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PubMed2005

Dynamic tissue perfusion measurement: a novel tool in follow-up of renal transplants.

BACKGROUND: The authors applied the novel method of noninvasive dynamic color Doppler sonographic parenchymal perfusion measurement to renal transplants. METHODS: Color Doppler sonographic videos of renal transplants from 38 renal transplant recipients were recorded under defined conditions. Specific tissue perfusion was calculated as mean flow velocity encoded by color Doppler signals of a region of interest during one full heart cycle. RESULTS: The authors could demonstrate significant differences of central versus peripheral cortical perfusion intensity (1.36 vs. 0.60 cm/sec) and a significant loss of perfusion intensity in the posttransplantation period in the peripheral cortex from 1.06 cm/sec in the first year to a minimum of 0.39 cm/sec in the 3- to 5-year interval, with stronger perfusion in longer surviving transplants: 0.71 cm/sec more than 9 years after transplantation. In the central cortex, a similar but less pronounced pattern could be demonstrated. A significant drop of parenchymal perfusion was found in patients with elevated serum creatinine (1.36 cm/sec in cases with normal and 0.82 cm/sec in those with elevated creatinine at the proximal cortical level). The perfusion ratio of the central 50% and the peripheral 50% shows marked changes over time: in the first year, the ratio was 2.99, climbing to 5.56 at the 3- to 5-year interval and declining later on. CONCLUSIONS: Cortical tissue perfusion in renal transplants was quantified noninvasively from color Doppler signal data in an easily accomplishable manner. Renal transplants showed a marked decline in tissue perfusion after transplantation. Perfusion is significantly lower in transplant function loss with elevated serum creatinine.

Adolescent↗
PubMed1984

P-31 nuclear magnetic resonance analysis of brain: II. Effects of oxygen deprivation on isolated perfused and nonperfused rat brain.

Phosphatic metabolite (perchloric acid extractable) concentrations of cerebral tissues were analyzed by phosphorus-31 nuclear magnetic resonance (P-31 NMR) spectroscopy following external perfusion of the isolated rat brain (30 min or 60 min) under the following conditions: (a) constant perfusion pressure with either fluorocarbon- or erythrocyte-based medium, and (b) constant perfusate flow rate (3 ml/min) with the erythrocyte-based medium. Metabolite concentrations of control perfused brains were compared with those in nonperfused controls to provide a basis for detecting any qualitative or quantitative changes in cerebral metabolite composition. Metabolic responses of perfused brains to ischemia (incomplete ischemia, 83% reduction in flow for 10 min; transient complete ischemia for 1.5 or 2 min) were evaluated immediately after the ischemic episode and at selected time points during reperfusion (3 and 15 min). Alterations in cerebral metabolite levels induced by hypoxia were analyzed using a nonperfused rat brain model. Irrespective of the perfusion method employed, the phosphatic metabolites of control perfused rat brains were identical quantitatively to those of the nonperfused controls. Cerebral ischemia resulted in significantly increased levels of ADP, AMP + IMP, Pi, fructose 1,6-diphosphate, and glycerol 3-phosphate (global ischemia only), whereas ATP and phosphocreatine (PCr) levels declined significantly. The magnitude of these changes varied with the severity of the ischemia; however, following 15 min of control reperfusion metabolite levels had reverted to preischemic values. Significant perturbations in tissue phosphoethanolamine (3.84 delta resonance) content were evident at various time points during ischemia and postischemic recovery, which varied according to the perfusion conditions. In contrast to the changes observed in response to ischemia, hypoxia affected only cerebral high-energy phosphate levels. ATP and PCr levels were reduced, while a concomitant, essentially equimolar, increase in Pi and ADP was observed. The present studies indicate that in terms of phosphatic metabolites, the control equilibrated isolated perfused rat brain is quantitatively and qualitatively indistinguishable from the nonperfused rat brain in vivo regardless of the perfusion conditions (constant flow versus constant pressure). The metabolic responses to ischemia and hypoxia, as measured by P-31 NMR, were consistent with the pattern of changes reported elsewhere. Overall, P-31 NMR spectroscopic evaluation of the intact rat brain provides a potential experimental context for dynamic measures of cerebral metabolism under exogenously controlled conditions. Th

Animals↗
PubMed1978

Autoregulation of plasma flow in the isolated perfused rat kidney.

