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Biomedical subjects

G Perez

Publications and source records attributed to G Perez.

At least 109 records · Page 6Linked to original sources
PubMed1980

Leukopenia, hypoxia, and complement function with different hemodialysis membranes.

Complement activation during exposure of plasma to cuprophan has been postulated to cause leukopenia and hypoxia in hemodialysis patients. To determine if hypoxia is related to leukopenia and if complement activation leads to a depletion of functional complement components, we dialyzed four patients three times sequentially against each of four types of membranes: cuprophan, regenerated cellulose, cellulose acetate, and polyacrilonitrile. Within 20 min there was a marked leukopenia with cuprophan from 5541 +/- 376 to 1216 +/- 94 (P less than 0.001) and with regenerated cellulose from 5541 +/- 411 to 1533 +/- 203 (P less than 0.001). With cellulose acetate, the change from 5558 +/- 400 to 3783 +/- 341 (P less than 0.001) was less dramatic, and with polyacrilonitrile the fall from 5591 +/- 381 to 464 +/- 401 (P less than 0.02) was minimal. After 2 and 4 hours of dialysis, a rebound leukocytosis was seen with cuprophan, regenerated cellulose, and cellulose acetate, but not with polyacrilonitrile. Transient thrombocytopenia occurred with cuprophan and regenerated cellulose. In spite of the variable degree of leukopenia, all membranes induced a similar and significant hypoxia, which was progressive throughout dialysis, even during the rebound leukocytosis. After 4 hours, the mean PO2 ranged from 91 to 93 mm Hg with all membranes. Functional hemolytic titers of whole complement, C3, C5, and C4 were normal prior to hemodialysis and failed to decrease after 4 hours with any membrane. It is concluded that hemodialysis leukopenia is membrane-dependent and is not the cause of hypoxia. In addition, hemodialysis complement activation does not lead to functional complement depletion and is of no clinical significance.

Adult↗
PubMed1980

Uptake and release of amino acids by normal and remnant kidneys: studies in the isolated perfused rat kidney.

In order to evaluate the capacity of normal and remnant kidneys to take up and release amino acids when plasma concentrations are increased above normal levels, we have determined the simultaneous net uptake or release of eight representative amino acids using the isolated perfused rat kidney model. Eight normal and five partially infarcted kidneys from Sprague-Dawley rats were perfused with Krebs-Ringer's bicarbonate buffer containing glucose 8 g/100 ml albumin and amino acids at concentrations approximately 10 times above normal plasma levels. Urine was collected every 15 min for 75 min, and perfusate samples were obtained at the midpoint of each urine collection. Amino acids were measured by gas-liquid chromatography. During perfusion, there was substantial net utilization of asparate, proline, alanine, and glycine by normal kidneys. In remnant kidneys the net uptake of amino acids tended to be lower than that of the normal kidneys. The fractional excretion of most amino acids by remnant kidneys was significantly higher than that of controls. These studies demonstrate the substantial capacity of the kidney to take up or release amino acids when presented with an increased load. The findings suggest that the fractional reabsorption of amino acids by residual nephrons of remnant kidneys is decreased.

Amino Acids↗
PubMed1980

Influence of nephrectomy on the glucoregulatory response to insulin administration in the rat.

Insulin sensitivity and resistance were examined in vivo in uremic rats by using tracer methods which permit the assessment of "non-steady-state" glucose kinetics. By relating the changes in the rates of glucose output by the liver (Ra), uptake by tissues (Rd), and metabolic clearance (MCR) to immunoreactive glucagon and insulin, it was possible to assess the tissue sensitivity to physiologic and supraphysiologic levels of these two hormones and the site of insulin resistance. The effect of an intravenous injection of insulin (100 mU) on glucose turnover was studied in acutely uremic rats 15 h after bilateral nephrectomy and in sham-operated controls, in the postabsorptive state. Glucose output by the liver and uptake by tissues were determined by the primed constant infusion technique using [3H]glucose. Under basal conditions, no significant difference in Ra and Rd between the two groups were observed, while a significant hyperglycemia and a reduced glucose metabolic clearance rate in the face of hyperglucagonemia and normal plasma insulin levels were observed in nephrectomized rats. After insulin injection, the glycemic curves were similar in the two groups, while Ra, Rd, and MCR displayed significantly lower values in nephrectomized rats in the face of higher plasma concentrations of insulin and glucagon. It was concluded that acute uremia in the rat is characterized by a loss of the normal ability of insulin to promote peripheral glucose uptake with retention of hepatic sensitivity to insulin.

