PubMed Health⌕ Search

Biomedical subjects

C P Carvounis

Publications and source records attributed to C P Carvounis.

At least 19 recordsLinked to original sources
PubMed2001

Unmeasured cations: probable cause of relatively low anion gap in chronic renal failure.

It is commonly believed that the electrolyte pattern in the patients with chronic renal failure (CRF) is associated with high anion gap (AG) and low serum bicarbonate (HCO3). However it was seen in many clinical studies that the AG is normal or only minimally increased in such patients. It is also known that organic cations, in particular guanidines, also increase in the serum of patients with CRF. We thus postulated that the relatively small increase in AG could be, in part, explained by the coexistent increase in unmeasured cations. If this is true, one may expect that the serum osmolality measured directly will be higher than the estimated one, leading to an osmolar gap (OG). Previous studies have shown that indeed OG exists in patients with CRF. We proceeded to determine SMA-7, AG, and OG simultaneously in ambulatory, undialyzed CRF patients with serum creatinine between 4 and 12 mg/dL. These investigations were also done on nine patients, after dialysis, who went on to have dialysis. The patients were divided into the normal AG (AG < or = 14) and a high AG (AG > 14) groups. There was no correlation of serum bicarbonate with degree of renal dysfunction. Serum AG influenced HCO3 only in the patients with high AG group (bicarbonate = 23.85-0.69 (deltaAG), r2 = 0.45). In patients with normal anion gap there was a good correlation between deltaAG and OG (deltaAG = 3.4-0.15 OG, r = 0.46, r2 = 0.21, p < 0.05). Thus serum bicarbonate appears to be controlled by both AG and OG. Following dialysis, OG decreased from 15.5 +/- 1.06 to 6.08 +/- 1.71, p < 0.01. We conclude that OG must be made up of unmeasured cations of low molecular weight as it normalizes the AG, and gets cleared after dialysis. These low molecular weight substances could be guanidines, such as guanidosuccinic acid and methylguanidine, which are increased by one hundred fold in CRF.

Acid-Base Equilibrium↗
PubMed2000

Prediction of acute renal failure by "bedside formula" in medical and surgical intensive care patients.

BACKGROUND: Prediction of which intensive care unit (ICU) patients are likely to develop acute renal failure (ARF) would be useful. However, scoring systems such as APACHE have been disappointing in this regard. We previously developed a bedside formula to predict ARF using only 3 parameters: serum albumin, urine osmolality, and presence of sepsis. METHODS: We prospectively evaluated 115 consecutive medical ICU (MICU) patients, comparing the bedside formula to APACHE II AND APACHE III as predictors of ARF or death and looking at nutritional parameters such as iron binding capacity, triceps skin fold, mid-arm circumference, and total lymphocyte count. We then evaluated 123 additional consecutive MICU and 98 consecutive surgical ICU (SICU) patients, comparing the bedside formula to APACHE II. RESULTS: The bedside formula was consistently more accurate than APACHE II in predicting ARF or in-hospital death in MICU patients. However, in SICU neither formula predicted ARF, and APACHE II predicted in-hospital death slightly better. No nutritional parameter other than albumin correlated with ARF. CONCLUSION: The bedside formula appears superior to APACHE II in predicting ARF or death in MICU but not SICU. This suggests that these two ICU populations are different.

APACHE↗
PubMed1998

Serum creatinine and blood urea nitrogen over a six-year period in the very old. Creatinine and BUN in the very old.

In a population of 141 very elderly subjects, there was a small but significant decline in BUN and creatinine at 3 years, which persisted at 6 years although partially attenuated. A similar pattern of falling BUN and creatinine was seen in the 31 subjects who began the study with mild azotemia. There was no significant change in the subjects' mean Body Mass Index during the 6-year period of observation. The azotemic subjects had a rate of death or dropout from the study similar to that of the entire cohort. Mean systolic blood pressure fell by 5.4 mm Hg (p < 0.05) and diastolic blood pressure by 2.1 mm Hg (p = NS) by 6 years. Users of diuretics or NSAID had a mean BUN and creatinine comparable to those not taking these medications. We conclude that BUN and serum creatinine do not necessarily increase with time in the old old, even in those with mild azotemia, hence, several determinations of these parameters may be needed to ensure accuracy. While renal function in the elderly probably does not improve with time, it may stabilize due to improvement in blood pressure. Use of diuretics and NSAID by functioning elderly individuals is not necessarily associated with worsening azotemia.