1. Autoregulation of renal plasma flow, by which flow remains constant despite changes in perfusion pressure, was studied in the isolated, perfused kidney of the rat. 2. Autoregulation did not occur in preparations perfused with a protein-free medium consisting of a balanced ionic solution resembling rat plasma in which 3% polyvinylpyrrolidone replaced the plasma proteins, changes in perfusion pressure over the normal autoregulatory range 100-150 mmHg produced a corresponding and linear change in venous outflow and no consistent change in renal vascular resistance. 3. Addition of human serum (5%, v/v) to the medium restored autoregulation; changes in perfusion pressure in the range 100-150 mmHg resulted in a stable plasma flow and a linear change in renal vascular resistance. The addition of bovine serum albumin (3 g/1.) to the protein-free medium restored autoregulation to a similar degree. 4. In kidneys perfused with the protein-free medium, the sensitivity of the renal vasculature to the vasoconstrictor drugs epinephrine and angiotensin II was only 1/40 the level seen in those kidneys perfused with media containing serum or albumin. 5. The experiments show that in the isolated, perfused kidney, autoregulation of plasma flow is not dependent on the presence of the globulin, angiotensinogen, in the perfusion medium; and suggest that failure of autoregulation in kidneys perfused with a protein-free medium could be attributed to the rapid decline in the sensitivity of the vascular smooth muscle to constrictor stimuli.

Angiotensin II↗
PubMed1982

Calcium ion dependence of myogenic renal plasma flow autoregulation: evidence from the isolated perfused rat kidney.

1. The independent roles of Ca2+ and glomerular filtration in the control of renal plasma flow autoregulation were examined in the isolated perfused rat kidney. Control kidneys autoregulated plasma flow between perfusion pressures of 120 and 160 mmHg. 2. Complete ischaemia, induced by clamping of the renal artery cannula for 1 h induced relative vasoconstriction and a loss of autoregulatory capacity. 3. The addition of either nifedipine (10(-7) M) or verapamil (10(-4) M) to the perfusion medium produced vasodilation and a loss of autoregulation. 4. Kidneys that were rendered non-filtering by raising the perfusate albumin concentration from 65 to 100 g/l appeared to shift autoregulatory capacity to a higher pressure range, whereas raising it to 150 g/l reduced autoregulation at all pressures studied. 5. The addition of ouabain (10(-3) M) restored autoregulation to the lower pressure range in non-filtering kidneys perfused with an albumin concentration of 100 g/l. Ouabain-treated non-filtering kidneys displayed a loss of autoregulation when perfused either with nifedipine or with reduced perfusate Ca2+. 6. Plasma flow was reduced in isolated kidneys perfused at pressures of 100 or 150 mmHg when ionized Ca2+ in the medium was raised from 0 to 1.8 mM. However, no decrement in flow was observed in kidneys perfused at 50 mmHg when ionized Ca2+ in the perfusate was raised to the same level. Thus the vasoconstrictive effect of raised ionized Ca2+ was pressure-dependent. 7. We conclude that renal plasma flow autoregulation occurs in the isolated kidney in the absence of glomerular filtration and is at least in part a myogenic phenomenon. Myogenic control of renal plasma flow autoregulation is regulated by smooth muscle permeability to Ca2+. Changes in smooth muscle Ca2+ permeability appear to be pressure-regulated.

Animals↗
PubMed1984

The direct inhibition of pancreatic electrolyte secretion by noradrenaline in the isolated perfused cat pancreas.

