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Biomedical subjects

M Ikegami

Publications and source records attributed to M Ikegami.

At least 217 records · Page 12Linked to original sources
PubMed1993

Prevalence of gastroesophageal varices supplied by intrahepatic portal branch.

The contribution of the intrahepatic portal branch to the gastroesophageal varices is rare. This anomalous pathway (a large left intrahepatic portal branch) was proved by portographic study and by imaging techniques in a 54-year-old man with cirrhosis. The overall prevalence of this type of collateral in the literature is only 1.9% in 908 patients with portal hypertension. In addition, all are via the left portal venous branch. It may be speculated that the mechanism of this variation is due to dilatation of the rest of the intrahepatic portal system via a small anastomosis due to portal hypertension.

Collateral Circulation↗
PubMed1993

Surfactant metabolism.

Alveolar surfactant pool sizes are small in the preterm animal with RDS, and these pool sizes probably increase to approximate those found in preterm animal without RDS by 3 to 4 days after birth. De novo synthesis and secretion of surfactant phospholipids are slow processes. Therefore, surfactant treatments are the only way to acutely increase the pool size. Surfactant phospholipids are very slowly catabolized in the preterm lung. The surfactant phospholipids used for treatment rapidly associate with lung tissue and are processed by recycling through lamellar bodies within type II cells. Surfactant proteins already present within the preterm lung can associate with the exogenous surfactant. These proteins have metabolic pathways quite different from those for the lipids. Surfactant treatments do not seem to interfere with endogenous metabolic pathways for surfactant synthesis and secretion. Surfactant treatments of infants with RDS are beneficial in part because of the favorable metabolism characterized by a preterm lung that can recycle surfactant and does not catabolize the exogenous surfactant.

Animals↗
PubMed1993

Surfactant metabolism.

Based on these metabolic studies of surfactant lipids in term lambs, in preterm lambs not treated with surfactant, and in preterm lambs that have been surfactant-treated, the following is a synthesis of the overall metabolism of surfactant. Preterm surfactant-deficient lungs seem to have all the synthetic and secretory pathways for surfactant phosphatidylcholine. Secretory kinetics are slow in preterm relative to term animals. Recycling pathways are active in the preterm lung, and surfactant used for treatment can be recycled. The major difference between the preterm or term lung and the adult lung is that there is almost no surfactant phosphatidylcholine catabolism in the developing lung. All assessments of surfactant metabolism are complicated by the different forms of surfactant within the airspaces that represent different functional surfactant pools. SP-A has secretory and reuptake kinetics quite different than those for phosphatidylcholine. De novo synthesized SP-A is secreted independently of lamellar bodies and may associate with surfactant lipids during the formation of tubular myelin. Surfactant treatments do not adversely affect endogenous synthetic and secretory phospholipid pathways by feedback inhibition. Therefore, surfactant treatments have two primary effects on the preterm lung: physiological effects related to surface properties, and metabolic effects resulting from the exogenous surfactant phospholipids functioning as substrate for the recycling pathways.

Animals↗
PubMed1993

Cardiopulmonary bypass significantly reduces surfactant activity in children.

Lung injury remains an important problem after cardiopulmonary bypass. The contribution of altered surfactant concentration or activity to pulmonary dysfunction after cardiopulmonary bypass is unclear. Recent evidence indicates that alveolar surfactant exists in specific aggregate forms that differ with respect to density, phospholipid composition, and function. A transition from surface active, higher density, large aggregates of surfactant to lower density, small aggregates that possess reduced surface activity has been demonstrated after experimental lung injury. The purpose of the present study was to examine surfactant aggregate fractions before and after bypass in children. Twelve acyanotic patients, aged 2 to 12 years, underwent intraoperative pulmonary function testing followed by bronchoalveolar lavage before incision and approximately 1 hour after termination of cardiopulmonary bypass. Saturated phosphatidylcholine pool sizes and total protein content of the small- and large-aggregate fractions of bronchoalveolar lavage fluid were determined. One hour after termination of cardiopulmonary bypass, the ratio of saturated phosphatidylcholine in small-aggregate as compared with that in large-aggregate fractions increased (mean +/- standard error) from 0.19 +/- 0.03 to 0.37 +/- 0.07 (p < 0.02), as did the ratio of saturated phosphatidylcholine to protein in the small-aggregate fraction (from 0.04 +/- 0.01 to 0.08 +/- 0.02, p < 0.05). Reductions in forced vital capacity (-19% +/- 5%), inspiratory capacity (-15% +/- 3%), and small airway flow rates (-32% +/- 6%) were also observed after bypass. These changes were accompanied by a fivefold increase in alveolar polymorphonuclear leukocyte content. The present study suggests that cardiopulmonary bypass of moderate duration in relatively healthy children is associated with surfactant changes that are similar in type and magnitude to those observed in experimental lung injury.

