorum↗
PubMed1993

Effect of dipyridamole on kidney function in cirrhosis.

Adenosine is a potent endogenous renal vasoconstrictor. To investigate the sensitivity of the renal circulation to adenosine in cirrhosis, we evaluated kidney function and vasoactive hormones in 20 patients with cirrhosis before and after administration of dipyridamole (0.4 mg/kg, intravenously), a drug that increases extracellular levels of adenosine. In patients with ascites and increased plasma renin activity (6.9 +/- 4.0 ng/ml.hr [mean +/- S.D.]) (n = 7), dipyridamole induced marked reductions in renal plasma flow (from 623 +/- 294 to 374 +/- 188 ml/min, p = 0.03), glomerular filtration rate (from 89 +/- 22 to 48 +/- 16 ml/min, p = 0.009), urine volume (from 7.1 +/- 2.1 to 1.5 +/- 1.1 ml/min, p = 0.0001), free water clearance (from 4.0 +/- 1.7 to 0.4 +/- 0.6 ml/min, p = 0.001) and sodium excretion (from 28 +/- 36 to 7 +/- 15 mu Eq/min, p = 0.05) in the absence of changes in arterial pressure, plasma renin activity and levels of aldosterone, norepinephrine and antidiuretic hormone. In patients without ascites (n = 5) and in patients with ascites and normal plasma renin activity (0.9 +/- 0.5 ng/ml.hr) (n = 8), renal plasma flow and glomerular filtration rate did not change significantly after dipyridamole administration, whereas excretion of sodium and free water was reduced. These results indicate that in cirrhotic patients with ascites and overactivity of the renin-angiotensin system, dipyridamole induces renal vasoconstriction in the absence of changes in systemic hemodynamics, suggesting that these patients are particularly sensitive to the renal vasoconstrictor effect of endogenous adenosine.

Ascites↗
PubMed1992

Assessment of the renin-angiotensin system in cirrhotic patients. Comparison between plasma renin activity and direct measurement of immunoreactive renin.

The renin-angiotensin system plays an important physiological role and has prognostic significance in cirrhotics with ascites. The degree of stimulation of this system is usually estimated by measuring plasma renin activity after incubation periods of 2-3 h. Recent investigations showed that the direct measurement of immunoreactive renin also estimates the degree of activity of the system. In this study, immunoreactive renin and plasma renin activity (measured at incubation periods of 10, 20, 50 and 180 min) were determined in ten healthy subjects, five hyperreninemic non-hepatic patients and 47 cirrhotics with ascites. Cirrhotic patients showed significantly higher plasma renin activity (5.1 +/- 0.9 ng/ml per h, p less than 0.05) and immunoreactive renin (145.4 +/- 24.4 pg/ml, p less than 0.01) than healthy subjects (1.2 +/- 0.15 ng/ml per h and 25.1 +/- 1.1 pg/ml, respectively). The angiotensin I generation rate was constant during the 3-h incubation in 22 cirrhotics and a close relationship (r = 0.956, p less than 0.001) between plasma renin activity (3.5 +/- 1.6 ng/ml per h) and immunoreactive renin (71 +/- 25 pg/ml) was observed in these patients. In the remaining 25 cirrhotics the generation rate of angiotensin I declined with time and the calculated plasma renin activity at 180 min was lower than the activity calculated at 10 min by 50.7%.(ABSTRACT TRUNCATED AT 250 WORDS)

Humans↗
PubMed1992

Abnormalities of thirst regulation in patients with chronic renal failure on hemodialysis.

To determine whether thirst mechanisms are altered in nondiabetic patients with chronic renal failure on hemodialysis, 4 patients with an average weight gain between dialysis sessions of more than 5% of dry body weight (group I), 5 patients with less than 3% weight gain (group II), and a group of 6 healthy subjects (group III) were submitted to infusion of hypertonic saline. After infusion the subjects had free access to water. Thirst was evaluated by visual analogue rating scales. Despite similar increments of effective plasma osmolality during saline infusion, patients of group I were thirstier than groups II and III (p less than 0.005 and p less than 0.01, respectively). Changes in thirst ratings were similar in groups II and III. Osmotic thresholds for thirst onset were similar in groups II and III (288.9 +/- 8.5 and 289.8 +/- 3.4 mosm/kg, respectively), but lower in group I (277.6 +/- 7.6 mosm/kg). Nevertheless, great variations were observed in the latter group. Thus, 2 patients showed thresholds for thirst within the normal range, whereas the others had low osmolar thresholds for thirst and baseline plasma osmolalities and high basal thirst scores. During the drinking period, the patients of group I drank more (14.2 +/- 2.8 ml/kg) than those of groups II (5.3 +/- 1.6 ml/kg; p less than 0.02) and III (10.2 +/- 1.6 ml/kg; n.s.) The plasma levels of angiotensin II in uremic patients were higher than in healthy subjects, although there were no differences between groups I and II and no correlation between basal angiotensin II levels and the interdialytic weight gain.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1991

Effect of V1-vasopressin receptor blockade on arterial pressure in conscious rats with cirrhosis and ascites.