Aged↗
PubMed1998

Renal involvement in the systemic inflammatory reaction syndrome.

Uncontrolled infection quite often leads to systemic inflammatory reaction syndrome (SIRS) and multiorgan dysfunction (MOD) syndrome. Thirty-five consecutive patients (19 males) fulfilling strict diagnostic criteria for SIRS were enrolled in two multicenter prospective double-blind trials involving new therapies for SIRS. The patients were followed prospectively up to day 28 after the enrollment. In the 35 patients with SIRS, males predominated in the age group below 40 (10/12, 83%) compared to the older group (nine males out of 23, 39%). Out of 16 females presenting with SIRS, only two were below the age of 40. This distribution was statistically different than our general MICU population. The serum albumin in these patients was uniformly low, with a mean of 22.5 gm/L. The bulk of SIRS patients (22/35; 63%) went on to develop acute renal failure (ARF). Although statistically not different, skin and peritoneal infections were more common in ARF group while pulmonary infections in non-ARF group. The majority of blood-cultures grew gram-positive organisms. Resolution of SIRS occurred within first 3 days in greater number of non-ARF survivors than ARF survivors (6/9, 66.7% vs. 6/16, 37.5%). Of the 22 ARF patients, 17 showed improvement in their renal function; the five who did not, died before day 28. The overall mortality (about 32%) was similar in both groups. Patients who developed both ARF and ARDS did not survive. In conclusion. SIRS occurs mostly in elderly patients, almost always in patients with low albumin levels. Premenopausal women seem to be protected. Blood cultures isolated a gram-positive organism in the majority of cases. Improvement in serum creatinine suggests good prognosis. The mortality in ARF and non-ARF groups is similar.

APACHE↗
PubMed1996

Effect of oral L-carnitine on serum myoglobin in hemodialysis patients.

Oral L-carnitine has been reported to lower the elevated serum myoglobin of renal failure in chronic peritoneal dialysis patients, and intravenous L-carnitine can improve muscle fatigue and cramps in chronic hemodialysis patients. In this study oral L-carnitine, 1.98 g/day, was administered to 6 chronic hemodialysis patients for 8 weeks. Serum levels of myoglobin, creatine kinase, and aldolase, as well as skeletal muscle symptoms (cramps during dialysis, fatigue, and weakness) were monitored biweekly for 12 weeks. Mean baseline serum myoglobin level was 337 +/- 34 ng/mL. By 6 and 8 weeks mean serum myoglobin was 234 +/- 39 and 233 +/- 40 ng/mL, significantly lower by the Friedman test (p < 0.05). Four weeks after carnitine was discontinued, mean serum myoglobin had risen to 320 +/- 118 ng/mL. Serum creatine kinase and aldolase levels were normal throughout the study. All 6 patients noted improvement in muscular symptoms, with maximal effect at 8 weeks, although 2 patients did not improve until 2 to 4 weeks after carnitine was stopped. We conclude that oral L-carnitine may lower serum myoglobin and improve muscle cramps and weakness in hemodialysis patients. The maximal effect of carnitine on myoglobin occurs 2 weeks before the maximal improvement in muscular symptoms.

Administration, Oral↗
PubMed1990

L-histidine augments the response to 1-deamino-8-D-arginine vasopressin in Brattleboro homozygous (di/di) rats.

