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D Z Levine

Publications and source records attributed to D Z Levine.

At least 37 records · Page 2Linked to original sources
PubMed1995

Ultrastructural and immunocytochemical evidence for the presence of polarised plasma membrane H(+)-ATPase in two specialised cell types in the chick embryo chorioallantoic membrane.

The chick embryo, confined in the eggshell, has to dispose/buffer the acid generated by its metabolism, as well as to release calcium from the shell which is used for growth. To localise H(+)-ATPase, electron microscope and immunocytochemical studies were conducted on chorioallantoic membranes of 15-17 d chick embryos. Ultrastructural studies of the villus cavity (VC) cells in the chorionic epithelium demonstrated that their apical plasma membrane, juxtaposed with the shell membranes, contains microvilli as well as microplicae which possess 9-10 nm studs at a density of 16,700 particles/micron2, a characteristic feature of the polarised H(+)-ATPase pump. Immunocytochemical staining, using a monoclonal antibody to the 31 kDa subunit of H(+)-ATPase, confirmed the presence of large amounts of the vacuolar H(+)-ATPase in the VC shells with a distribution highly polarised towards the eggshell membranes. Immunoelectron-microscopic localisation studies using a rabbit antiserum to whole bovine H(+)-ATPase and immunogold technique, confirmed the localisation of H(+)-ATPase at the apical microvilli/microplicae as well as in the subapical vesicles. In the allantoic epithelium, the presence of mitochondria-rich (MR) cells was confirmed; it was shown that these cells extend through the full thickness of this epithelium. The MR cells also contained large numbers of 9-10 nm studs, typical of proton secreting cells, in their apical plasma membrane. This was confirmed by immunocytochemical staining which showed abundant localisation of H(+)-ATPase in these cells; this localisation was, however, diffuse rather than apical.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1995

Ciguatera: current concepts.

Ciguatera poisoning develops after ingestion of certain coral reef-associated fish. With travel to and from the tropics and importation of tropical food fish increasing, ciguatera has begun to appear in temperate countries with more frequency. The causative agents are certain varieties of the protozoan dinoflagellate Gambierdiscus toxicus, but bacteria associated with these protozoa may have a role in toxin elaboration. A specific "ciguatoxin" seems to cause the symptoms, but toxicosis may also be a result of a family of toxins. Toxicosis develops from 10 minutes to 30 hours after ingestion of poisoned fish, and the syndrome can include gastrointestinal and neurologic symptoms, as well as chills, sweating, pruritus, bradycardia, tachycardia, and long-lasting weakness and fatigue. More severe features are rare. In this review, the pathophysiologic features and symptoms of ciguatera are reviewed and compared with those of other seafood-related syndromes. Although no definitive therapy is known, the most promising treatment for ciguatera is intravenous administration of mannitol. Physicians should warn patients who are traveling to endemic areas about this toxicosis.

Animals↗
PubMed1994

In vivo modulation of rat distal tubule net HCO3 flux by VIP, isoproterenol, angiotensin II, and ADH.

To examine the in vivo effects of agonists reported to influence bicarbonate flux (JtCO2), microperfusion experiments were carried out on distal tubules of normally fed or overnight-fasted rats. As we previously reported, distal tubules from fed rats reabsorbed no bicarbonate, whereas overnight-fasted rats consistently reabsorbed bicarbonate (JtCO2 10 +/- 3 pmol.min-1.mm-1; P < 0.01). Vasoactive intestinal peptide and isoproterenol infused intravenously (7.3 and 4.0 micrograms.kg-1.h-1, respectively) in fasted rats suppressed JtCO2 and, in the case of vasoactive intestinal peptide, elicited net bicarbonate secretion (JtCO2 -10 +/- 2 and -4 +/- 4 pmol.min-1.mm-1, respectively). In fed rats, angiotensin II infused at a rate of 1.2 micrograms.kg-1.h-1 stimulated bicarbonate reabsorption (JtCO2 16 +/- 3 pmol.min-1.mm-1), while antidiuretic hormone infused at 0.024 micrograms.kg-1.h-1 elicited a similar response (17 +/- 4 pmol.min-1.mm-1), both values being significantly different from control. These results, therefore, demonstrate for the first time that these agonists can modulate JtCO2 at the distal tubule site in vivo and therefore may be potential regulators of systemic acid-base balance.

Absorption↗
PubMed1994

Distal tubule unidirectional HCO3 reabsorption in vivo during acute and chronic metabolic alkalosis in the rat.

