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PubMedDate not supplied

Calcium ionophore-activated neutrophils prestimulated with endotoxin increase pulmonary arterial pressure and vascular leakage in isolated perfused rat lungs: role of platelet-activating factor.

The influence of stimulated polymorphonuclear neutrophils on pulmonary arterial pressure and vascular leakage in isolated perfused rat lungs was investigated. We exposed isolated neutrophils to various stimuli in vitro, instilled the cells in the lung perfusate, and studied the effects on pulmonary arterial pressure and passage of fluorescently labeled dextran (4100 dalton) from the pulmonary circulation into the lung. We found that neutrophils stimulated with the calcium ionophore A23187 or with E. coli endotoxin had no significant influence on the pressure or the passage of dextran. On the other hand, neutrophils preincubated with endotoxin and then stimulated with A23187 caused significant increases, both in pulmonary arterial pressure and accumulation of dextran in the lung. Both these effects were attenuated by BN 52021, a specific platelet-activating factor antagonist, and by nordihydroguaiaretic acid, an agent that inhibited the generation of platelet-activating factor in A23187-stimulated neutrophils. These findings demonstrate that activated neutrophils can increase pulmonary arterial pressure and lung fluid accumulation and suggest that endotoxin-stimulated activated neutrophils exert at least some of their action via generation of platelet-activating factor.

Animals↗
PubMed1992

Blocking effects of OPC-21268 and OPC-31260 (vasopressin V1- and V2-receptor antagonists) on vasopressin-induced constrictions in isolated, perfused dog femoral arteries.

Using a perfusion technique of isolated vessels, constrictor responses to vasopressin (VP) and norepinephrine (NE) were investigated in perfused dog femoral arteries. Both OPC-21268, a selective V1-antagonist, and OPC-31260, a selective V2-antagonist, significantly shifted the VP-induced dose response curves to the right without influencing the NE-induced ones. The blocking effects of OPC-31260 were much greater than those of OPC-21268, suggesting that there may probably be functional V1- and V2-receptors in isolated dog femoral arteries that mediate vasoconstriction.

Angiotensin Receptor Antagonists↗
PubMed1984

Method of isolation-perfusion of the liver in the pig.

A method was developed in the pig for isolation-perfusion of the liver using a pump-oxygenator that infused blood through the portal vein after vascular isolation and collected the hepatic venous effluent in a closed recirculating system. Portal and vena caval blood flows were diverted around the liver by an intracaval conduit or by an external shunt. Leakage from the perfusion circuit into the systemic circulation was measured using radioactive albumin tracer. Ten pigs were perfused for 30 or 60 minutes at 37 C or 41 C. Nine animals survived treatment with transient elevations of hepatic enzymes but with no clinical or pathologic signs of permanent hepatic damage.

Animals↗
PubMed1990

Selective neurohormonal interactions in islet cell secretion in the isolated perfused human pancreas.

To investigate the effects of stimulant interactions on alpha- and beta-cell secretions, the differential effects of gastric inhibitory polypeptide (GIP) and cholinergic stimulation (CS) on insulin (IRI) and glucagon (IRG) release were examined during euglycemic, single-pass perfusion in the isolated human pancreas. Pancreata obtained from 12 cadaver organ donors were perfused for 15-min test periods with (a) 1 nM GIP (b) intrinsic CS via bipolar electrical stimulation (10 V, 5 msec, 10 Hz) of the splanchnic neural fibers during simultaneous perfusion with 4 microM phentolamine and 6 microM propranolol, or (c) GIP and CS. The integrated response of IRI and IRG demonstrated that IRI release was stimulated 308 +/- 52 microU/g-min by GIP, 366 +/- 73 microU/g-min by CS, and 560 +/- 50 microU/g-min by GIP and CS (P less than 0.05). IRG release was stimulated 111 +/- 33 pg/g-min by GIP, 34 +/- 12 pg/g-min by CS, and 90 +/- 36 pg/g-min by GIP and CS. Combined hormonal and cholinergic stimulation was additive for IRI release, but not for IRG release. We conclude that the interaction of neural and hormonal islet cell stimuli is cell-type specific. This may result in selective impairment of hormone release after pancreatic denervation.

Adolescent↗
PubMedDate not supplied

Influence of sodium palmitate on the cellular action of potentials of the left ventricle of isolated, perfused guinea-pig heart.