The continuous infusion of noradrenaline into the arterial supply of the isolated saline-perfused pancreas caused a dose-dependent rise in perfusion pressure, a reduction in perfusion rate and an inhibition of pancreatic secretion. With increasing dose there was always a greater reduction in secretion rate than there was of perfusate flow rate. Manual reduction of the perfusion rate resulted in a reduction in secretion rate. When noradrenaline reduced the perfusate flow by 44.2 +/- 6.0% the secretion rate fell by 76.6 +/- 14.1%. Manual reduction of the perfusion flow rate by a similar amount (43.0 +/- 5.7%) only reduced the secretion rate by 41.4 +/- 7.0%. The infusion of noradrenaline, when all calcium had been removed from the perfusate, caused only a small increase in perfusion pressure with little change in the perfusion flow whilst at the same time the inhibition of electrolyte secretion was relatively unaffected. The vasomotor and secretory effects of noradrenaline were abolished by phentolamine. It is concluded that noradrenaline inhibits pancreatic electrolyte secretion by a direct action on the secretory cell and indirectly by vasoconstriction and that both these effects are mediated through the alpha-receptor.

Animals↗
PubMed1991

Enhanced fluid uptake in frog mesenteric capillaries associated with plasmin perfusion.

1. We have measured the permeability of single capillaries of the mesenteries of decerebrated frogs, before and during perfusion with solutions containing the fibrinolytic enzyme, plasmin. 2. The hydraulic permeability (Lp) and the effective oncotic pressure exerted across the vessel walls (sigma delta pi) were measured using the method of Michel (1980). The vessels were sequentially perfused with a control frog Ringer solution containing either Ficoll 70 or bovine serum albumin (BSA) at concentrations of 40 mg ml-1 or a mixture of Ficoll 70 (40 mg ml-1) and BSA (10 mg ml-1), and then with a second Ringer perfusate containing plasmin (1 mg ml-1) but in all other respects identical to the control solution. 3. In sixteen out of seventeen experiments, perfusion with plasmin increased sigma delta pi. In eleven of these experiments the increase was very large such that sigma delta pi exceeded the in vitro value for perfusate oncotic pressure. 4. In the same seventeen vessels plasmin perfusion was associated with a fall in Lp from a mean value of 10.3 x 10(-7) cm s-1 cmH2O-1 to one of 7.7 x 10(-7) cm s-1 cmH2O-1. The fall in Lp was not significant. 5. In five of the seventeen vessels, a second control perfusion was made after exposure to plasmin. There was no evidence that Lp had increased above or sigma delta pi had fallen below the initial control value. 6. In a further six experiments, the effects of plasmin were investigated in the absence of other perfusate macromolecules. No significant changes in Lp or sigma delta pi were observed. 7. In a further eight vessels, the effects of plasmin on fluid filtration were investigated with the tissues cold and then at room temperature. In all eight vessels plasmin reduced filtration or increased fluid reabsorption to a greater extent when the tissue temperature was 17 degrees C than when it was 4 degrees C. 8. The large increases in sigma delta pi which we have observed during perfusion of single vessels with plasmin-containing solutions are consistent with the development of substantial local osmotic gradients at the capillary wall following the enzyme's action upon substrates at the endothelial cell surface, one of which could be fibrin. Alternatively, plasmin might stimulate endothelial cells to liberate molecules which locally amplify the oncotic pressure exerted by the perfusate macromolecules. These effects are more marked at room temperature than at 4 degrees C.

Animals↗
PubMed1985

Cl- requirement for saliva secretion in the isolated, perfused rat submandibular gland.

Replacement of perfusate Cl- with Br- reduced by 37% the volume of saliva secreted by isolated, perfused rat submandibular glands exposed to 10(-6) M acetylcholine. Replacement of perfusate Cl- with SO4(2-) reduced fluid secretion by 73%, while replacement of bicarbonate with HEPES or addition of acetazolamide had no effect on salivary flows or volumes. Furosemide (10(-3) M) reduced saliva secretion when added to Cl- -(73%) or Br- -containing (56%) perfusates and also to HEPES- (95%) or acetazolamide-containing (82%) perfusates. Perfusion of the glands with furosemide or SO4- containing perfusates resulted in significantly reduced salivary Cl- concentrations and increased residual anion (Na+-K+-Ca2+-Cl-) concentrations, while perfusion with solutions containing acetazolamide or with HCO3- -free (HEPES) perfusates resulted in opposite changes in salivary anions. Addition of furosemide to HEPES- or acetazolamide-containing perfusates reversed these changes and caused a reduction in salivary Cl- concentrations and an increase in residual anion concentrations. It is concluded that 1) extracellular Cl- is required for saliva secretion in the rat submandibular gland, 2) the required external Cl- enters the salivary cells by a furosemide-sensitive transport system, which is likely to be similar to a Na+-K+-Cl- cotransport system described in other epithelia, 3) HCO3- is not normally required for saliva secretion but can sustain it partially when Cl- transport is inhibited by either furosemide or Cl- replacement, and 4) salivary electrolyte changes induced by Cl- or HCO3- replacement or by furosemide probably represent combined effects on acinar secretion and transductal electrolyte transport.