Animals↗
PubMed1980

Urea synthesis by perfused rat liver in experimental uremia.

Urea synthesis was examined in experimental uremia using the isolated perfused rat liver in order to assure strict control of substrate (NH4Cl) presented to the liver. Acute uremia was created in female Sprague-Dawley rats by bilateral nephrectomy (n = 7) 48 h prior to studies. Chronic uremia (8--14 weeks) was produced by right nephrectomy and segmental infarction of the left kidney in 7 rats. At infusion rates of NH4Cl (8.3 mumol/min) which resulted in prehepatic perfusate ammonia levels approximately twice the previously described Km value, livers of chronically uremic rats had slightly higher rates of urea production than controls (controls: 0.41 +/- 0.03; chronic uremia: 0.54 +/- 0.04 mumol/min/g of wet liver weight; p less than 0.02). In acute uremia, urea production was higher (0.66 +/- 0.05 mumol/min/g) than in sham-operated rats (0.59 +/- 0.05 mumol/min/g) but the differences did not achieve statistical significance. Simultaneously performed taurocholate transport studies did not reveal significant functional differences between the livers of uremic and control animals. The data suggest that urea production by livers of uremic rats is increased when compared to that of control animals.

Acute Disease↗
PubMed1980

Altered glucoregulatory response to physiological infusions of epinephrine and glucagon in hyperthyroidism.

To study the mechanism of altered glucose homeostasis in hyperthyroidism, the effects of a 2-h physiological infusion of epinephrine (0.05 microgram/kg x min) or glucagon (3 ng/kg x min) on glucose kinetics and glucoregulatory hormones were determined in nine normal subjects and five untreated hyperthyroid patients. Under basal conditions, hyperthyroid patients exhibited increased glucose turnover (2.2 +/- 0.09 vs. 1.62 +/- 0.1 mg/kg x min in normals), a modest hyperglycemia, hyperglucagonemia, and normal levels of plasma insulin, cortisol, and GH. In normal subjects, epinephrine induced a sustained increase in plasma glucose (45 mg/dl), reflecting a transient 100% rise in glucose output, and a sustained 28% decrease in glucose clearance. In hyperthyroid patients, the rise in plasma glucose was significantly lower (22 mg/dl) due to a smaller but sustained increase in glucose output (45%) and the lack of a fall in glucose clearance. Plasma insulin rose to a peak 80% higher than baseline in hyperthyroid patients, whereas in normals it initially declined and then rose to levels 50% higher than basal. Plasma glucagon displayed only minor changes in both groups. Glucagon infusion induced similar increments in plasma glucagon levels in the two groups (120-150 pg/ml). Insulin, cortisol, and GH remained unchanged. Plasma glucose rose by 4 mg/dl in hyperthyroid patients and by 11 mg/dl in normal subjects. The net increments were significantly lower in the former group (P < 0.05-0.01). Glucose output increased by 40% in normals and returned to baseline by 75 min, whereas it increased by only 15% in hyperthyroid patients and remained above baseline until the end of the infusion. Glucagon had no appreciable effect on glucose clearance in either group. We conclude that hyperthyroidism is characterized by 1) increased glucose turnover and hyperglucagonemia in the basal state, 2) a reduced glucemic response to physiological infusions of epinephrine and glucagon, 3) a sustained response of glucose production to epinephrine and glucagon, and 4) the lack of epinephrine-induced suppression of glucose clearance, presumably due to an exaggerated response of insulin secretion to epinephrine.