Studies in vitro have shown that L-histidine increases the hydroosmotic response to vasopressin. We examined whether this phenomenon occurs also in vivo. Homozygous Brattleboro rats (di/di) were fed a regular diet (0.5% histidine) or a diet enriched with histidine and received 1 ng of 1-deamino-8-D-arginine vasopressin (dDAVP) daily. Addition of histidine (1% by weight) increased post-dDAVP urine osmolality to a level higher than that of control (502 +/- 62 vs. 316 +/- 36 mosmol/kg, P less than 0.05). Similar results were seen with 3.0% and 5.5% dietary histidine. There were significant increases in free-water reabsorption and in the ratio of free-water reabsorption to osmolar clearance, but no difference in osmolal clearance. No significant effect was found with supplemental histidine of 0.5% or less. The cause for these findings appears not to be the metabolism of histidine, since the nonmetabolizable D-histidine had a significant, albeit smaller, effect, and the isonitrogenous addition of albumin, alanine, arginine, or glutamine was ineffective. In part, histidine may operate by increasing cAMP since the renal cAMP content in response to vasopressin is increased in histidine-fed rats (13.1 +/- 0.9 vs. 9.8 +/- 0.8 nmol/g dry weight, P less than 0.01). The role of prostaglandins appears less clear. Histidine greatly decreased urinary PGE2 during baseline (1.5 +/- 0.3 vs. 7.0 +/- 2.3 micrograms/mg creatinine, P less than 0.001), but it profoundly augmented urinary prostaglandin excretion after dDAVP stimulation (40.0 +/- 4.2 vs. 7.0 +/- 2.0 micrograms/mg creatinine, P less than 0.001).

Animals↗
PubMed1989

Water flow in the toad urinary bladder in response to vasopressin: role of potassium.

In agreement with previous reports, we found that absence of K+ from the serosal bath of the toad urinary bladder substantially impairs vasopressin and cAMP-stimulated water flow. The decreased response to vasopressin appears unrelated to prostaglandin production since inhibition of endogenous prostaglandins by pretreatment with naproxen 10(-5) M failed to prevent the effect seen with K+-free Ringer's. The resistance to vasopressin does not appear to be directly related to epithelial K+ concentrations, in that maneuvers leading to decreased intracellular K+ failed to produce a similar effect. A more likely explanation appears to be that K+-free Ringer's induces an increased cytosolic Ca++ which, in turn, decreases the hydrosmotic effects of vasopressin. Several lines of evidence argue in favor of such an explanation: (a) Increased cytosolic Ca++ had been found in other tissues with low extracellular K+; (b) The resistance to vasopressin decreases with decreased serosal Ca++; (c) The effects of K+-free Ringer's are not additive in situations believed to have increased epithelial Ca++, i.e. replacement of serosal Na+ with choline; (d) The effects of K+-free serosal bathing medium could be both prevented and/or reversed if already established by increasing serosal bath, and presumably intracellular, pH, which is believed to decrease intracellular Ca++.

Animals↗
PubMed1988

Effects of histidine on vasopressin action: role of decreased prostaglandin production.

Addition of histidine to the serosal bath of the toad bladder increases the hydrosmotic response of vasopressin in this tissue. Because this represents primarily the effect of the imidazole ring of histidine, which is a known inhibitor of the production of prostaglandins, we evaluated whether histidine increases the response to vasopressin through decreased prostaglandin production. Histidine increases the response to vasopressin much more than 10(-5) M naproxen, even though the latter was equipotent to histidine in reducing prostaglandin E2 (PGE2) production. Furthermore, histidine was additive to naproxen in increasing the hydrosmotic effect of vasopressin, without causing a further decrease in PGE2 production. These findings suggest that histidine has an effect over and above that due to inhibition of prostaglandin synthesis. Our results suggest that histidine enhances the permeability of the tissue beneath the luminal membrane, an effect not found with naproxen. We propose that histidine increases the hydrosmotic response to vasopressin through at least two distinct mechanisms: 1) it decreases prostaglandin synthesis and thus increases luminal permeability; 2) it decreases the resistance to water movement of the tissues beneath the luminal membrane.

Amphotericin B↗
PubMed1986

Nutritional status of maintenance hemodialysis patients.

Fat and fat-free tissues were determined in hemodialysis patients using either anthropometric measurements or indirectly from total body water (TBW) determined from urea kinetics. A very close correlation between the two methods in determining either fat or fat-free tissue (r greater than 0.8, n = 43) was shown. Twenty-two patients were followed for 2 yr. We found that fat increased while fat-free tissue decreased over that period of time. The latter appears to reflect methodological problems since both fat-free determinations depend upon TBW rather than somatic proteins. This was further confirmed by finding a proportional decrease in TBW with time, while creatinine appearance rate remained unaffected. Adherence to prescribed diet was monitored through diet records and periodic determination of urea N appearance rate during interdialysis periods. Our present studies determined body composition of hemodialysis patients and examined the relative validity of the commonly used methods. We demonstrate that no malnutrition occurs with time in patients adhering to their prescribed diet.

