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PubMed1981

Role of calcium and albumin in the autoregulation of renal perfusate flow.

1. We investigated the role of calcium and albumin on the perfusate flow in isolated perfused rat kidneys. The initial perfusion medium was Krebs-Henseleit bicarbonate solution with 1.82 mm-calcium without albumin. Perfusate flow autoregulation occurred above 100 mmHg.2. Raising albumin concentration to 20 and 60 g/l. abolished autoregulation and increased perfusate flow.3. Keeping ionized calcium at 1.82 mm restored autoregulation in medium containing 20 and 60 g albumin/l. However, in 60 g albumin/l. autoregulation occurred at a significantly higher flow.4. 1.82 mm-ionized calcium appears to be a critical level for autoregulation of flow in these experiments, for autoregulation was not obtained in 60 g albumin/l. medium containing 1.80 mm-ionized calcium. On the other hand, autoregulation occurred in medium containing 1.83 mm-ionized calcium, but at a lower perfusate flow.5. Raising albumin concentration to 120 g/l. increased perfusate flow from 14.6+/-0.8 to 20.8+/-0.7 ml./min.g (n = 5, P < 0.01) in the presence of 1.82 mm-total calcium, and from 11.6+/-1.0 to 15.8+/-0.7 ml./min.g (n = 5, P < 0.01) in 1.82 mm-ionized calcium. The effect of raising albumin concentration was reversible.6. Removing the capsule from the kidneys abolished the increased flow in response to raising albumin concentration.7. We conclude that (a) the mechanism for the autoregulation of renal perfusate flow in isolated perfused kidneys is critically dependent on an extremely narrow range of ionized calcium concentration in the perfusion medium, below this range, autoregulation is not achieved; above it, however, autoregulation is achieved, but during intense vasoconstriction; (b) raising albumin concentration in the perfusion medium increases perfusate flow and abolishes autoregulation by lowering extracellular ionized calcium and by raising intrarenal tissue pressure.

Animals↗
PubMed1991

Hypoxic vasodilatation in isolated, perfused guinea-pig heart: an analysis of the underlying mechanisms.

1. The mechanisms underlying hypoxic dilatation of coronary arteries were studied in isolated guinea-pig hearts perfused with physiological salt solution at 37 degrees C. The hearts were perfused at a constant rate of 3-10 ml min-1; coronary perfusion pressure (CPP) and isovolumetric left ventricular pressure (LVP) were measured with piezoresistive transducers. 2. Addition of the K+ channel opener cromakalim (500 nM) to the perfusate caused a maximal vasodilatation in beating hearts, i.e. a decrease in CPP of about 50%. Switching from normal perfusate (partial pressure of O2 (PO2), 650-700 mmHg) to hypoxic perfusate (PO2, 9-10 mmHg) caused a similar vasodilatation. Both of these effects were prevented by 2 microM-glibenclamide, a blocker of ATP-sensitive potassium channels. Hypoxic vasodilatation was accompanied by a marked decrease in LVP, which was reduced by 56 +/- 22% (mean +/- S.D.) in the presence of glibenclamide. 3. In hearts arrested by increasing the K+ concentration of the perfusate to 15 mM, the addition of the adenosine-uptake inhibitor dipyridamole evoked a maximal vasodilatation and this was inhibited by 76 +/- 7% in the presence of glibenclamide. 4. The adenosine antagonist 8-phenyltheophylline (8-PT; 5 microM) inhibited the vasodilatation induced by dipyridamole by 88 +/- 10%. In contrast, hypoxic vasodilatation was unaffected by 5 microM 8-PT. This suggests that hypoxic dilatation of coronary arteries is not mediated by release of adenosine from cardiomyocytes. 5. In order to test whether release of endothelium-derived relaxing factor (EDRF) contributed to hypoxic vasodilatation we blocked EDRF synthesis with N omega-nitro-L-arginine (NNA). When applied at a perfusion rate of 10 ml min-1 to arrested hearts, 10 microM-NNA increased CPP by 35% and prolonged the delay between application of hypoxic solution and half-maximal vasodilatation from 52 +/- 9 to 129 +/- 29 s. 6. Under control conditions the relation between perfusion rate and the CPP measured in the steady state was linear. In the presence of 10 microM-NNA coronary resistance was increased more than twofold at low perfusion rates; at perfusion rates between 4 and 10 ml min-1 coronary resistance decreased progressively. This change in the pressure-flow relationship may be responsible for the alterations in the time course of hypoxic vasodilatation induced by NNA. 7. In order to test whether changes in energy metabolism in coronary smooth muscle cells were responsible for hypoxic vasodilatation we blocked glycolysis by replacing the glucose in the perfusate with deoxyglucose (DOG).(ABSTRACT TRUNCATED AT 400 WORDS)