Adult↗
PubMed1978

Volume as a determinant of plasma aldosterone in anephric man.

Previous studies from this laboratory have demonstrated that the redistribution of blood volume and concomitant central hypervolemia induced by water immersion to the neck (NI), produces a prompt and profound suppression of plasma renin activity (PRA) and plasma aldosterone concentration (PA) without concomitant alterations in serum sodium and potassium concentrations. The NI model was utilized to assess the responsiveness of PA to volume expansion in 12 anephric subjects. The patients were studied on 2 occasions, 48 h after their last dialysis: during a seated control study (7 of the patients) and during 3 h of NI (all 12 patients). The conditions of seated posture and time of day were identical. Blood for PRA, PA, and cortisol was obtained at 30-min intervals for 5 h. PRA was undetectable in all patients. NI failed to alter PA. Plasma cortisol declined progressively throughout NI; serum potassium concentration remained unchanged. An identical NI study in normal subjects suppressed PA by 60%. These data demonstrate that when plasma composition and posture are maintained constant, marked central hypervolemia does not alter PA in anephric man. The present findings support the role of the renin-angiotensin system as the prepotent mediator of volume-induced changes in PA.

Adult↗
PubMed1977

Removal of guanidinosuccinic acid by hemodialysis.

The dialysis clearance of guanidinosuccinic acid (GSA) was measured in vitro and in vivo in patients undergoing maintenance hemodialysis. The in vitro (44 +/- 5 [SEM] ml/min) and in vivo (40 +/- 7 ml/min) clearances were similar to and lower than those of urea and creatinine. Plasma GSA concentrations predialysis (210 +/- 49 microgram/100 ml) were higher then those of controls ( less than 40 microgram/100 ml) and decreased substantially at the end of a single hemodialysis (percent decrease: 53 +/- 5). Marked increase of plasma GSA concentrations 12 h postdialysis were found in only two cases. An attempt was made to derive a single curve predicting plasma GSA decline during dialysis using the data obtained in these patients. The removal data suggest that the space of distribution of GSA approximates the extracellular fluid volume.

Guanidines↗
PubMed1977

Studies on the mechanism underlying the influence of alanine infusion on glucose dynamics in the dog.

These experiments have been designed to study the influence of alanine infusion of glucose dynamics in the dog and to further elucidate the role of pancreatic hormones in the interaction of alanine with glucose homeostasis. The primed constant infusion of glucose-2-t was used in order to quantitate the rates of glucose production by the liver (Ra) and glucose utilization (Rd). In a first group of experiments, the intravenous infusion of alanine at the rate of 2 mg./kg./min. produced a moderate enhancement of plasma insulin (IRI), while pancreatic glucagon (IRG) increased more consistently. This different pattern of IRI and IRG response caused the insulin/glucagon molar ratio to decline progressibely throughout the experiment. Both rates of glucose turnover increased significantly during alanine infusion. Since Ra rose more rapidly thanRd did initially, hyperglycemia developed. Later, glucose production slowly decreased and, in spite of the sustained hyperglucagonemia, reached levels very close to the baseline in the second part of the experiment. A significant direct correlation between Ra and IRG was found, while the changes in Ra correlated inversely with those in I/G molar ratio. In a second group of experiments, alanine was infused at the same dose together with 0.4 microng./kg./min. of cyclic somatostatin. In the first part of the infusion, IRG fell more than IRI did, so that I/G ratio increased. Later, IRI levels maintained at low values while IRG returned slowly to the baseline and consequently I/G ratio significantly decreased. Glucose production fell rapidly soon after the beginning of the infusion, and therefore hypoglycemia developed. Later, Ra increased progressively to levels above baseline and plasma glucose returned to the preinfusion levels. As in the the first group of experiments, a significant direct correlation between Ra and IRG and an inverse correlation between the changes in Ra and I/G ratio were observed. These experiments demonstrate that alanine infusion produces an acceleration of glucose turnover and that a clear interrelationship between the release of glucose by the liver and the mobilization of pancreatic hormones exists. Finally, the experiments with somatostatin indicate that hyperglucagonemia is one of the mechanisms underlying the stimulatory effect of alanine on glucose production.