Bronchoalveolar Lavage Fluid↗
PubMed1993

[Effect of verapamil on urinary calcium and oxalate excretion in renal stone formers].

The effect of the calcium antagonist verapamil on urinary calcium and oxalate excretion was examined and compared with that of trichlormethiazide to evaluate whether verapamil is useful in the prevention of calcium oxalate renal stones. Twenty-four-hour urine of 16 renal stone formers was measured at the outpatient clinic before and after administration of 120 mg/day verapamil for a mean duration of 2.7 months (range, 2 weeks to 6 months). The 24-hour urine was analyzed for creatinine, calcium, oxalic acid, magnesium and citric acid and the results compared with those in 20 renal stone formers who were administered trichlormethiazide. Verapamil was found to significantly reduce the urinary oxalate excretion of the 5 hyperoxaluric (> or = 50 mg/day) patients but no significant effect on urinary calcium, magnesium or citric acid was observed. Conversely, trichlormethiazide significantly decreased urinary calcium excretion in the hypercalciuric (> or = 250 mg/day) patients. Calcium oxalate risk index of hypercalciuric and hyperoxaluric patients was significantly reduced after the administration of verapamil. These findings suggest that verapamil is effective in reducing urinary oxalate excretion in the hyperoxaluric patients.

Calcium↗
PubMed1993

Reduced gastric mucosal blood flow in patients with portal-hypertensive gastropathy.

Although congestive gastric mucosal circulation has been suggested in patients with portal-hypertensive gastropathy, whether it is due to "active" (overflow) or "passive" (stasis) congestion is not known. To answer this question, we assessed regional gastric mucosal blood flow with laser Doppler flowmetry in 57 patients with portal hypertension and 30 controls. Twelve patients had portal-hypertensive gastropathy of the antrum: in eight it was mild and in four it was severe. Portal-hypertensive gastropathy of the corpus was seen in 32 patients: it was mild in 24 and severe in 8. Thus prevalence of portal-hypertensive gastropathy was higher in the corpus than in the antrum (p < 0.01). In the antrum, gastric mucosal blood flow was significantly lower (p < 0.05) in patients with severe portal-hypertensive gastropathy (0.54 +/- 0.27 V) than in controls (1.12 +/- 0.44 V), whereas the values in patients without portal-hypertensive gastropathy (0.90 +/- 0.35 V) and with mild portal-hypertensive gastropathy (0.91 +/- 0.31 V) were not significantly different from the values in controls (p < 0.05 on one-way analysis of variance). In the corpus, gastric mucosal blood flow was significantly lower in patients with mild (0.75 +/- 0.25 V) or severe portal-hypertensive gastropathy (0.42 +/- 0.22 V) than in controls (1.16 +/- 0.37 V) (p < 0.01 and p < 0.01, respectively) whereas the value in patients without portal-hypertensive gastropathy (0.99 +/- 0.37 V) was not significantly different from values in controls (p < 0.01 on one-way analysis of variance).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1992

Effects of antenatal thyrotropin-releasing hormone, antenatal corticosteroids, and postnatal ventilation on surfactant mobilization in premature rabbits.

OBJECTIVE: The effects of antenatal hormones on postnatal surfactant mobilization were evaluated in preterm rabbits. STUDY DESIGN: Pregnant rabbits were treated with vehicle, betamethasone, or thyrotropin-releasing hormone for 2 days before cesarean section at 29 days' gestation (term 31 days). Newborns were mechanically ventilated or allowed to spontaneously breathe, and groups were compared by analysis of variance. RESULTS: Neither antenatal corticosteroids nor thyrotropin-releasing hormone increased radiolabeled precursor incorporation, alveolar wash or total lung saturated phosphatidylcholine pools, lung clearance of radiolabeled rabbit surfactant, or estimated net secretion of saturated phosphatidylcholine. However, saturated phosphatidylcholine pools in alveolar wash increased 2.7-fold during the first 24 hours in spontaneously breathing rabbits versus 2.1-fold in mechanically ventilated thyrotropin-releasing hormone-treated and control rabbits (p less than 0.05). In addition, estimated net secretion of precursor-derived saturated phosphatidylcholine was 50% higher after 24 hours in spontaneously breathing rabbits. CONCLUSION: Mechanical ventilation may have hindered the mobilization of surfactant saturated phosphatidylcholine pools to the alveolar space after birth in preterm rabbits, but maternal hormonal therapies did not appear to influence this adaptive process or change surfactant metabolism.