During metabolic alkalosis (MA) associated with 2 days of dietary chloride restriction, there is net bicarbonate secretion by rat distal tubules in vivo, whereas after 5 wk of chloride depletion alkalosis there is net bicarbonate reabsorption. To examine unidirectional components of net bicarbonate reabsorption during chronic MA, we measured distal tubule unidirectional bicarbonate secretion (Jsec) and reabsorption (Jreab), as well as the inhibitor sensitivity of Jreab. In control, 2-day, and 7-day alkalosis, Jsec was similar. Jreab, however, was only present in 7-day MA (17 +/- 3 pmol.min-1.mm-1, P < 0.05). This Jreab was completely suppressed by perfusion with 10(-7) M bafilomycin A1, partially suppressed with 10(-5) M Schering (Sch)-28080 (4 +/- 2 pmol.min-1.mm-1, P < 0.1), and converted into a secretory flux by 3 mM amiloride. We conclude that adaptation to chloride depletion MA from the acute secretory phase to the chronic state, where plasma bicarbonate is sustained at elevated levels, does not involve suppression of distal tubule Jsec but rather enhanced Jreab, which is sensitive to bafilomycin, Sch-28080, and amiloride.

Absorption↗
PubMed1994

In vivo adaptation of bicarbonate reabsorption by rat distal tubules during acid loading.

We carried out in vivo microperfusion experiments in acid-loaded rats to characterize the adaptive response of the unidirectional components secretory flux (Jsec) and reabsorptive flux (Jreab)] of distal tubule bicarbonate reabsorption and to test the hypothesis that Jreab is dependent on bafilomycin A1-sensitive H(+)-adenosinetriphosphatase activity. During 18 h of severe acidosis there was a significant decrease in Jsec (-15 +/- 3 vs. -38 +/- 5 pmol.min-1.mm-1, P < 0.05) and a significant increase in Jreab (37 +/- 6 vs. 0 +/- 5 pmol.min-1.mm-1, P < 0.05), which was insensitive to 10(-5) M bafilomycin A1, 10(-5) M Sch-28080, and 3 mM amiloride. After 3 days of acid loading, these same inhibitors reduced Jreab by approximately 60%. However, when water flux was completely inhibited by isosmotic perfusion, a significant Jreab (15 +/- 2 pmol.min-1.mm-1) resistant to 10(-5) M bafilomycin A1 persisted, as in severe acidosis. In reabsorbing distal tubules of overnight-fasted rats, Sch-28080 elicited no inhibition, whereas bafilomycin A1 and amiloride had significant effects (28 +/- 5, 24 +/- 4, respectively, vs. 50 +/- 4 pmol.min-1.mm-1 for fasted rats, P < 0.05). Thus, although Jsec is reduced in the transition from mild to severe metabolic acidosis of 18-h duration, the predominant effect is a stimulation of bafilomycin A1-resistant Jreab.

Acclimatization↗
PubMed1993

Induction of intercalated cell changes in rat pups from acid- and alkali-loaded mothers.

We evaluated the effects of acid-base changes in pregnant and lactating dams on intercalated cell morphology and populations in newborn and 2-wk-old rats. Collecting ducts were studied with transmission electron microscopy with intercalated cells identified by the presence of 10-nm studs in the cytoplasmic face of apical membranes (A-type intercalated cells) or basolateral membranes (B-type intercalated cells). In newborn and 2-wk-old pups from dams with metabolic alkalosis, there was a significantly larger percentage of B-type intercalated cells and a smaller percentage of A-type intercalated cells. Acid loading with NH4Cl, however, did not produce an increase in the percentage of A-type intercalated cells, but reduced the percentage of B-type intercalated cells. We conclude that maternal metabolic alkalosis is associated with an increase in the percentage of B-type intercalated cells, suggesting that the initial differentiation of intercalated cells is responsive to maternal acid-base disturbances.

Acid-Base Imbalance↗
PubMed1993

Poor ultrafiltration during nighttime dialysis in CAPD patients and its effects on fluid balance.

To evaluate fluid retention during the long nighttime peritoneal dwell in continuous ambulatory peritoneal dialysis (CAPD) patients, we measured remaining volumes in 70 patients. In only 50% of these patients were more than 2 L of fluid recovered; in 30% between 1.5 and 2 L were recovered; and in 17% of patients we retrieved less than 1.5 L of peritoneal fluid. In 3 of these patients, who were edematous and had marked pitting edema, we shortened the nighttime dwell by having the patients awaken after 4 hours and drain the dwell. This resulted in 3-5 kg of weight loss in each patient, when compared with each patient's previous use of long nighttime dwells. Finally, we propose in this report two automated methods whereby the period of nighttime dialysis can be controlled, while patients sleep, using a system of timer clamps.

Edema↗
PubMed1991

Differentiation of renal intercalated cells in fetal and postnatal rats.