Influence of sodium palmitate on the cellular action potentials of the left ventricle of isolated, perfused guinea-pig heart. Acta Physiol. Pol. 1975, 26 (1): 1-11. Transmembrane action potentials (APs) were recorded from the left ventricle and glucose uptake was estimated in the isolated guinea-pig hearts perfused with Langendorff method. After the control period the perfusion fluid was changed for the solution of altered composition containing: 1) 0.5 mM of palmitate complexed with 4% albumin and no glucose; 2) 0.1 mM or 0.5 mM of palmitate added to solution containing 11 mM of glucose; 3) substrate-free solution; 4) solution equilibrated with 5% CO-2 + 95% N-2. In all experimental groups marked shortening of AP duration was observed accompanied by the shortening of the functional refractory period and by the desynchronization of repolarization. The effect of perfusion with the substrate-free solution was similar to that evoked by substituting palmitate for glucose. In all the groups except for anoxia, fibrillation either occurred spontaneously or it was evoked by early extra stimuli. Fibrillation was reversible in all groups except for substitution 0.5 mM palmitate for glucose. Under anoxic conditions loss of excitability was observed, and shortening of AP was smaller than under palmitate. Glucose uptake was inhibited by 30% in the presence of 0.5 mM of palmitate, but not by 0.1 mM of palmitate. Thus changes in the shape of AP are not related to the glucose uptake. The possible effect of palmitate on inhibition of cellular respiration and glycolysis is discussed.

Action Potentials↗
PubMed2006

Protective effects of regulatory amino acids on ischemia-reperfusion injury in the isolated perfused rat liver.

OBJECTIVE: Some amino acids (AAs) display potent regulatory activities on cell metabolism, including via anti-oxidative defences. The aim of this study was to evaluate the protective effect of these AAs on warm ischaemia-reperfusion (I/R) injury in the isolated perfused rat liver. MATERIAL AND METHODS: Livers from fasted male Sprague-Dawley rats were isolated and perfused without (control group) or with (AP group) a mixture of regulatory AAs (glutamine, histidine, leucine, methionine, proline, phenylalanine, tryptophan and alanine). After 45 min of perfusion, warm ischaemia was induced for 45 min by clamping the portal vein catheter; thereafter, reperfusion was performed for 30 min. RESULTS: TNF-alpha production was significantly lower in the AP group during reperfusion ( CONTROL: 39+/-7 versus AP: 16+/-2 pg min-1 g-1, p<0.05), and lactate dehydrogenase (LDH) release decreased significantly during the last 15 min of reperfusion ( CONTROL: 0.13+/-0.03 versus AP: 0.04+/-0.02 IU min-1 g-1, p<0.05), despite similar levels of oxidative stress. The addition of regulatory AAs was not associated with variations in portal flow, bile flow, hepatic glucose or urea metabolism. However, significant changes in intrahepatic glutamine ( CONTROL: 1.4+/-0.2 versus AP: 2.6+/-0.5 micromol g-1, p < 0.05) together with higher glutamate release in the AP group ( CONTROL: 10.2+/-5.4 versus AP: 42.6+/-10.9 nmol min-1 g-1, p < 0.05) indicated modifications in nitrogen metabolism. CONCLUSIONS: Taken together, the lower TNF-alpha production, suggesting decreased inflammatory response, the decrease in LDH release in the AP group, demonstrating a better preservation of liver viability, and the increase in hepatic glutamine indicate that AAs play an important role in the liver's response to I/R.

Algorithms↗
PubMed1986

Effect of coupling of 2-nor-2-formylpyridoxal 5'-phosphate to stroma-free hemoglobin on oxygen affinity and tissue oxygenation. Studies in the isolated perfused rat liver under conditions of normoxia and stagnant hypoxia.

Hemoglobin in stroma-free solution (7 gm/100 ml) was modified by covalently cross-linking the beta-chains with 2-nor-2-formylpyridoxal 5'-phosphate (NFPLP). The coupling efficiency was approximately 65%. The oxygen dissociation curve of the coupling mixture was shifted to the right, with a P50 of 30 mm Hg vs. 15 mm Hg for the nonmodified solution. The effect of the modification on tissue oxygenation was studied in the isolated perfused rat liver at normoxia and at hypoxia induced by decrease of flow rate at constant Po2 and hemoglobin concentration. The two perfusates used were a nonmodified hemoglobin solution and the coupling mixture. The chemical modification of the hemoglobin molecule did not affect the vascular resistance in the liver tissue. During normoxia the NFPLP-induced decrease in oxygen affinity was reflected in a higher venous Po2. The differences in the other oxygen-sensitive parameters were not significant. The decrease in O2 supply induced by a decrease of perfusion flow rate (stagnant hypoxia) resulted in a decrease in venous Po2, O2 consumption, and bile flow rate, and an increase in the cytoplasmatic redox level (lactate/pyruvate ratio) and the mitochondrial redox level (beta-hydroxybutyrate/acetoacetate ratio). During hypoxia the changed oxygen affinity of the modified hemoglobin solution was reflected in small but significant differences between both perfusates in the venous Po2 and both redox levels. No change in O2 consumption and bile flow rate was observed. When compared with earlier low-flow perfusions of the isolated rat liver with erythrocytes, the oxygen affinity of hemoglobin solutions appears not to be rate limiting for the O2 consumption, probably because of better tissue perfusion with hemoglobin solutions.