Adenosine↗
PubMed1989

Increased sinusoidal volume and solute extraction during retrograde liver perfusion.

Retrograde isolated liver perfusion has been used to probe acinar functional heterogeneity, but the hemodynamic effects of backward flow have not been characterized. In this study, extraction of a long-chain fatty acid derivative, 12-N-methyl-7-nitrobenzo-2-oxa-1,3-diazol-amino stearate (12-NBDS), was greater during retrograde than during anterograde perfusion of isolated rat liver. To determine whether hemodynamic differences between anterograde and retrograde perfused livers could account for this finding, the hepatic extracellular space was measured for both directions of flow by means of [14C]sucrose washout during perfusion as well as by direct measurement of [14C]sucrose entrapped during perfusion. A three- to fourfold enlargement of the total hepatic extracellular space was found during retrograde perfusion by both approaches. Examination of perfusion-fixed livers by light microscopy and morphometry revealed that marked distension of the sinusoids occurred during retrograde perfusion and that this accounts for the observed increase in the [14C]sucrose space. These findings support the hypothesis that maximum resistance to perfusate flow in the isolated perfused rat liver is located at the presinusoidal level. In addition, increased transit time of perfusate through the liver and greater sinusoidal surface area resulting from sinusoidal distension may account for the higher extraction of 12-NBDS and possibly other compounds by retrograde perfused liver.

4-Chloro-7-nitrobenzofurazan↗
PubMed2002

Increased coronary perfusion augments cardiac contractility in the rat through stretch-activated ion channels.

The role of stretch-activated ion channels (SACs) in coronary perfusion-induced increase in cardiac contractility was investigated in isolated isometrically contracting perfused papillary muscles from Wistar rats. A brief increase in perfusion pressure (3-4 s, perfusion pulse, n = 7), 10 repetitive perfusion pulses (n = 4), or a sustained increase in perfusion pressure (150-200 s, perfusion step, n = 7) increase developed force by 2.7 +/- 1.1, 7.7 +/- 2.2, and 8.3 +/- 2.5 mN/mm(2) (means +/- SE, P < 0.05), respectively. The increase in developed force after a perfusion pulse is transient, whereas developed force during a perfusion step remains increased by 5.1 +/- 2.5 mN/mm(2) (P < 0.05) in the steady state. Inhibition of SACs by addition of gadolinium (10 micromol/l) or streptomycin (40 and 100 micromol/l) blunts the perfusion-induced increase in developed force. Incubation with 100 micromol/l N(omega)-nitro-L-arginine [nitric oxide (NO) synthase inhibition], 10 micromol/l sodium nitroprusside (NO donation) and 0.1 micromol/l verapamil (L-type Ca(2+) channel blockade) are without effect on the perfusion-induced increase of developed force. We conclude that brief, repetitive, or sustained increases in coronary perfusion augment cardiac contractility through activation of stretch-activated ion channels, whereas endothelial NO release and L-type Ca(2+) channels are not involved.

Animals↗
PubMed1985

Isolated perfused head of rainbow trout. I. Gas transfer, acid-base balance, and hemodynamics.