Animals↗
PubMed1982

Flow dependence of norepinephrine extraction by isolated perfused rat lungs.

Disposition of perfused norepinephrine (NE) was studied in isolated rat lungs at several perfusate flows, including that occurring in vivo. Lungs were ventilated with 95% O2-5% CO2 and perfused at 37 degrees C with recirculating medium initially containing 90 nM [14C]NE. In agreement with previous studies the fraction of NE removed in a single pass through the pulmonary vasculature was 0.30 +/- 0.03 by lungs perfused at low flow (10 ml/min; 7.2 ml.min-1.g lung-1). This extraction ratio decreased with increasing flow, so that in lungs perfused at 45 ml/min (31.8 ml.min-1.g lung-1) the extraction ratio was 0.09 +/- 0.01. The concentration of NE metabolites in the perfusate reservoir increased with time of perfusion. The rate of appearance of deaminated and O-methylated metabolites in the recirculating perfusion medium was not markedly influenced by flow. NE that accumulated in lung was metabolized before reentry into the perfusion medium. These results indicate that extraction of NE by rat lung is markedly dependent on flow and suggest that removal of NE by lung is not highly efficient at normal organ perfusion rates.

Animals↗
PubMed1983

Hyperreactivity of coronary vasculature in platelet-perfused hearts from diabetic rats.

Coronary vascular responsiveness to platelet-produced eicosanoids was examined in isolated perfused hearts of alloxan-diabetic rats. Coronary perfusion pressure was increased in isolated hearts of control and diabetic rats on perfusion with platelets and arachidonic acid (AA). However, the increase in perfusion pressure was approximately twofold higher in hearts of diabetic rats when compared with those isolated from control rats. This was associated with increased thromboxane B2 (TxB2) and prostaglandin F2 alpha (PGF2 alpha) production that was comparable in platelet-perfused hearts of control and diabetic animals. Ibuprofen, a cyclooxygenase inhibitor, blocked the increase in perfusion pressure and TxB2 and PGF2 alpha production by greater than 90% in both control and diabetic hearts perfused with platelets and AA. Dazoxiben, a thromboxane synthetase inhibitor, blocked the increase in perfusion pressure by 50%, totally inhibited TxB2 production, but increased PGF2 alpha production by 60% in both groups of platelet-perfused hearts. Increased levels of PGF2 alpha and possibly other constrictor eicosanoids (e.g., leukotriene D4) may account for the partial constriction observed in platelet-perfused hearts with dazoxiben. Results of the present study suggest that vascular reactivity to vasoconstrictor eicosanoids is increased in hearts of diabetic animals.

Animals↗
PubMed1987

Dexamethasone potentiates hypoxic vasoconstriction in salt solution-perfused rat lungs.

Isolated rat lungs perfused with blood or plasma develop good hypoxic pressor reactivity, but those flushed of blood and perfused solely with physiological salt solution (PSS) show decreased or no hypoxic vasoconstriction. Because the handling of rats during collection of blood increases the plasma corticosterone levels, we wondered whether the difference between blood and PSS perfusion was due partly to higher glucocorticoid activity with blood than with PSS. Treatment of lung donors with the synthetic glucocorticoid dexamethasone (2 mg/kg im 3 h before isolation) or addition of dexamethasone (4.2 X 10(-6) M) to the perfusate increased markedly the hypoxic pressor reactivity of rat lungs perfused with PSS plus albumin (4 g/100 ml). In comparison, dexamethasone did not cause a significant increase in the already vigorous hypoxic pressor reactivity of blood-perfused lungs, but it reversed the blunted pressor reactivity of lungs perfused with blood collected from adrenalectomized rats. The potentiation of hypoxic vasoconstriction by dexamethasone required greater than 40 min to develop and was inhibited by a 100-fold higher concentration of progesterone, a glucocorticoid receptor antagonist. Although dexamethasone and the cyclooxygenase blocker meclofenamate (3.1 X 10(-5) M) caused similar decreases in perfusate levels of cyclooxygenase metabolites, the glucocorticoid was much more effective in inducing hypoxic vasoconstriction in PSS-perfused lungs. Thus a reduction of cyclooxygenase metabolism might have contributed to, but did not fully account for, the glucocorticoid effect. Dexamethasone also caused small increases in base-line perfusion pressure and in pressor reactivity to angiotensin II.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenalectomy↗
PubMed1988