3-Hydroxybutyric Acid↗
PubMedDate not supplied

Renal excretion mechanisms of the antiviral nucleoside analogue AM 188 in the rat isolated perfused kidney.

1. AM 188 is an antiviral guanosine analogue that undergoes extensive renal excretion in humans. The present study was designed to investigate the disposition of AM 188 over a range of concentrations in the rat isolated perfused kidney (IPK) to explore the mechanisms involved in its renal handling. 2. Right kidneys of male Sprague-Dawley rats (n = 23) were isolated and perfused in recirculating mode with Krebs'-Henseleit (pH 7.4) buffer containing 0.65% bovine serum albumin, 3.6% dextran, amino acids and glucose. [14C]-Inulin was added to the perfusate reservoir to permit estimation of glomerular filtration rate (GFR). [3H]-AM 188 and unlabelled AM 188 were added to the perfusate as a bolus initially, followed by a constant rate of infusion at 5, 25, 125, 500 or 1000 microg/min to achieve initial target perfusate concentrations of 1, 5, 25, 100 or 200 microg/mL, respectively. During the 130 min over which AM 188 was infused, urine was collected in 10 min intervals (commencing 10 min after the bolus dose) and perfusate was collected at the mid-point of these intervals to permit calculation of the renal clearance (CLR) of AM 188. Binding of AM 188 in perfusate, measured using ultrafiltration, was negligible. 3. The bolus dose and infusion regimen produced relatively stable AM 188 concentrations in perfusate in the 5, 25 and 125 micro g/min groups and progressively increasing concentrations in the 500 and 1000 microg/min groups. High-pressure liquid chromatography analysis of IPK perfusate and urine suggested that there was no or negligible metabolism of AM 188 in the kidney. The CLR/GFR ratio for AM 188 (mean+/-SD) was 5.76 +/- 1.57, 5.99 +/- 0.52, 6.02 +/- 1.47, 3.38 +/- 0.26 and 1.08 +/- 0.42 in the 5, 25, 125, 500 and 1000 microg/min groups, respectively, showing significant reductions at the two highest infusion rates (P < 0.05). Although there was no difference between the five groups in the distribution of AM 188 between kidney tissue and perfusate (KT/P), at the end of perfusion the corresponding urine-to-tissue concentration ratio declined significantly in the 1000 microg/min group. 4. AM 188 undergoes substantial net renal secretion over a wide range of perfusate concentrations. A reduction in renal clearance at perfusate concentrations above 25 microg/mL could be due to saturation of carrier-mediated transport at the brush border membrane and/or a solubility limitation leading to precipitation of AM 188 in tubular cells and/or tubular urine.

Algorithms↗
PubMed1993

Association of galactosamine-induced hepatitis in the rat with hyperhyaluronanaemia and decreased hyaluronan uptake by the isolated, perfused liver.

Plasma hyaluronan (HA) concentration and the rate of HA uptake by the isolated, perfused liver were measured in rats treated with saline, D-galactosamine (GaI-NH2, 50 mg/100 g body wt), gadolinium chloride (GdCl3) (0.5 mg/100 g body wt), and GdCl3 + GaI-NH2. GdCl3 was given 24 hr before GaI-NH2 or saline. Plasma L-alanine:2-oxoglutarate aminotransferase (EC 2.6.1.2), a marker for hepatocyte damage, was increased by 8 hr and remained elevated for 24 hr after GaI-NH2 injection. GdCl3 did not affect plasma enzyme levels when given alone or in association with, but prior to, GaI-NH2. Plasma HA levels were increased (200%) within 24 hr after GaI-NH2 administration. A plateau was reached at 8 hr, which was maintained for at least 24 hr. Although GdCl3 alone did not affect plasma HA levels, it slightly delayed the increase in HA concentration in GaI-NH2-treated rats. Livers, isolated 24 hr after GaI-NH2 treatment, exhibited a severe depression (approximately 67%) of HA uptake. GdCl3 did not prevent this suppression. The data presented indicate that: (1) one of the sinusoidal endothelial cell-dependent functions of the liver, i.e. removal of HA from the blood stream, is profoundly impaired during galactosamine-induced hepatitis, and (2) the adverse effect of GaI-NH2 on this sinusoidal endothelial cell function may not be dependent on CdCl3-suppressible Kupffer cell functions.