Branchial gas transfer, acid-base balance, and hemodynamics were critically evaluated and compared in Ringer-perfused and blood-perfused heads of rainbow trout. Blood perfusion stimulated O2 uptake and CO2 excretion across the gills to values more representative of intact fish. The stimulatory effect of blood on gas transfer was due to increased O2 carrying capacity (O2 uptake) and the presence of erythrocytic carbonic anhydrase (CO2 excretion). Adding carbonic anhydrase to Ringer enhanced CO2 excretion in a manner similar to blood. During Ringer perfusion, arteriovenous pH gradients were abnormal (arterial pH less than venous pH). Perfusion with blood or addition of carbonic anhydrase to Ringer reversed the pH gradients to typical in vivo levels. Branchial vascular resistance to flow was abnormally high in both Ringer- and blood-perfused preparations, primarily as a result of low dorsal aortic pressure. Input pressure increased during blood perfusion and was similar to ventral aortic pressure in vivo. Perfusion with Ringer may have caused irreversible deterioration of gill function as indicated by decreased arterial Po2 and O2 extraction effectiveness after a rapid switch from Ringer to blood perfusion. The results are discussed with reference to the suitability of perfused trout head preparations for studying gill gas transfer, acid-base balance, and hemodynamics. Comparisons are made between the perfused head preparation and intact fish as well as with other types of perfused gill preparations.

Acid-Base Equilibrium↗
PubMed1989

Spontaneous injury in isolated sheep lungs: role of perfusate leukocytes and platelets.

Perfusion of isolated sheep lungs with blood causes spontaneous edema and hypertension preceded by decreases in perfusate concentrations of leukocytes (WBC) and platelets (PLT). To determine whether these decreases were caused by pulmonary sequestration, we continuously measured blood flow and collected pulmonary arterial and left atrial blood for cell concentration measurements in six lungs early in perfusion. Significant sequestration occurred in the lung, but not in the extracorporeal circuit. To determine the contribution of these cells to spontaneous injury in this model, lungs perfused in situ with a constant flow (100 ml.kg-1.min-1) of homologous leukopenic (WBC = 540 mm-3, n = 8) or thrombocytopenic blood (PLT = 10,000 mm-3, n = 6) were compared with control lungs perfused with untreated homologous blood (WBC = 5,320, PLT = 422,000, n = 8). Perfusion of control lungs caused a rapid fall in WBC and PLT followed by transient increases in pulmonary arterial pressure, lung lymph flow, and perfusate concentrations of 6-ketoprostaglandin F1 alpha and thromboxane B2. The negative value of reservoir weight (delta W) was measured as an index of fluid entry into the lung extravascular space during perfusion. delta W increased rapidly for 60 min and then more gradually to 242 g at 180 min. This was accompanied by a rise in the lymph-to-plasma oncotic pressure ratio (pi L/pi P). Relative to control, leukopenic perfusion decreased the ratio of wet weight to dry weight, the intra- plus extravascular blood weight, and the incidence of bloody lymph. Thrombocytopenic perfusion increased lung lymph flow and the rate of delta W, decreased pi L/pi P and perfusate thromboxane B2, and delayed the peak pulmonary arterial pressure. These results suggest that perfusate leukocytes sequestered in the lung and contributed to hemorrhage but were not necessary for hypertension and edema. Platelets were an important source of thromboxane but protected against edema by an unknown mechanism.

Animals↗
PubMed1991

Permeability characteristics of isolated perfused rat lungs.

We examined the factors that influence the permeability characteristics of isolated perfused rat lungs and compared the ex vivo permeability-surface area product (PS) with that obtained in vivo. In lungs perfused for 20 min with homologous blood or a physiological salt solution (PSS) containing 4 g/100 ml albumin, mean PS values, obtained by the single-sample method of Kern et al. [Am. J. Physiol. 245 (Heart Circ. Physiol. 14): H229-H236, 1983], were 9.9 +/- 0.6 (SE) and 6.8 +/- 0.3 cm3.min-1.g wet lung-1.10(-2), respectively. These values were similar to lung PS obtained in intact rats (7.7 +/- 0.4 cm3.min-1.g wet lung-1.10(-2). In perfused lungs, PS values were influenced by the perfusate albumin concentration, the length of perfusion time, and the degree of vascular recruitment. Twenty minutes after lung isolation, PS was 126% higher in lungs perfused with albumin-free PSS containing Ficoll than in lungs perfused with albumin-PSS. Moreover, PS in Ficoll-PSS-perfused lungs increased even higher after 2 h of perfusion, and this time-dependent increase in PS was attenuated by addition of 0.1 g/100 ml albumin to the perfusate. Two hours of ex vivo ventilation with hypoxic (0 or 3% 0(2)) or hyperoxic (95% 0(2)) gas mixture did not affect PS values in perfused lungs. However, PS was elevated in lungs perfused ex vivo with protamine, which causes endothelial cell injury, or in lungs from rats exposed in vivo to human recombinant tumor necrosis factor.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1997