Changes in coronary pressure-flow relation after transition from blood to Tyrode perfusion.

In six isolated, diastolic-arrested, maximally vasodilated cat hearts, we studied changes in coronary pressure-flow relations (zero-flow pressure intercept, resistance) during the first 25 min, after a change of perfusate, from blood to Tyrode. The apparent intercept (zero-flow) pressure changed from 2.0 +/- 0.94 (+/- SD) kPa during blood perfusion to 2.5 +/- 0.55, 2.6 +/- 0.68, 2.5 +/- 0.94, and 2.7 +/- 1.34 kPa during Tyrode perfusion for 2:15, 5:30, 10:30, and 25:00 min, respectively. Intercept pressures during Tyrode perfusion were significantly different from the intercept pressure during blood perfusion, except for the one measured after 25 min of Tyrode perfusion (P less than 0.05). Resistance (defined as the ratio of perfusion pressure and flow at 10 kPa perfusion pressure) steadily rose to approximately 170% of the value during blood perfusion. The observation that the apparent intercept pressure is maintained, when a particle-free (Newtonian) isotonic perfusate is used, may indicate that this intercept is not a result of blood rheology alone. The increase rather than decrease in resistance suggests an effect of edema, which increases interstitial volume at the expense of intravascular volume.

Animals↗
PubMed1985

Isolated perfused head of rainbow trout. II. Ionic fluxes.

Branchial ionic transport processes were evaluated and compared in Ringer-perfused and blood-perfused heads of rainbow trout. Rates of Na+ and Cl- influx were similar to in vivo levels at the onset of perfusion. Na+ uptake deteriorated more rapidly over time during Ringer perfusion, whereas Cl- uptake was relatively stable regardless of the perfusate employed. Transepithelial potentials (TEP) were similar to values reported for intact freshwater teleosts and were unstable only during the initial period of blood perfusion. The TEP was extremely dependent on the external concentration of NaCl. Ammonia excretion (JNH4+net) was normal during both types of perfusion, although blood did have a stabilizing effect on JNH4+net over time of perfusion. JNH4+net was stimulated by the addition of carbonic anhydrase to Ringer, without a concomitant increase in Na+ uptake. Branchial net fluxes of Na+ and Cl- were stable but slightly negative and in this regard represented slightly stressed intact animals. Net acid flux (JH+net), however, was similar to in vivo rates. Na+ and Cl- uptake displayed Michaelis-Menten kinetics. The affinity constant (Km) for Na+ uptake was typical of intact fish during both Ringer and blood perfusion, whereas Km for Cl- uptake was abnormally high in both cases. The results are discussed with reference to the suitability of the perfused trout head preparation for studying gill ionic fluxes in vitro.

Animals↗
PubMed1986

Pulmonary microvascular responses to arachidonic acid in isolated perfused guinea pig lung.