An ultrastructural study was conducted on the kidneys from rat fetuses and pups from ages ranging from birth to 8 weeks to identify the time of appearance of each of the two intercalated cell types. With transmission electron microscopy. A-intercalated cells were recognized by their large apical microvilli and microplicae as well as by the numerous subapical vesicles. Their identification was confirmed by the presence of typical studs at the cytoplasmic face of the apical plasma membrane. By scanning electron microscopy the cells were recognized by their typical microplicae at the apical surface. In 19-day-old fetuses and newborns. A-intercalated cells were numerous in the epithelium lining the renal pelvis and inner medullary intercalated ducts. Two weeks after birth they disappeared from these regions but became numerous at the outer medullary collecting ducts and also at the cortical collecting ducts although to a lesser degree. B-intercalated cells were recognized by the scarcity of microvilli, the absence of microplicae, and the large number of basal infoldings. Their identification was confirmed by the presence of studs at the cytoplasmic face of the basolateral membrane. B-cells started to appear 3 weeks after birth and increased thereafter. We speculate that the particular stages at which the two cell types differentiate might be related to changes in acid-base status.

Aging↗
PubMed1991

Burning pain in an extremity. Breaking the destructive cycle of reflex sympathetic dystrophy.

The pathogenesis of reflex sympathetic dystrophy is controversial, but the condition can result from a major or seemingly minor injury to a limb, or even an insult to an organ, such as stroke or myocardial infarction. Onset can be sudden or insidious. The syndrome is characterized primarily by localized, deep, burning pain in a limb--pain that may not follow any logical distribution. Nonpitting edema, skin hyperesthesia, and guarding of the limb usually accompany the pain. If treatment is not instituted, deformity, contracture, and wasting of the limb can eventually occur. With appropriate therapy, the process can be stopped and often reversed. The keys are a high index of suspicion, early diagnosis, and aggressive treatment.

Clinical Protocols↗
PubMed1991

Distal tubule bicarbonate reabsorption during rebound metabolic alkalosis.

Rebound metabolic alkalosis is a transient alkalemia that is seen during recovery from NH4Cl-induced metabolic acidosis. The persistent elevation of plasma bicarbonate concentration is the result of continuing excretion of net acid by the kidney. Bicarbonate transport by inner medullary collecting ducts has been reported by others to proceed normally (i.e., bicarbonate reabsorption continues in this segment) during rebound metabolic alkalosis. No other segmental responses have been evaluated. Since the surface distal tubule of the rat is known to both reabsorb and secrete bicarbonate in vivo, it was of interest to determine the response of this segment. Our results show that the distal tubule microperfused in vivo during rebound metabolic alkalosis continues to reabsorb significant amounts of bicarbonate, despite the presence of systemic alkalemia that we have previously shown to be associated with distal tubule bicarbonate secretion.

Absorption↗
PubMed1991

Bicarbonate secretion in vivo by rat distal tubules during alkalosis induced by dietary chloride restriction and alkali loading.

To examine in vivo the separate effects on distal tubule JtCO2, of dietary chloride restriction, bicarbonate loading, and changes in luminal chloride concentration, we microperfused distal tubules at a physiologic flow rate (8 nl/min) with solutions containing either 45 or 0 mM chloride (after gluconate substitution). Rats were fed a diet containing zero, minimal, or normal amounts of chloride, while drinking either water or a solution of 0.15 M sodium bicarbonate. Neither extracellular fluid volume contraction nor negative chloride balance ensued. Analysis of covariance with repeated measures demonstrated that dietary chloride, drinking sodium bicarbonate, and perfusion with either 45 mM or zero chloride, each have separate and significant modulating effects on distal tubule bicarbonate secretion. During mild alkalemia, there is modest bicarbonate secretion which is significantly different from zero (-9.9 +/- 3.2 pmol.min-1.mm-1, P less than 0.01), and which is suppressed after perfusion with zero chloride. In contrast, during more pronounced metabolic alkalosis after supplemental bicarbonate drinking, the bicarbonate secretory flux is brisk (-26 +/- 3 pmol.min-1.mm-1) and significantly different from zero and persists (-11 +/- 3 pmol.min-1.mm-1) even during perfusion with zero luminal chloride. Accordingly, in this two-day model of alkalosis induced by dietary chloride restriction, there is regulatory secretion of bicarbonate by distal tubules in vivo which is modulated by luminal chloride concentration.

Absorption↗
PubMed1990

Interstitial cystitis. An overlooked cause of pelvic pain.

Interstitial cystitis is a disease primarily of young and middle-aged women that is characterized by pelvic pain, urinary frequency, and dyspareunia. Its cause is unknown, but defects in the protective glycosaminoglycan layer of the bladder mucosa may be responsible. The diagnosis is mainly one of exclusion. Cystoscopy reveals characteristic glomerulations in the bladder mucosa. Of the available treatments, the most common are intermittent hydrodilation of the bladder and intermittent intravesical instillation of dimethyl sulfoxide. Other methods and medications are currently under investigation. Although interstitial cystitis is uncommon, its potentially devastating effects may be modified or even averted if primary care physicians are familiar with its presentation and maintain a high index of suspicion.