Alanine Transaminase↗
PubMed1982

Dosimetry in isolation perfusion of the limbs by assessment of perfused tissue volume and grading of toxic tissue reactions.

The optimal single dosage of melphalan in isolation perfusion of the limbs for malignant melanoma was assessed. For this purpose a method to determine the volume of the isolated region in the individual patient and a grading system for the reaction of the normal tissues were introduced. A strictly standardized pharmacosurgical routine was developed that permitted an analysis of the correlation between dosage and the grade of toxic reaction in 90 perfusions. The optimal dosage of a cytostatic drug was considered to be the highest amount tolerated at an acceptable risk. Melphalan at 10 mg/l perfused tissue was determined as the likely optimum. This dose provoked remarkably little variation in toxicity, all reactions falling within a safe range. No exception to the applicability of this dosage was encountered.

Arm↗
PubMed1983

Evaluation of the isolated perfused heart of mice, with special reference to vasoconstriction caused by intracoronary acetylcholine.

A perfusion model of isolated hearts (left in situ) was developed in mice. The heart was perfused retrogradely, according to the Langendorff technique, under a fixed flow rate of about 4 ml/min with physiological saline solution. Left ventricular (LV) cavity pressure, LV dP/dt max, heart rate, and arterial perfusion pressure were measured. Stable levels of mechanical parameters were reached within 30 min following the start of perfusion and were maintained for more than three hours. Single doses of acetylcholine (ACh, 0.003-1 microgram) administered into the coronary perfusion system elicited a dose-dependent increase (vasoconstriction) followed by a decrease (vasodilation) in perfusion pressure. Coronary vasoconstriction in response to ACh was especially prominent. LV systolic pressure, LVdP/dt max, and heart rate resulted in a decrease followed by an increase. A single injection of atropine (10 micrograms) antagonized both cardiac and vascular (vasoconstrictor and dilator) effects of ACh. The present studies substantiate the validity of this experimental model for the assessment of the action of drugs on the heart and coronary vasculature.

Acetylcholine↗
PubMed1986

Ex-vivo isolated perfusion of the pancreas in the Syrian golden hamster.

The technique of ex-vivo isolated pancreatic perfusion has been a valuable method for investigation of the physiology of the exocrine and endocrine pancreas. We have adapted the technique of isolated pancreatic perfusion for use in the Syrian golden hamster, an animal used widely in studies of pancreatic carcinogenesis. The technique involves surgical harvest of the pancreas with its aortic and portal venous blood supply intact and perfusion of the pancreas with a modified Krebs buffer at 37 degrees C. Physiological function of the perfused pancreas system was examined in 27 Syrian hamsters. In tests of endocrine function, the perfused pancreas responded by increasing insulin secretion within 1 min of elevating perfusate glucose concentration, and also secreted insulin promptly in response to 10 mM arginine. In exocrine studies, the flow of pancreatic juice was stimulated by the addition of 0.8 X 10(-9) M secretin to the perfusate, and amylase output was significantly increased by the addition of 0.2 X 10(-9) M cholecystokinin (CCK-8). The ex-vivo isolated perfused pancreas in the hamster thus appears to respond appropriately to physiological stimuli and is a valuable additional tool for studies of the hamster pancreas.

Animals↗
PubMed2005

Effects of meconium aspiration in isolated perfused rat lungs.