Influence of the perfusate temperature on lung preservation: is there an optimum?

The optimal temperature of the pulmonary flush perfusate is still a matter of controversy. At present, a temperature of 10 degrees C is favored. This study deals with the structural and functional impact of different perfusate temperatures on lung preservation. In an extracorporeal rat heart-lung model lungs were preserved with Perfadex solution of 4, 15 and 25 degrees C and submitted to 2 h ischemia. Heart-lung blocks harvested from male rats were perfused with Krebs-Henseleit solution and ventilated with room air. Lungs were perfused with deoxygenated perfusate via the working right ventricle while the coronary arteries were retrogradely perfused with oxygenated perfusate. Oxygenation capacity (dPO2), peak inspiratory pressure (PIP) and pulmonary vascular resistance were measured. After establishment of baseline functional parameters hearts were arrested with 10 ml St. Thomas cardioplegia and lungs were flushed with 20 ml Perfadex solution. The heart-lung block was then stored for 2 h at 10 degrees C. Reperfusion was performed thereafter under the same conditions. At the end of the trial the lung tissue water was measured by the wet/dry ratio. The perfusion time of the groups flushed with 15 or 25 degrees C perfusate was significantly lower than that of the 4 degrees C group. After 20 min reperfusion dPO2 of the groups flushed with 15 or 25 degrees C was superior to those submitted to a 4 degrees C flush perfusion. PIP was significantly lower in the 15 degrees C group than in the 4 and 25 degrees C groups. The wet/dry ratio revealed the smallest water content in the 15 degrees C group. We conclude that the post-ischemic lung function is dependent on the temperature of the flush perfusate. Among the tested temperatures, perfusion at 15 degrees C showed the best results. The optimum may therefore lie in this range.

Animals↗
PubMed1999

Pharmacokinetics of cisplatin administered by continuous hyperthermic peritoneal perfusion (CHPP) to patients with peritoneal carcinomatosis.

The pharmacokinetics of cisplatin administered by continuous hyperthermic peritoneal perfusion (CHPP) was characterized in patients with peritoneal carcinomatosis. Cisplatin was added into the perfusate with escalating doses from 100 mg/m2 to 400 mg/m2. The hyperthermic perfusion was maintained for 90 minutes with a flow rate of 1.5 L/min and a target peritoneal temperature of 42.5 degrees C after a tumor debulking procedure. Samples of both the perfusate and blood were obtained during the perfusion and 30 minutes after the perfusion. Cisplatin plasma and perfusate concentrations were determined by flameless atomic absorption spectrometry with a lower limit of detection of 2 ng/ml and a coefficient of variation (CV) < 10%. Fifty-six patients were enrolled in the study. The mean (+/- SD) percentage of cisplatin present in the perfusate at the completion of perfusion was 27.8% +/- 20% of the total dose. The maximum cisplatin concentrations in the perfusate were 10 times higher than those in plasma. The area under the concentration-time curve (AUC) of the perfusate was 13 times higher than the AUC of plasma. A two-compartment model with an additional peritoneal cavity compartment fits to the data best based on the Akaike information criterion. However, the interpatient variability was considerably high (CV < 100%). In conclusion, cisplatin administered by hyperthermic peritoneal perfusion resulted in a pharmacological advantage by obtaining higher and direct drug exposure to the tumor in the peritoneal cavity while limiting systemic absorption and toxicity. Using a complex two-compartment model, the authors were able to characterize the pharmacokinetics of cisplatin given intraperitoneally via this technique.