We examined the effects of arachidonic acid (AA) on pulmonary hemodynamics and fluid balance in Ringer- and blood-perfused guinea pig lungs during constant-flow conditions. Mean pulmonary arterial (Ppa), venous (Pv), and capillary pressures (Pcap, estimated by the double-occlusion method) were measured, and arterial (Ra) and venous resistances (Rv) were calculated. Bolus AA injection (500 micrograms) caused transient increases (peak response 1 min post-AA) in Ppa, Pcap, and Rv without affecting Ra in both Ringer- and blood-perfused lungs. The response was sustained in blood-perfused lungs. AA had no effect on the capillary filtration coefficient in either Ringer- or blood-perfused lungs. AA stimulated the release of thromboxane B2 and 6-ketoprostaglandin F1 alpha in both Ringer- and blood-perfused lungs, but the responses were sustained only in the blood-perfused lungs. Meclofenamate (1.5 X 10(-4) M), a cyclooxygenase inhibitor, abolished the AA-induced pulmonary hemodynamic responses in both Ringer- and blood-perfused lungs, whereas U-60257 (10 microM), a lipoxygenase inhibitor, attenuated the response only in the blood-perfused lungs. In conclusion, AA does not alter pulmonary vascular permeability to water in either Ringer- or blood-perfused lungs. AA mediates pulmonary venoconstriction and thus contributes to the rise in Pcap. The venoconstriction results from the generation of cyclooxygenase-derived metabolites from lung parenchymal cells and blood-formed elements. Lipoxygenase metabolites may also contribute to the vasoconstriction in the blood-perfused lungs.

6-Ketoprostaglandin F1 alpha↗
PubMed1987

Constant-flow perfusion of the hindlimb vascular bed in conscious dogs.

Hindlimb vascular bed pressure-flow relationships were evaluated in seven conscious dogs using a newly developed controlled-flow perfusion technique. For controlled-flow perfusion, blood was diverted from a common carotid artery to a roller pump for perfusion of the left hindlimb vascular bed via an artificial vascular graft anastomosed to the left external iliac artery. An occlusion cuff positioned around the external iliac artery proximal to the graft arrested normal hindlimb blood flow during perfusion. Collateral flow was minimized by ligating all other major arteries supplying the left hindlimb. Hindlimb perfusion pressure, measured via the left deep femoral artery, decreased to a plateau value of 19.7 +/- 3.4 mmHg when pump flow was zero. Pressure-flow relationships were evaluated while the dogs were at rest by changing flow in small "square-wave" steps for 3 min each and measuring the steady-state perfusion pressure at each step. The hindlimb was perfused over a wide range of flows (25-450 ml/min) that resulted in perfusion pressures ranging from 40 to 175 mmHg. The hindlimb pressure-flow relationship obtained was indicative of net passive vascular behavior. That is, resistance to flow decreased with increases in flow, such that a curvilinear pressure-flow relationship occurred that was convex to the pressure axis. We conclude that the hindlimb circulation of resting conscious dogs can be perfused using controlled-flow perfusion techniques. These techniques can also be applied to other vascular beds and should be useful for evaluating peripheral vascular responses to drugs and reflexogenic alterations.

Animals↗
PubMed1991

Perfusate cytochrome c reduction in isolated rabbit lungs.

The reduction of ferricytochrome c within the perfusate in isolated lung perfusion systems has been demonstrated previously. We carried out the present study 1) to determine what reducing agents might be responsible for this reduction and 2) to determine whether the cytochrome c (cyto c) reduction within the recirculating perfusion system can be accounted for by relatively stable reducing agents released into the perfusate or whether some of the reduction is dependent on short-lived agents and/or proximity to the source of the agents within the lungs. Experiments were carried out with the use of isolated rabbit lungs perfused for 1 h in a recirculating system. In one group of experiments, ferricytochrome c was included in the recirculating perfusion system. In another group, the cyto c was added to produce the same concentration in samples after they were removed from a cyto c-free recirculating system. The recirculating cyto c was reduced at a rate of approximately 1.76 mumol/h, and approximately 22% was inhibitable by superoxide dismutase. Most of the rest could be inhibited by ascorbate oxidase within the recirculating perfusate. When the ferricytochrome c was added to the samples removed from the cyto c-free perfusion system, virtually the entire cyto c reducing capacity was inhibitable by ascorbate oxidase. Although reduced glutathione did accumulate in the recirculating perfusate, the quantity was not sufficient to have an important role in the cyto c reduction. We conclude that most of the cyto c reducing capacity within the lung perfusate could be accounted for by ascorbate released from the lungs.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Effect of blood and albumin on pulmonary hypertension and edema in perfused rabbit lungs.