Our objective was to study meconium-induced lung injury in isolated perfused rat lungs exposed to anoxia. Our working hypothesis was that meconium-induced lung injury is independent of preexisting hypoxia, and that hypoxia will increase severity of lung injury observed after meconium aspiration. We compared five different groups of animals (n = 5) for pulmonary arterial pressure (PAP), weight lung changes, and TNFalpha expression. Group I had lungs instilled with 4 ml of normal saline. Group II had lungs exposed to 5 min of anoxia. Group III had lungs instilled with 4 ml of 30% filtered human meconium. Group IV had lungs exposed to 5 min of anoxia and then instilled with 4 ml of 30% filtered human meconium. Group V had lungs instilled with 4 ml of 30% unfiltered human meconium. Our subjects were adult Sprague-Dawley rats. The isolated rat lung model was prepared according to Levey and Gast (J Appl Physiol 1966;21:313-316). Lungs were ventilated with room air. Anoxia was caused by the use of N(2). The pulmonary artery was cannulated, and pulmonary arterial pressure and lung weight were measured. Lung weight and pulmonary arterial pressure were monitored for 120 min, and TNFalpha levels were measured in effluent at 15, 30, 60, and 120 min. Experiments were done at the Michael Reese Hospital (Chicago, IL). At the end of the experiment, PAP reached its highest values in group V (10.0 +/- 1.7 mmHg). Final PAPs in groups I-IV were: 4.85 +/- 0.3, 4.99 +/- 0.4, 5.93 +/- 0.3, and 7.25 +/- 0.51 mmHg, respectively). Lung wet weight increased significantly only in groups IV and V vs. group I; at 120 min, they were: 0.96 +/- 0.3 g, P < 0.01, and 1.5 g +/- 0.2 g, P < 0.01, respectively. TNFalpha levels did not change significantly over time in group I. TNFalpha is a marker as well as proprietor of pulmonary inflammatory response. TNFalpha reached its highest levels in groups IV and V: 595 and 753 pg/ml at 120 min, respectively. In conclusion, a short episode of anoxia prior to meconium aspiration may increase lung sensitivity to meconium-induced lung injury. This effect may be moderated by the TNFalpha present in the pulmonary circulation.

Animals↗
PubMed1992

The effects of surfactants on the permeability of isolated perfused fish gills to urea.

1. The diffusional transfer capacity of [14C]urea in isolated perfused trout (Oncorhynchus mykiss) gills in the presence of sodium n-dodecylsulphate (SDS), n-dodecyltrimethylammonium bromide (DTAB) and p-t-octylbenzene oxyethylene10 (Triton X-100) has been measured over a range of surfactant concentrations. 2. Urea has been shown to be transported transcellularly through the respiratory cells of the gill secondary lamellae by passive diffusion. Each surfactant was found to markedly increase the rate of diffusion and the diffusional transfer capacity reached a steady-state at a particular surfactant concentration. 3. The steady state flux was increased by surfactant in the sequence DTAB greater than SDS greater than Triton X-100 and the surfactant concentrations in terms of the critical micelle concentration (CMC) at which the diffusional transfer capacities reached limiting values were 0.92 x CMC (SDS), 0.53 x CMC (DTAB) and 2.5 x CMC (Triton X-100). 4. Compared to interactions between isolated epithelial cells and the surfactants, the rates at which the surfactants changed the urea flux were slow, suggesting that the mucus layer plays a significant role in protecting the epithelial cells of the secondary lamellae from disruption. 5. Relative to the other surfactants, DTAB had the most marked effect on both the rate of flux change and on the magnitude of the change, at concentrations which are low relative to the CMC, suggesting a more specific interaction with the negatively charged mucus layer consistent with the toxic effects of quaternary ammonium compounds on aquatic organisms.

Animals↗
PubMed2002

Decreased activity of hepatic P-glycoprotein in the isolated perfused liver of the adjuvant arthritis rat.

1. We investigated the hepatobiliary transport of doxorubicin in the isolated perfused liver prepared from the adjuvant arthritis rat, an animal model for rheumatoid arthritis, to examine the hepatic P-glycoprotein activity in the adjuvant arthritis rat. 2. Liver was isolated from the normal and the adjuvant arthritis rat and perfused for 60 min with recirculating buffer and the perfusate and bile samples were collected at timed interval. 3. The elimination of doxorubicin in the adjuvant arthritis rat tended to be reduced, but it was not significantly different from the normal rat. Biliary clearance (CL(bile)) in the normal rat was 1.93 +/- 0.48 ml min(-1), whereas, CL(bile) in the adjuvant arthritis rat was significantly decreased to 0.40 +/- 0.13 ml min(-1). 4. CL(bile) was markedly decreased to about 0.15 ml min(-1) in the presence of 100 microM verapamil in both types of rat. Methotrexate treatment had no effect on CL(bile) in both the normal and adjuvant arthritis rat (2.18 +/- 0.22 and 0.47 +/- 0.22 ml min(-1), respectively). 5. The results suggest that the hepatic P-glycoprotein activity was markedly decreased in the adjuvant arthritis rat and the effect of methotrexate on the hepatic P-glycoprotein activity did not corresponded to its anti-inflammatory effect.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1987

Lactate metabolism of isolated, perfused fetal, and newborn pig hearts.