Adult↗
PubMed1992

Edema and tumor perfusion: characterization by quantitative 1H MR imaging.

Tumor perfusion is of central importance to the clinical oncologist because it has a direct effect on the success of cancer therapy. Yet determining whether a tumor is well or poorly perfused is difficult without the use of invasive techniques, because the variables that affect tumor perfusion are poorly understood. Quantitative MR imaging of tumor edema may provide a means of characterizing tumor perfusion, of studying heterogeneity of perfusion within the tumor mass, or of monitoring changes in tumor perfusion after therapy. A combination of factors often results in production of a large amount of edema within cranial or extracranial tumors. Any tumor that is encapsulated, whether by a fibrous tumor capsule or by a structure such as the cranium, will have an elevation in interstitial fluid pressure because dissipation of fluid is hindered. Elevated pressure of interstitial fluid acts to occlude tumor capillaries, so edema can cause a striking reduction of tumor perfusion. Because MR imaging can potentially be used for quantitative imaging of tumor edema, it may provide a means of indirectly measuring tumor perfusion. A review of the literature suggests that diffusion-weighted MR imaging may be better than T1- or T2-weighted MR imaging for quantitative imaging of tumor edema. I do not propose that diffusion-weighted imaging can measure perfusion directly; rather I hypothesize that a diffusion-weighted image can be correlated with tumor edema. Because edema indirectly regulates perfusion through the mechanism of interstitial fluid pressure, I propose an indirect correlation between the diffusion-weighted image and regional tissue perfusion. If the relationship between tumor perfusion and the pharmacokinetics of chemotherapeutic agents is better understood, MR imaging of tumor edema may even aid in predicting the delivery of drugs to a tumor.

Brain Edema↗
PubMedDate not supplied

The perfused guinea-pig lung revisited: a study of EDRF-no system.

Adult male guinea pigs from both sexes were anaesthetized with pentobarbital (40mg/Kg). After tracheotomy the lungs were perfused with Krebs-Henseleit solution at 37 degrees C in a non recirculated system composed of a perfusion pump, a transducer to measure pressure and another one to measure bronchial resistance. In all groups studied histamine injections were made at the doses of 50, 100, 200 and 400 microg/ml as a bolus. Propranolol (1 microg/ml) added to the perfusate, promoted a remarkable increase in perfusion pressure (p<0.001) and a significant augmentation in bronchoconstriction (p<0.05). When indometacin (10 microg/ml) was added to the perfusate, a great increase in histamine induced bronchoconstriction was observed, that was followed by a remarkable increase in perfusion pressure. Methylene blue at the dose of 8.25 microg/ml increased bronchorreativity as well as the perfusion pressure significantly. L-arginine (3.5 microg/ml) added to the perfusate, did not promote reactivity. The addition of L-arginine plus NADPH (1 microg/ml), promoted a significant decrease in bronchoconstriction (p<0.01). In both cases, perfusion pressure increased when compared to controls. Nitroarginine (2.5 microg/ml) greatly increased perfusion pressure with no change in bronchoconstriction. Therefore, we conclude that nitric oxide (NO) is a very important modulator for keeping the low perfusion pressure and bronchodilation of the isolated perfused guinea pig lung.

Adrenergic beta-Antagonists↗
PubMed1977

[The passage of nitrogenous compounds through the wall of perfused sheep rumen (author's transl)].