Adrenal Cortex Hormones↗
PubMed1992

Platelet-activating factor antagonists decrease lung protein leak in preterm ventilated rabbits.

OBJECTIVE: The preterm ventilated lung is characterized by an increased protein leak from the pulmonary vascular spaces into the air spaces, which interferes with lung function and plays a role in neonatal respiratory distress syndrome. To investigate the role of platelet-activating factor in this process, platelet-activating factor antagonists were given to preterm ventilated rabbits. STUDY DESIGN: New Zealand White rabbits were delivered on day 28 of 31 days' gestation. Each rabbit pup received saline solution or one of two platelet-activating factor antagonists and were ventilated for 30 minutes with measurement of compliance, surfactant pool size, and protein leak into and out of the lung. Statistical analysis was performed with analysis of variance followed by Student-Newman-Keuls correction for multiple comparisons. RESULTS: There were no differences in lung compliance, surfactant pool size, or protein leak out of the air spaces among any of the groups. Treatment with the platelet-activating factor antagonists decreased the protein leak into the air spaces by greater than 50% and into the lung as a whole by 40% (p less than 0.01). CONCLUSION: Platelet-activating factor plays a role in the protein leak seen in the preterm lung, which contributes to neonatal respiratory distress syndrome.

Animals↗
PubMed1992

Surfactant protein A metabolism in preterm ventilated lambs.

Surfactant protein A (SP-A) metabolism was studied in vivo in 33 preterm ventilated lambs at 138 +/- 1 days gestational age by measuring recoveries of exogenously administered surfactant containing both radiolabeled SP-A and labeled saturated phosphatidylcholine (Sat PC) given via the trachea at birth. Endogenously secreted SP-A was also labeled with [35S]methionine and followed over 24 h. The exogenously labeled SP-A left the alveolar pool more rapidly than did Sat PC over the first 5 h of life (P less than 0.05), and both exogenously labeled SP-A and Sat PC were detected within lamellar bodies by 2 h, indicating uptake from the airspaces. The quantity of SP-A in alveolar washes increased about twofold from birth to 5 h of age, whereas alveolar Sat PC pools were constant over 24 h. The SP-A endogenously labeled with [35S]methionine was recovered at highest specific activities in the alveolar washes at 10 and 45 min after birth with no labeled SP-A detectable in lamellar body fractions until 2 h. The curve for endogenous SP-A labeling of lamellar bodies was similar to that for exogenous labeling, indicating that SP-A was initially secreted by a pathway independent of lamellar bodies with subsequent SP-A labeling of lamellar bodies. The kinetics of SP-A metabolism were very different than for Sat PC in preterm lambs.

Animals↗
PubMed1992

Localization of alveolar surfactant clearance in rabbit lung cells.

Localization of surfactant phospholipid clearance in lung cells was investigated in vivo in rabbits using radiolabeled dipalmitoylphosphatidylcholine (DPPC) and 1,2-dihexa-decyl-sn-glycero-3-phosphocholine (DPPC-ether), a phospholipase A1- and A2-resistant analogue of DPPC. After intratracheal injection of liposomes of the labeled lipids associated with unlabeled surfactant, adult rabbits were killed in groups of three to five at 0, 4, 12, and 24 h with recovery of bronchoalveolar lavages for alveolar macrophages and surfactant. Type II cells and tissue-associated macrophages were isolated on Percoll gradients following elastase and trypsin digestion of the lungs. Radiolabel recoveries as saturated phosphatidylcholine were measured in alveolar wash, alveolar macrophages, lung tissue, and the type II cell and mixed cell bands from the Percoll gradients. Cost accounting of label demonstrated similar recoveries at 0 h, but significantly more DPPC-ether compared with DPPC in cells at later times, indicating ineffective degradation of the DPPC-ether. Internalization of the lung tissue-associated labels into cells was time dependent. At all times, greater than 65% of the cell-associated labels were recovered in type II cells, indicating the primary role for these cells in clearing alveolar surfactant phospholipid in vivo. The total contribution of alveolar macrophages to the overall clearance was approximately 20%.