Adipose Tissue↗
PubMed1985

Independent action of prostaglandins and kinins on vasopressin-stimulated water flow.

The kallikrein-kinin and the prostaglandin systems are both important modifiers of vasopressin action. This study examines whether the systems are dependent on one another for their action. Four groups of toad hemibladders were examined. In groups 1 and 2 animals the endogenous prostaglandin system was inhibited. Inhibition of kallikrein by aprotinin caused vasopressin-stimulated water flow to increase further (24.8 +/- 4.9 to 34.5 +/- 4.8 microliters/min) while potentiation of kinins by captropril caused vasopressin-stimulated water flow to decrease (45 +/- 6.3 to 30.5 +/- 5.4 microliters/min). In groups 3 and 4 endogenous kallikrein was inhibited by aprotinin. The addition of prostaglandin E2 caused vasopressin-stimulated water flow to decrease (17.5 +/- 2.7 to 5.71 +/- 1.0 microliter/min) while the inhibition of endogenous prostaglandins caused vasopressin-stimulated water flow to increase (26.7 +/- 3.4 to 39.2 +/- 3.5 microliters/min). Thus, the inhibitory effects of prostaglandins and kinins on vasopressin-stimulated water flow are independent of one another.

Animals↗
PubMed1985

Cell determinants of vasopressin-stimulated water flow.

I present a technique that permits evaluation of the permeability to water of the luminal membrane of the toad urinary bladder, independently of constraints to water flow imposed by the remainder of the tissue. This technique essentially depends on fixation of the luminal membrane with 1% glutaraldehyde for 5 min, and subsequent elimination of cytosolic constraints by decreasing the tonicity of the serosal bath to 1/2 normal strength. The increased hydraulic conductivity found with serosal hypotonicity is readily reversible, as the bladder returns to an isotonic serosal bath. By evaluating water flow in luminally fixed bladders during bathing in normal and hypotonic bath, one may identify the relative contribution of the luminal membrane and the "cytosol" on water flow. Using this technique, I found that the effect of the prostaglandin inhibitor Naproxen to increase vasopressin-stimulated water flow is due to increased luminal membrane permeability. The effect of histidine to increase vasopressin-stimulated water flow, however, depends on increased permeability of both the luminal membrane as well as the underlying structures. The action of serosal hypertonicity to induce water flow is due to an increased luminal permeability. However, serosal hypertonicity decreases "cytosolic" permeability, so that its overall function is a composite effect of its action at the luminal membrane and the "cytosolic" level.

Animals↗
PubMed1985

Importance of amino acids on vasopressin-stimulated water flow.

The presence of several naturally occurring amino acids in the serosal bath of toad urinary bladder significantly alters the hydrosmotic response of this tissue to vasopressin. We found that histidine, glutamate, and lysine increase vasopressin-stimulated water flow by 75%, 60%, and 43%, respectively. In contrast, alanine did not alter vasopressin-stimulated water flow, whereas glutamine decreased it by 25%. The effect of each amino acid represents intracellular events because their effects on theophylline-stimulated water flow were similar to those found with vasopressin. However, the site of action of amino acids varied, with some operating at steps before and others at steps after cyclic AMP generation. The fact that the metabolically inactive D-histidine and D-glutamate are as effective as their metabolically active L-counterparts suggests that the action of amino acids depends upon some physicochemical properties of their molecules. The ability of amino acids to influence the hydrosmotic effects of vasopressin was shown to be independent of prostaglandin generation, ionic composition, and molecular charge. In the case of histidine, we were able to obtain some understanding of the mechanism responsible for its action. We first showed that the effect of histidine does not depend upon its metabolism. In addition to D-histidine being as effective as the metabolically active L-histidine, we also showed that histidine is effective when its metabolism is abolished by low ambient temperature and also when its incorporation into proteins was prevented by cycloheximide. These findings suggest that histidine operates through some physicochemical property localized on its molecule. We were able to show that this property resides on the imidazole part of histidine. Imidazole, similar to histidine, increases vasopressin-stimulated water flow. Methylation of histidine on the imidazole ring completely abolished its effectiveness in increasing vasopressin-stimulated water flow. In contrast, methylation of histidine at the side chain increased vasopressin action similar to that found for histidine. We provide evidence that the physicochemical property of the imidazole ring of histidine is that of chelating Zn++ intracellularly, and that the intracellular site of action of histidine is closely linked to microtubules formation and/or action.