The role of lactate as an energy substrate in fetal (0.9 gestation) and newborn (2 day old) hearts was investigated in isolated, perfused hearts. Perfusions were performed with Krebs-Henseleit buffer supplemented with glucose (5 mM) in combination with varying concentrations of lactate. Isolated working heart perfusions, in which the heart ejects the buffer at controlled pressure, were carried out with glucose (5 mM) alone and with glucose (5 mM) and lactate (5 mM) combined. With glucose as sole substrate, lactate was produced by the heart and glucose uptake accounted for approximately two-thirds of oxygen consumption. When both glucose and lactate were provided, lactate accounted for more than 80% of oxygen consumption and profoundly suppressed glucose uptake. Further investigations using retrograde perfusion through the aorta demonstrated that lactate uptake was consistently observed when exogenous lactate concentrations exceeded 1.25 mM. Glucose uptake was suppressed with lactate concentrations as low as 0.5 mM and progressive suppression occurred with increasing lactate concentrations. Fetal and newborn pig hearts utilize lactate as a primary substrate for energy production when lactate concentrations are in the physiological range.

Adenosine Triphosphate↗
PubMedDate not supplied

Modulatory role of endothelium-derived relaxing factors on the response to vasoconstrictors and flow-pressure curve in the isolated perfused rat kidney.

The aim of this study was to compare the effects of the blockade of nitric oxide (NO) and of endothelium-derived hyperpolarizing factor (EDHF) on the response to vasoconstrictors (VC) and on the flow-pressure curve in the isolated perfused rat kidney. To this end, dose-response curves to phenylephrine and BaCl2 were studied in the renal vasculature under basal conditions and after the infusion of N(omega)-nitro-L-arginine methyl ester (L-NAME) and tetraethylammonium (TEA) in endothelium-intact and endothelium-denuded (CHAPS-treated) preparations. In another experiment, renal flow-pressure curves were obtained under basal conditions and after the infusion of L-NAME or TEA. The flow-pressure curve was obtained by increasing renal perfusion flow (RPF) from 2.5 to 15 ml/min/g kidney weight (KW) over the basal level (5 ml/min/g KW). L-NAME or TEA produced a leftward shift of the dose-response curves of both VC, and the simultaneous administration of L-NAME and TEA produced a greater shift to the left in the pressor response curves. CHAPS treatment produced a leftward shift of the dose-response curves of both VC, and the dose-response curves were not significantly modified by the infusion of L-NAME or TEA. L-NAME markedly shifted the flow-pressure curve upward, especially at higher levels of RPF. However, the administration of TEA, perfusate solution (Tyrode) or D-NAME did not significantly change the flow-pressure curve. These results suggest that NO is released in response to VC as well as to increased perfusion flow in the isolated renal vascular bed. However, EDHF release seems to be stimulated by VC but not by increased perfusion flow.

Animals↗
PubMed1986

An isolated perfused rat lung preparation for the study of aerosolized drug deposition and absorption.

The isolated, perfused rat lung preparation was modified to allow characterized solid aerosol delivery. Deposition and airway-to-perfusate transfer of disodium fluorescein from 3-4 micron dae solid aerosols were studied under different ventilatory regimes. The lungs inhaled from an aerosol stream of constant concentration via a tracheal cannula. Air displacement from a sealed artificial thorax housing the lungs provided the driving force for inhalation. The lungs were suspended in a physiologically normal position and both left and right sides of the heart were cannulated for constant rate perfusate flow. Fractional deposition was inversely proportional to respiratory frequency implying that sedimentation was the primary deposition mechanism. Increasing tidal volumes similarly enhanced the ratio of amount deposited/amount administered. Fluorescein transfer to the perfusate occurred from the lung regions containing intact vasculature, was apparent first-order, and independent of perfusate flow. The average rate constant for transfer was 0.057 +/- 0.02 min-1 (t1/2 = 12.2 +/- 4.2 min-1). The ratio of transferable amount/amount deposited appeared to indicate the depth of aerosol penetration. This increased at high respiratory frequency and tidal volume, while decreasing with increasing aerosol particle size. Potential applications of the model are discussed in the light of these results.

Absorption↗