5-Hydroxytryptophan↗
PubMed1976

Influence of prostaglandins on plasma glucagon levels in the rat.

The effect of PGE1and PGA1 intravenous infusion (2/mug/min) on plasma glucose and glucagon levels was investigated in normal, sympathectomized and propranolol-treated rats. PGE1 infusion significantly increased glucose and glucagon levels, while PGA1 had no effect. Since the dose of PGE1 used in this study was able to reduce the arterial blood pressure by about 20%, the possibility that PGE1 acted indirectly through a reflex sympathetic overactivity was tested. The increases in plasma glucagon induced by PGE1 occurred also in sympathectomized or in beta-blocked animals. Thus, it was possible to exclude a sympathetic mediation or a direct stimulation of pancreatic beta-receptors as a likely mechanism of PGE1 action.

Animals↗
PubMed1976

Theophylline stimulation of gluconeogenesis from alanine in normal and sympathectomized rats.

The influence of theophylline ethylenediamine (100 mg/kg i.p.) on gluconeogenesis was studied in normal and in adrenodemedullated and reserpinized rats after overnight fasting by measuring the time-course of Alanine-14C incorporation into Glucose-14C. In the normal rat, theophylline produced a moderate hyperglycemia associated with an increased conversion of alanine to glucose at all time intervals. In addition, a marked rise of plasma levels of insulin and glucagon was observed. In sympathetctomized rats, plasma glucose and gluconeogenesis were again enhanced by theophylline, but the pattern of these modifications differed from that of normal rats since the peak values occurred earlier. Subsequently, both parameters rapidly declined reaching values lower than controls at the end of the experiment. Insulin response to theophylline was higher in sympathectomized animals in comparison to normal rats, while glucagon response was approximately of the same magnitude in the two groups. From these findings it was concluded that theophylline is able to stimulate gluconeogenesis from alanine both in the normal and sympathectomized rat. The different pattern of alanine conversion to glucose seems to depend on the different participation of insulin and catecholamines in the two groups.

Alanine↗
PubMed1976

Participation of beta receptors in reflex vasodilatation in the dog.

The effects of propranolol, given by direct intraarterial injection, on the reflex vasodilatation induced in the atropinized isolated gracilis muscle by rapid intravenous administration of norepinephrine, were studied in dogs. In these studies, both atropine and atropine plus propranolol did not significantly alter the maximum fall in vascular resistance in the perfused gracilis muscle following intravenous norepinephrine; however, if the reflex responses were evaluated as integrated areas of vasodilatation, atropine attenuated the vasodilatation and the administration of propranolol further attenuated the reflex. In fact, the value of the integrated areas of vasodilatation was 52.8 +/- 9 mmHg/min in the basal state, 39 +/- 6 mmHg/min after administration of atropine, and 24 +/- 7 mmHg/min after propranolol, whereas the integrated areas of the systemic hypertension did not show any modification. These results prompt us to conclude that the adrenergic beta receptors participate in the reflex vasodilatation, although the mechanism of their action needs further elucidation.

Animals↗
PubMed1976

The biosynthesis of guanidinosuccinic acid by perfused rat liver.

The metabolic pathway for the synthesis of guanidinosuccinic acid was studied in the rat. Labeled guanidinosuccinic acid was isolated from the urine of animals given L-[guanidino-14C]arginine intraperitoneally but did not appear in the urine after administration of D,L-[guanidino-14C]canavanine. Radioactive arginine and nonradioactive aspartic acid and arginine were infused in the isolated, perfused rat liver. After 20 min, small amounts of both labeled and unlabeled guanidinosuccinic acid and large amounts of urea were detected in radiochromatograms of the perfusate. These results support the theory that guanidinosuccinic acid is formed in the liver from transamidination of arginine to aspartic acid.

Animals↗