1,2-Dipalmitoylphosphatidylcholine↗
PubMed1992

Different ventilation strategies alter surfactant responses in preterm rabbits.

The effect of ventilation strategy on in vivo function of different surfactants was evaluated in preterm rabbits delivered at 27 days gestational age and ventilated with either 0 cmH2O positive end-expiratory pressure (PEEP) at tidal volumes of 10-11 ml/kg or 3 cmH2O PEEP at tidal volumes of 7-8 ml/kg after treatment with one of four different surfactants: sheep surfactant, the lipids of sheep surfactant stripped of protein (LH-20 lipid), Exosurf, and Survanta. The use of 3 cmH2O PEEP decreased pneumothoraces in all groups except for the sheep surfactant group where pneumothoraces increased (P < 0.01). Ventilatory pressures (peak pressures - PEEP) decreased more with the 3 cmH2O PEEP, low-tidal-volume ventilation strategy for Exosurf-, Survanta-, and sheep surfactant-treated rabbits (P < 0.05), whereas ventilation efficiency indexes (VEI) improved only for Survanta- and sheep surfactant-treated rabbits with 3 cmH2O PEEP (P < 0.01). Pressure-volume curves for sheep surfactant-treated rabbits were better than for all other treated groups (P < 0.01), although Exosurf and Survanta increased lung volumes above those in control rabbits (P < 0.05). The recovery of intravascular radiolabeled albumin in the lungs and alveolar washes was used as an indicator of pulmonary edema. Only Survanta and sheep surfactant decreased protein leaks in the absence of PEEP, whereas all treatments decreased labeled albumin recoveries when 3 cmH2O PEEP was used (P < 0.05). These experiments demonstrate that ventilation style will alter a number of measurements of surfactant function, and the effects differ for different surfactants.

Air Pressure↗
PubMed1992

Antenatal ambroxol effects on surfactant pool size and postnatal lung function in preterm ventilated rabbits.

Following maternal treatments with 50 mg/kg/day ambroxol for 2 or 3 days before delivery at 28 days gestation, preterm rabbits were ventilated to evaluate lung function. Subsequently, surfactant saturated phosphatidylcholine (SatPC) pool sizes were measured. One half of the ambroxol treated and control rabbits were given surfactant at delivery. Although surfactant improved lung function comparably for control and ambroxol treated rabbits, ambroxol treatments did not change ventilatory pressure requirements, compliances, or the recovery of intravascular labeled albumin in the lungs. Ambroxol treatments tended to increase lung volumes as evaluated by pressure-volume curves. The ambroxol treatments significantly increased lung tissue SatPC by 22%, but there were no changes in alveolar SatPC pool values. These results do not indicate a large effect of ambroxol on lung function in preterm rabbits.

Ambroxol↗
PubMed1992

Metabolism of exogenously administered surfactant in the acutely injured lungs of adult rabbits.

Acute lung injury was induced in adult rabbits with a subcutaneous injection of N-nitro-so-N-methylurethane (NNNMU). Clearance of saturated phosphatidylcholine (Sat.PC) from a treatment dose of exogenous surfactant (100 mg/kg) in the injured lungs of these rabbits was similar to normal, control rabbits when measured 24 h after treatment. However, total Sat.PC pool sizes in both the alveolar wash and total lung at this time point were significantly lower for the injured lungs than for the control lungs (p less than 0.05), implying altered endogenous surfactant metabolism in response to surfactant treatment in the injured animals. Although both injured and control animals had comparable ratios of small to large surfactant aggregates, as measured by differential centrifugation of alveolar wash 5 min after treatment, by 24 h this ratio had increased 5-fold in the control animals and remained unchanged in the injured animals. This indicated diminished conversion of large surfactant aggregates to the smaller forms in lung injury. In vivo functional studies of these aggregates were performed by intratracheal injection into surfactant-deficient preterm rabbits. Large aggregates from normal adult rabbits given surfactant had superior functional properties than did the surfactant used for treatment alone, which in turn was better than large aggregates isolated from NNNMU-injured rabbits treated with surfactant. This indicates that the alveolar environment influenced the function of the exogenously administered surfactant differently in normal and injured rabbits.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1992

Lung albumin recovery in surfactant-treated preterm ventilated lambs.