Cystitis↗
PubMed1990

Luminal chloride modulates rat distal tubule bidirectional bicarbonate flux in vivo.

The effects of replacing luminal chloride with gluconate on distal tubule bicarbonate transport were studied in vivo in normally fed rats, overnight-fasted rats, and rats made mildly alkalotic by administration of desoxycorticosterone acetate (DOCA). In paired microperfusions of the same tubule with 0 or 55 mM Cl at 25 nl/min, net secretion of bicarbonate by distal tubules of fed rats was inhibited by chloride replacement. Zero chloride perfusion in DOCA rats also resulted in an inhibition of net bicarbonate secretion at 25 nl/min. In contrast, replacement of 45 mM chloride also perfused at 25 nl/min in fasted rats caused an increase in net bicarbonate reabsorption. To further characterize the effects of changes in luminal chloride, experiments were undertaken in fasted rats with 0, 45, and 100 mM chloride-containing solutions perfused at 8 and 25 nl/min. Perfusion with zero Cl resulted in net bicarbonate reabsorption at 8 nl/min that increased markedly with high flow, whereas bicarbonate reabsorption did not change significantly during perfusion at high flow with a 45-mM Cl perfusate. In marked contrast, perfusion with a 100-mM Cl solution resulted in only minimal bicarbonate reabsorption at 8 nl/min with significant secretion observed at high flow. Thus, chloride-free perfusates inhibit bicarbonate secretion and enhance bicarbonate reabsorption, while high chloride perfusates elicit net bicarbonate secretion in usually reabsorbing distal tubules.

Acid-Base Equilibrium↗
PubMed1990

Body fluid volume status in hemodialysis patients: the value of the chest radiograph.

Thirty-six pairs of chest radiographs in stable patients undergoing long-term hemodialysis were taken immediately before and after dialysis. They were evaluated in pairs, without indication as to before or after, for radiologic signs of fluid retention, and to identify if changes in these signs could be correlated with body weight and removal of body fluid by dialysis. The radiologic signs assessed were those of increased blood volume (degree of pulmonary vascularity, vascular pedicle width (VPW), transverse cardiac diameter (TD), and azygos vein width (AVW), of interstitial pulmonary edema (perihilar haze, Kerley B lines, bronchial wall thickening and thickening of the minor fissure) and pleural effusion. At least one sign of interstitial pulmonary edema was present in 28 (78%) of the pre-dialysis chest radiographs, and resolved with dialysis in all but three (8%). Pleural effusions were present in 10 (28%), of which 5 (14%) persisted after dialysis and 5 resolved. Pulmonary vascularity was found difficult to assess quantitatively, and AVW was not found to be a useful indicator of volume status. Vascular pedicle width decreased significantly with dialysis and was a useful indicator of volume status. The most reliable indicator, however, was the transverse diameter of the heart, the simplest of the measurements used. Both TD and VPW may be useful in estimating dry weight when clinical assessment is difficult.

Azygos Vein↗
PubMed1989

Distal tubule bicarbonate reabsorption in NH4Cl acidotic rats.

NH4Cl acidosis--a common experimental model of hyperchloremic metabolic acidosis--elicits complex intrarenal responses whereby the fall in plasma bicarbonate concentration can be restored to normal after the initial acid load. Using the technique of in vivo micropuncture of surface distal tubules of the rat kidney, we attempted to further define controlling mechanisms underlying the enhanced bicarbonate reabsorption in this setting. Specifically, we wished to determine the dependence of distal tubule bicarbonate reabsorption (JtCO2) on sodium transport, water reabsorption, and carbonic anhydrase activity. Surface distal tubules of Sprague-Dawley rats made acidotic by ammonium chloride gavage (arterial blood pH: 7.15 +/- 0.01, [HCO3]: 14.8 +/- 0.5 mM) were perfused in vivo at 8 and 24 nL/min with 4 different isoosmotic, 25 mM bicarbonate solutions: Group 1 was perfused with 60 mM Na, Group 2 with 60 mM choline, Group 3 with 60 mM choline + 3 x 10(-4) M amiloride, and Group 4 with 60 mM Na + 10(-3) M acetazolamide. At 8 nL/min, significant bicarbonate reabsorption occurred with all perfusates. JtCO2 was 65 +/- 4, 59 +/- 5, 58 +/- 6, and 40 +/- 4 pmol.min-1.mm-1, in Groups 1, 2, 3, and 4, respectively. However, JtCO2 in Group 4 was significantly less than that in Groups 1 and 2 (p less than 0.01 and p less than 0.05, respectively). Amiloride added to the low sodium perfusate did not reduce bicarbonate reabsorption. We conclude that bicarbonate reabsorption in distal tubules of acidotic rats is acetazolamide-sensitive and is not significantly sustained by sodium or water movements.

Absorption↗