Experiments were performed by the method of the extracorporeal perfusion of sheep rumen lasting 150 minutes. After 60 minutes of perfusion, 20 g of enzymatic casein hydrolyzate were applied to the rumen. Ammonia, urea, and total nitrogen were determined in the samples of perfusate, and ammonia and pH were determined in the rumen content. Considerable amounts of ammonia accumulated in the perfusate in the course of the experiment. At the end of perfusion, the concentration of NH3-N reached an average value of up to 12 mg per 100 ml. The level of urea in the perfusate decreased only in the first phase of perfusion (before the application of casein hydrolyzate to the rumen) and remained unchanged in the subsequent phase. It is assumed that part of urea-N from the perfusate after urea hydrolysis, taking place already in the rumen wall, returned to the perfusate in the form of ammonia. In the first phase of perfusion the passage of nitrogen from the blood into the rumen took place, in the second phase its absorption from the rumen into the blood was observed. The urea-N ratio from the passage of total nitrogen into the rumen ranged between 4.63% and 13.84%, but the concentration of total nitrogen in the perfusate decreased by 7-15% and that of urea nitrogen by 37-42%. It follows from the results that a major part of endogenous nitrogen passing from perfusate to the rumen was represented by proteins and/or their peptidic splits.

Ammonia↗
PubMed1987

Nascent lipoproteins from recirculating and nonrecirculating liver perfusions and from the hepatic Golgi apparatus of African green monkeys.

Perfusate apoB-100-containing lipoproteins from the isolated, perfused livers of African green monkeys consist of significant amounts of d greater than 1.006 g/ml particles in addition to very low density lipoproteins (VLDL). Distinguishing characteristics of these perfusate lipoproteins are the relative abundance of surface lipids and deficiency of core lipids. The present studies were performed to determine the likelihood that the d greater than 1.006 g/ml perfusate lipoproteins are secretion products instead of products of post-secretory modification (e.g., lipolysis) of secreted VLDL. [14C]Leucine from the perfusate became incorporated into the apoB of each of the perfusate lipoprotein classes to a similar extent in both recirculating and nonrecirculating perfusions. When endogenously radiolabeled perfusate VLDL from one liver was recirculated through a second liver, only about 15% of the radiolabeled protein appeared in the d greater than 1.006 g/ml fraction. The particle morphology and the cholesterol and apoB distribution between VLDL and d greater than 1.006 g/ml fractions were similar in recirculating and nonrecirculating perfusions. A Golgi apparatus-rich fraction was isolated from the homogenates of fresh liver samples and the isolated Golgi VLDL and d greater than 1.006 g/ml lipoproteins exhibited morphologic evidence of extra surface material analogous to that seen in perfusate. Taken together, these data support the possibility that significant amounts of d greater than 1.006 g/ml lipoproteins, many with surface-rich properties, are nascent, secretory products of the primate liver. The low level of lecithin:cholesterol acyltransferase (LCAT) in this perfusion system appears to permit detection of these secretion products and it is significant to note that the perfusate lipoprotein profile, which is unlike that of normal plasma, is similar to that of LCAT-deficient patients.

Animals↗
PubMed1983

Ecto-5'-nucleotidase does not catalyze vectorial production of adenosine in the perfused rat liver.

From the results obtained in perfused rat hearts, Frick and Lowenstein proposed that ecto-5'-nucleotidase catalyzes a vectorial reaction in which AMP hydrolysis is accompanied by transfer of adenosine across the cell membrane (Frick, G.P., and Lowenstein, J.M. (1978) J. Biol. Chem. 253, 1240-1244). We have examined by the use of perfused rat livers, the uptake mechanism of adenosine generated from AMP by ecto-5'-nucleotidase. Recirculating perfusion of rat livers was performed with a buffered saline containing [2-3H]AMP at an initial concentration of 5 microM. One-half of the [2-3H] AMP was dephosphorylated by 0.8 min of perfusion; less than 13% of the radioactivity of hydrolyzed [2-3H] AMP was located in [2-3H]adenosine plus [2-3H]inosine appearing in the perfusate. Addition of 6-[(4-nitrobenzyl)thio]-guanosine, an inhibitor of the nucleoside transport system, at 120 microM to the perfusate caused a 3.9-fold increase in the amount of the [2-3H]AMP-derived 3H-nucleosides appearing in the perfusate. Moreover, in a perfusion in which uridine was added to the perfusate at 2.6 mM to compete with the [2-3H] AMP-derived [2-3H]adenosine for the nucleoside transport system, more than 87% of the radioactivity of hydrolyzed [2-3H]AMP was located in [2-3H]adenosine appearing in the perfusate; the result indicates that the uridine added to the perfusate efficiently trapped the [2-3H]adenosine formed from [2-3H]AMP. These results support an uptake mechanism of the AMP-derived adenosine in which the adenosine formed by ecto-5'-nucleotidase in the blood-sinusoidal plasma membrane of hepatocytes, is taken up by the nucleoside transport system located at the plasma membrane side by side with ecto-5'-nucleotidase. The results therefore indicate that the ecto-5'-nucleotidase of hepatocytes does not catalyze vectorial production of adenosine, in contrast to the previous report on perfused rat hearts.