Preterm ventilated animals and infants with respiratory distress syndrome (RDS) develop proteinaceous alveolar edema. To study the effect of postnatal age on intravascular radiolabeled albumin accumulation into lungs, preterm lambs at 132 days gestational age were ventilated after treatment with sheep surfactant or cow surfactant extract for periods as long as 24 h. Lambs not treated with surfactant were studied for only 5 h because of severe respiratory failure. All lambs were given radiolabeled albumin by intravascular injection 1 h before they were killed, and the net recovery of the labeled albumin was measured in the lung tissue and air space as quantified by alveolar lavage. Net 1-h radiolabeled albumin recoveries in the lungs decreased from 5 to 6% soon after birth to 0.9% at 24 h in the surfactant-treated groups (p less than 0.01). At 3 h there was less labeled albumin recovery by alveolar lavages in lambs treated with sheep surfactant than in control lambs and lambs treated with cow surfactant extract (p less than 0.05). Protein in alveolar washes from lambs treated with cow surfactant extract exceeded that in lambs treated with sheep surfactant at 3 h (p less than 0.05), but protein recoveries had decreased to similar values by 24 h, indicating a net clearance of air-space protein. These studies demonstrate a sixfold decrease in net albumin accumulation from birth to 24 h of age despite continued ventilation and oxygen exposure of the premature lamb lungs.

Animals↗
PubMed1992

In vitro conversion of surfactant subtypes is altered in alveolar surfactant isolated from injured lungs.

Pulmonary alveolar surfactant can be separated into different subtypes on the basis of their buoyant densities. These subtypes have been characterized as ultraheavy and heavy forms, which are surface-active, and light forms, which are less surface active. The ratio of these subtypes was altered in an animal model of acute lung injury that contributed to the physiologic abnormalities. We used an in vitro method of surface-area cycling to compare conversion of heavy subtypes isolated from injured and from normal lungs. Lung injury was induced in adult rabbits with a subcutaneous injection of N-nitroso-N-methylurethane (NNMU). Conversion of NNMU-injured heavy subtypes to light subtypes was significantly greater than normal heavy subtype conversion at each time point studied from 60 to 180 min of cycling (p less than 0.01). Surfactant protein A (SP-A) was added to heavy subtypes, with no effect on conversion when 1.5% SP-A was added, but the addition of 4.5, 10.5, and 22.5% caused complete conversion to ultraheavy forms with no cycling. With subsequent cycling, there was greater conversion from ultraheavy to lighter subtypes for normal surfactant material than for NNMU-injured material (p less than 0.05). We conclude that the altered ratio of surfactant subtypes in the alveolar lavage of injured lungs was due to a greater conversion of these subtypes within the alveolar space. Furthermore, SP-A may play an important role in the metabolism of alveolar surfactant both in normal and in injured lungs.

Animals↗
PubMed1992

[Evaluation of kidney graft function with dynamic MRI--preliminary report].

The value of dynamic magnetic resonance imaging (MRI) in the examination of the function of transplanted kidneys was examined. Dynamic MRI was performed on 14 renal transplant patients. After the injection of Gd-DTPA (dimeglumine gadopentetate), we used small tip angle gradient echo (STAGE) technique with a flip angle of 20 degrees. The cortex was higher in signal intensity of well functioning grafts than the medulla before the injection in Gd-DTPA. Signal intensity of the cortex decreased after 30 seconds. After 1 minute the signal intensity of the cortex recovered and low intensity band meaning passage of Gd-DTPA at corticomedullary differentiation was displayed. Signal intensity of the medulla decreased after 3 minutes. Signal intensity of the parenchyma of transplanted kidney after 5 minutes was much the same as that before injection. Image of poor functioning grafts displayed unclear figures. Time-intensity values of both cortex and medulla in well functioning grafts decreased rapidly after about 2 minutes, and rose thereafter. Time-intensity curves of both cortex and medulla were almost flat on and after 5 minutes. Time-intensity curves of both cortex and medulla in poor functioning grafts were almost flat through out the examination. We concluded that effective parameters of the graft function for the time-intensity curve were delta I1 and delta I2. Dynamic MRI was suggested to be useful in the evaluation of kidney graft function.

Contrast Media↗