Perfusate composition may alter pulmonary hemodynamics and edema formation in perfused lungs. Perfusion for 3 h with Krebs-Henseleit solution with 3% bovine serum albumin did not produce pulmonary hypertension, pulmonary edema (assessed by lung wet-to-dry wt ratio), or increased macromolecular permeability (assessed by 125I-albumin uptake). Addition of blood to hematocrit levels of 10 or 20% resulted in pulmonary hypertension during the final hour of perfusion but not pulmonary edema or increased macromolecular permeability. Pulmonary hypertension during blood perfusion was primarily due to increased precapillary resistance. Perfusion with buffer solution without albumin produced edema and increased macromolecular permeability but not pulmonary hypertension. In lungs perfused with blood (20% hematocrit), thromboxane B2 levels increased in parallel with the pulmonary hypertension, and inhibition of cyclooxygenase or thromboxane synthase with indomethacin or dazmegrel prevented pulmonary hypertension. Perfusion with leukopenic blood (from prior nitrogen mustard administration or from filtration) also prevented pulmonary hypertension. We conclude that blood perfusion produces pulmonary hypertension via thromboxane A2 generation, which depends on leukocyte activation, and that perfusion with buffer solutions without albumin produces edema and increased permeability without pulmonary hypertension.

Albumins↗
PubMed1999

Beat-to-beat modulation of heart rate is coupled to coronary perfusion pressure in the isolated heart.

A goal of clinicians caring for heart transplant recipients has been to use heart rate variability as a noninvasive means of diagnosing graft rejection. The determinants of beat-to-beat variability in the surgically denervated heart have yet to be elucidated. We used an isolated, blood buffer-perfused porcine heart preparation to quantitatively assess the relationship between coronary perfusion and sinus node automaticity. Hearts (n = 9) were suspended in a Langendorff preparation, and heart rate (HR) fluctuations were quantified while perfusion pressure was modulated between 70/50, 80/60, 90/70, and 100/80 mmHg at 0.067 Hz. In 32 of 32 recordings, the cross spectrum of perfusion pressure vs. HR showed the largest peak centered at 0.067 Hz. In eight of nine experiments during nonpulsatile perfusion, HR accelerated as perfusion pressure was increased from 40 to 110 mmHg (mean increase 24.2 +/- 3.0 beats/min). HR increased 0.34 beats/min per mmHg increase in perfusion pressure (least squares linear regression y = -25.8 mmHg + 0.34x; r = 0.88, P < 0.0001). Administration of low- and high-dose nitroglycerin (Ntg) resulted in a modest increase in flow but produced a significant decrease in HR and blunted the response of HR to changes in perfusion pressure (HR increase 0.26 beats. min-1. mmHg-1, r = 0.87, P < 0.0001 after low-dose Ntg; 0.25 beats. min-1. mmHg-1, r = 0.78, P < 0.0001 after high-dose Ntg). These experiments suggest that sinus node discharge in the isolated perfused heart is mechanically coupled to perfusion pressure on a beat-to-beat basis.

Animals↗
PubMed1979

Free fatty acid and glucose metabolism during hypothermic perfusion of canine kidneys.

Canine kidneys were subjected to continuous nonpulsatile perfusion using 200 ml of a perfusate containing 50 g/l albumin. When optimal oxygenation was achieved, perfusate K+ contents were unchanged for 24 h, indicating adequate membrane function but tended to increase thereafter. Lowered oxygen pressures resulted in significant cellular K+ loss during the first hours of perfusion. During oxygenated perfusion, glucose and free fatty acids (FFA) were oxidized in considerable amounts with a preferential consumption of octanoate. A capacity for long-chain FFA oxidation became obvious when the octanoate had been used up, but the amount of these FFA in the perfusate depended preferentially on FFA being liberated from tissue lipids during the 1st day of perfusion. Glucose consumption rates were highest during the first 2 days of perfusion but the subsequent reduction of the metabolic rate was not accompanied by an accumulation of lactate. Thus medium-chain FFA and glucose should be supplied to the continuously perfused kidney in hypothermia and optimal oxygenation of the perfusate should be guaranteed. However, it seems to be unnecessary to supply exogenous long-chain FFA.

Albumins↗