Angiotensin II blockade with saralasin in human cirrhosis with ascites is associated with a significant reduction in arterial pressure, indicating that endogenous angiotensin II plays an important role in the maintenance of systemic hemodynamics in this condition. The aim of the current study was to investigate whether vasopressin also contributes to the maintenance of arterial pressure in cirrhosis with ascites. The study was performed using three groups of cirrhotic rats with ascites and three groups of control animals. The administration of d(CH2)5Tyr(Me)AVP, a selective antagonist of the vascular effect of vasopressin, to 10 cirrhotic rats induced a significant reduction in mean arterial pressure (from 94 +/- 4 to 85 +/- 4 mm Hg; P less than 0.001) and a significant increase in plasma renin activity (from 24.3 +/- 4.9 to 34.3 +/- 5.9 ng/mL.h; P less than 0.02) and plasma norepinephrine concentration (from 1474 +/- 133 to 2433 +/- 253 pg/mL; P less than 0.01). Similar results were observed following saralasin administration in a second group of 5 cirrhotic rats [mean arterial pressure decreased from 97 +/- 4 to 85 +/- 5 mm Hg (P less than 0.0001); and plasma renin activity and norepinephrine concentration increased from 18.4 +/- 5.8 to 40.3 +/- 5.7 ng/mL.h (P less than 0.02) and from 1383 +/- 70 to 2312 +/- 334 pg/mL (P less than 0.05), respectively]. The simultaneous blockade of angiotensin II and vasopressin in a third group of cirrhotic rats resulted in a significantly greater reduction of mean arterial pressure (from 97 +/- 6 to 74 +/- 6 mm Hg; P less than 0.05). No changes in arterial pressure were observed in the three groups of control rats. These findings indicate that endogenous vasopressin is as important as angiotensin II in the maintenance of arterial pressure in cirrhotic rats with ascites and support the contention that arterial hypotension is the initial event leading to the stimulation of the renin-angiotensin system and vasopressin in this animal model of cirrhosis.

Angiotensin II↗
PubMed1991

Plasma and saliva levels of PGI2 and TXA2 in the headache-free period of classical migraine patients. The effects of nicardipine.

The levels of Prostacyclin (PGI2) and Thromboxane A2 (TXA2) were assayed simultaneously (RIA) in the plasma and saliva of 9 patients suffering from classical migraine attacks. The assays were done during an attack-free period. In relation to the control group we observed a significant decrease in the plasma levels of PGI2 together with a sharp increase in TXA2 in saliva. When the patients were treated with nicardipine, a calcium antagonist, the TXA2 increase in saliva did not occur. These results suggest both a systemic and local effect in the classical migraine attacks. We explain and discuss our results by referring to the PGI2: TXA2 equilibrium system. Nicardipine action might be related to its ability to reduce the calcium entry into the cell induced by thromboxane.

Adolescent↗
PubMed1991

Temporal relationship between the decrease in arterial pressure and sodium retention in conscious spontaneously hypertensive rats with carbon tetrachloride-induced cirrhosis.

It has been proposed that the initial event of sodium retention in cirrhosis is a peripheral arteriolar vasodilation causing underfilling of the arterial vascular compartment and stimulation of the renin-aldosterone and sympathetic nervous systems. To test this hypothesis, systolic blood pressure, sodium balance and urinary excretion of sodium and aldosterone were sequentially measured in 13 conscious spontaneously hypertensive rats submitted to a cirrhosis induction program with carbon tetrachloride and phenobarbital and in 14 control hypertensive animals. No significant differences were found between control and cirrhotic rats in any of the measured parameters during the first 7 wk of the study. The eighth week sodium retention developed in cirrhotic rats as indicated by a positive sodium balance and a marked decrease of sodium excretion. At the same time a significant reduction in systolic blood pressure and a great increase in urinary excretion of aldosterone were detected. These changes were more marked the ninth week of the study. In cirrhotic rats there was a highly significant direct correlation between systolic blood pressure and urinary sodium excretion. Postmortem examination showed a histological picture of cirrhosis in all animals given carbon tetrachloride and ascites in six of them. These results indicate that the onset of hyperaldosteronism and sodium retention in conscious spontaneously hypertensive rats with carbon tetrachloride-induced cirrhosis is chronologically related to a significant decrease in arterial pressure, thus supporting the "peripheral arterial vasodilation hypothesis" of ascites.

Aldosterone↗
PubMed1990

Effects of intravenous amino acid infusion and dietary proteins on kidney function in cirrhosis.

Acute intravenous amino acid infusion or a high-protein diet increases renal plasma flow and the glomerular filtration rate in healthy subjects. Conversely, a low-protein diet reduces renal plasma flow and glomerular filtration rate. The aim of this study was to investigate the effect of intravenous amino acid infusion and dietary proteins on kidney function in cirrhosis. Protocol 1: renal plasma flow and glomerular filtration rate were measured before and during intravenous administration of a 10% amino acid solution (0.043 ml/kg/min) to eight compensated cirrhotic patients (group 1), nine nonazotemic cirrhotic patients with ascites (group 2) and seven cirrhotic patients with ascites and functional renal failure (group 3). Amino acid administration induced a significant increase in renal plasma flow and glomerular filtration rate in all groups studied. Renal plasma flow and glomerular filtration rate increased by 16% and 14%, respectively, in group 1; 31% and 22% in group 2 and 25% and 21% in group 3. Protocol 2: Renal plasma flow and glomerular filtration rate were measured in nine cirrhotic patients with ascites after 11 days on a low-protein diet (0.5 gm/kg body weight/day) and also after the patients followed for 11 days a moderately high-protein diet (1.5 gm/kg body weight/day). The moderately high-protein diet was associated with a significant increase in renal plasma flow (12%) and glomerular filtration rate (13%) compared with values obtained while the patients followed the low-protein diet. Plasma glucagon levels increased markedly during the intravenous administration of amino acid and the intake of the moderately high-protein diet.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acids↗