5'-Nucleotidase↗
PubMed1982

[Studies on pressure-flow relationships in the pulmonary vascular bed, during antegrade and retrograde pulsatile perfusion of an excised canine lung lobe preparation].

Pulsatile pressure-flow relationships were studied in order to clarify the mechanical property of the pulmonary vascular bed. The left or right lower lobe of the dog was excised. Then, its pulmonary artery, pulmonary vein and bronchus were attached to a perfusion system. The lobe was perfused either via pulmonary artery (antegrade perfusion) or via pulmonary vein (retrograde perfusion) employing Harvard 1405 pulsatile pump. Positive pressure ventilation was maintained by a respirator throughout the experiment. From the pressure and flow wave, pulmonary vascular input impedance and total hydrauric power were computed by means of Fourier analysis. Pulmonary vascular resistance during retrograde perfusion was lower than that obtained during antegrade perfusion in a high flow state. The data suggests that the pulmonary vascular bed shows more passively distensible character during retrograde perfusion compared with antegrade perfusion. In the control flow state (inflow pressure of 15 mmHg and outflow pressure of 5 mmHg), however, above mentioned relationship was reversed (statistically significant). As outflow pressure was elevated, also, pulmonary vascular bed showed more remarkable distensibility during retrograde perfusion than during antegrade perfusion. With regard to the input impedance modulus and phase, there is no difference between the antegrade and retrograde perfusion of an excised lung lobe. Therefore, pulmonary arterial tree and pulmonary venous tree have a similar mechanical property, which determines the pulmonary vascular impedance. The rate of pulsatile power (Wp)/total hydrauric power (Wt) was 15-25% during antegrade perfusion, and Wp/Wt had minimum value at an inflow pressure of 14.5-15.5 mmHg. It may be stated that this value indicates the best condition for the pulmonary arterial smooth muscle.

Animals↗
PubMed1980

[Cardioplegic haemoglobin-perfusion for myocardial protection. Experiments on isolated rat-hearts (author's transl)].

On isolated normothermic and constant-pressure perfused rat-hearts cardioplegic haemoglobin-perfusion was compared with conventional cardioplegic perfusion without haemoglobin. The addition of 4% haemoglobin to the cardioplegic solution guarantees oxygen demand of the pharmacologically arrested heart at physiological PO2 (about 100 mm Hg) of the perfusion-solution, while conventional cardioplegic perfusion without haemoglobin needs arterial PO2 > 600 mm Hg and guarantees oxygen demand of the arrested normotherm rat-heart only under condition of sufficient coronary flow. The coronary flow during constant-pressure cardioplegic haemoglobin-perfusion was about 58% higher than during cardioplegic perfusion without haemoglobin. Interstitial oedema after perfusion for 1 hour was more intense after perfusion with the conventional cardioplegic solution than after cardioplegic haemoglobin-perfusion. Normothermic ischaemia of 20 minutes after perfusion with cardioplegic haemoglobin-solution was connected with a smaller drop of creatinephosphate and adenosinetriphosphate than after conventional cardioplegic perfusion, electron-optical preparations showed smaller changes of the structure. The use of cardioplegic haemoglobin-solutions in heart-surgery and the advantages of cardioplegic haemoglobinperfusion are discussed.