Amino Acids↗
PubMed1982

Graft infection and bacteremia with Listeria monocytogenes in a patient receiving hemodialysis.

Patients receiving hemodialysis are particularly susceptible to infection. We report a case of Listeria monocytogenes bacteremia and graft infection developing in a patient receiving hemodialysis. Vancomycin hydrochloride therapy was initiated in anticipation of a staphylococcal infection, and continued as the patient's clinical course improved. Ultimately the arteriovenous graft required excision. Identification of the organism and drug susceptibilities are described. To our knowledge, this is the first case report of both an L monocytogenes arteriovenous graft infection and the use of vancomycin in the treatment of this infection.

Blood Vessel Prosthesis↗
PubMed1981

Multiple sites for interaction of prostaglandin and vasopressin in toad urinary bladder.

The interaction of vasopressin with prostaglandins were examined in the toad bladder by determining water flows, cAMP levels, and cAMP-dependent protein kinase activity. Both water flow and activation of cAMP-kinase in response to vasopressin were enhanced after prostaglandin inhibition, consistent with inhibition of vasopressin-induced cAMP generation by endogenous prostaglandins. On the other hand exogeneous PGE stimulated cAMP generation. PGE1 (10(-7) M) alone did not increase water flow but activated kinase more than vasopressin only. Addition of PGE1 (10(-7) M) and vasopressin inhibited water flow as compared with vasopressin along but increased the kinase ratio above that with vasopressin only. PGE2 (10(-5) M) increased the cAMP content and kinase ratio even more than vasopressin but again resulted in no water flow. Addition of vasopressin and PGE2 (10(-5) M) increased water flow but did not alter cAMP content or the kinase ratio compared with PGE2 alone. Similar results were obtained with PGE1. Accordingly, prostaglandin dissociates cAMP levels and kinase ratio from the hydroosmotic response, suggesting that PGE2 inhibits steps distal to cAMP. Consistent with this, in bladders pretreated with naproxen or meclofenamate, PGE2 (10(-8) to 10(-6) M) inhibited the response to submaximal doses of cAMP (5 mM) or 8-bromo-cAMP (0.03 mM). Furthermore, pretreatment with naproxen significantly enhanced the response to cAMP (5 mM). These studies provide evidence for vasopressin-PGE interaction at the site of cAMP generation and also at a step(s) unrelated to cAMP generation.

Animals↗
PubMed1981

Role of the endogenous kallikrein-kinin system in modulating vasopressin-stimulated water flow and urea permeability in the toad urinary bladder.

This study investigates the endogenous kallikrein-kinin system's role as a modulator of vasopressin action in the toad urinary bladder. Kalli-krein inhibition by aprotinin, which results in decreased kinin production, significantly increased both vasopressin and 8-Br-cyclic (c) AMP-stimulated water flow. Kinin potentiation by the kininase II inhibitor captopril (SQ 14225) significantly decreased vasopressin and 8-Br-cAMP-stimulated water flow. In contrast to water flow, vasopressin-stimulated urea permeability was decreased by aprotinin and increased by captopril. We conclude that the endogenous kallikrein-kinin system represents a significant modulator of vasopressin action and it permits separate control of vasopressin-stimulated water flow and solute transport.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1979

Membrane pathways for water and solutes in the toad bladder: I. Independent activation of water and urea transport.

Vsopressin activates a number of transport systems in the toad bladder, including the systems for water, urea, sodium, and other small solutes. Evidence from experiments with selective inhibitors indicates that these transport systems are to a large extent functionally independent. In the present study, we show that the transport systems can be separately activated. Low concentrations of vasopressin (1 mU/ml) activate urea transport with virtually no effect on water transport. This selective effect is due in part to the relatively greater inhibitor action of endogenous prostaglandins on water transport. Low concentrations of 8-bromoadenosine cyclic AMP, on the other hand, activate water, but not urea transport. In additional experiments, we found that varying the ratio of exogenous cyclic AMP to theophylline activated water or urea transport selectively. These studies support the concept of independently controlled systems for water and solute transport, and provide a basis for the study of individual luminal membrane pathways for water and solutes in the accompanying paper.

Animals↗