Adenosine Triphosphate↗
PubMed1995

Functional and ultrastructural features of ethanol/bile salts interaction in the isolated perfused rat liver.

We investigated whether bile salts (BS) with different hydrophobic-hydrophilic properties interact with ethanol on bile secretion, enzyme (aspartate transaminase [AST], lactate dehydrogenase [LDH]) release in the perfusate, liver ultrastructure, and vesicular exocytosis in the isolated perfused rat liver. Ethanol (0.1 or 1%) promoted a rapid decrease of bile flow and BS secretion in livers perfused with taurocholate (TCA), the physiologic BS in the rat (-28% decrease of baseline values with 0.1% and -34% with 1% ethanol). The inhibitory effect of ethanol on bile flow and BS secretion was significantly (P < .02) attenuated by perfusing liver with the hydrophilic BS, tauroursodeoxycholate (TUDCA), and it was exacerbated (P < .02) by perfusion with the hydrophobic BS, taurodeoxycholate (TDCA). The release of AST and LDH in the perfusate was unaffected by 0.1% ethanol, but increased threefold to fivefold by 1% ethanol in TCA-perfused livers. This cytolitic effect of ethanol was not observed in TUDCA-perfused livers, but it was enhanced (P < .03) by perfusion with TDCA. No ultrastructural abnormalities were found in either TCA- or TUDCA-perfused livers, with or without 1% ethanol. Only minimal changes were found in livers perfused with TDCA alone, but, in the presence of TDCA, 1% ethanol induces marked mitochondrial damage. The biliary excretion of the fluid phase marker horseradish peroxidase was inhibited by ethanol, an effect reversed by TUDCA (P < .02) and exacerbated by TDCA (P < .04). In conclusion, this study demonstrates that hydrophilic BS such as TUDCA counteract the inhibitory effect of ethanol on bile secretion and vesicular exocytosis as well as the ethanol-induced cytolitic effect in the isolated perfused rat liver. In the presence of hydrophobic BS such as TDCA, the exposure to ethanol promotes a marked inhibition of bile secretion and vesicular exocytosis as well as prominent mitochondrial damage.

Animals↗
PubMed1993

Long-term heart preservation by intermittent perfusion with crystalloid medium.

This study was undertaken to determine whether hearts preserved with intermittent coronary perfusion would recover physiologic function after a prolonged period of hypothermic preservation. Intermittent perfusion is commonly used for cardioplegia, but its efficacy in long-term heart preservation has not yet been demonstrated. Five groups of isolated rat hearts were studied (n = 7 per group): (1) fresh nonpreserved control hearts; (2) hearts preserved with continuous low-pressure perfusion via the aorta; (3) hearts preserved with cycles of 5 minutes of perfusion followed by 25 minutes of nonperfusion; (4) hearts preserved with cycles of 10 minutes of perfusion followed by 25 minutes of nonperfusion; (5) hearts preserved with submersion storage without perfusion. An oxygenated extracellular-type crystalloid medium (oxygen tension = 820 +/- 5 mm Hg) was used as a preservation medium; preservation was for 12 hours. During preservation, the coronary resistance of the intermittent perfusion-preserved hearts increased significantly, and these hearts produced significantly more excess lactate than did hearts in the other two preservation groups. The submersion-stored hearts exhibited no postpreservation ventricular function in an isolated perfused working rat heart system. The poststorage function of the other four groups, which was quantified during a 4-hour, 37 degrees C perfusion period at constant heart rate, indicated that there were no significant group differences with respect to output or energetics (coronary flow, aortic output, cardiac output, myocardial oxygen consumption, and external work efficiency). The intermittent perfusion-preserved hearts had significantly lower postpreservation contractile function (left ventricular systolic pressure, peak rates of left ventricular pressure development and relaxation, peak aortic flow rate, stroke work, and peak power) and higher left ventricular end-diastolic pressure compared with the control group. Although hearts preserved with intermittent perfusion had a loss of contractile function and decreased compliance compared with fresh hearts, after preservation they had better function than did hearts preserved with submersion storage and the same function as hearts preserved with continuous perfusion.

Animals↗