Some effects of autologous and homologous blood or plasma overtransfusions in the dog

1965 ◽  
Vol 209 (4) ◽  
pp. 673-679 ◽  
Author(s):  
R. A. Huggins ◽  
E. L. Smith ◽  
S. Deavers

Plasma volume, protein concentration, mean arterial pressure, urticaria, and survival rates were observed in morphine-pentobarbitalized dogs overtransfused with either dextran, homologous blood, reconstituted homologous blood, autologous frozen stored, homologous frozen stored, or fresh plasma. The principal reaction and only difference between responses with autologous plasma and homologous blood and plasma was the development of urticaria with homologous blood (10%), homologous plasma (70–90%), and reconstituted homologous blood (100%). Significant amounts of fluid and protein were lost with all overtransfusions; this loss was not correlated with the urticaria. Of five dogs developing urticaria, three had an increased plasma histamine level. Diphenhydramine hydrochloride reduced the incidence of urticaria from 100 to 20%. Blood group incompatibility was not involved. There was a direct relationship between handling of blood and urticaria, and it is postulated that, during handling, a substance is activated which causes the release of endogenous histamine and production of urticaria.

1990 ◽  
Vol 259 (5) ◽  
pp. H1317-H1324
Author(s):  
R. D. Manning

Studies were performed in 14 conscious, anephric dogs to clarify the role of blood volume in the genesis of hypertension. The dogs were splenectomized and had plasma protein concentration (PPC) reduced to 2.7 g/dl by daily plasmapheresis for 9 days. This hypoproteinemia resulted in a 20% decrease in both blood volume and mean arterial pressure. On the 10th day the dogs were nephrectomized. On the 11th day after a 3-h control period with plasmapheresis, lactated Ringer equivalent to 10 or 20% of body weight was intravenously infused. By 25 h postinfusion blood volume had not increased, and the dogs were still hypotensive. At 25 h plasma protein mass was returned to normal by intravenous infusion of autologous plasma, the average blood volume of the three low PPC groups increased approximately 50%, and the arterial pressure increased greater than 60%. The decrease in PPC shifted the regression of blood volume on sodium space down the blood volume axis. In conclusion, the dependence of arterial pressure on blood volume was demonstrated by the decrease in both blood volume and arterial pressure after PPC reduction, the constancy of blood volume and pressure during Ringer infusion, and the increase in both volume and pressure after plasma infusion.


1997 ◽  
Vol 82 (1) ◽  
pp. 348-353 ◽  
Author(s):  
John D. Grimme ◽  
Susan M. Lane ◽  
Michael B. Maron

Grimme, John D., Susan M. Lane, and Michael B. Maron.Alveolar liquid clearance in multiple nonperfused canine lung lobes. J. Appl. Physiol. 82(1): 348–353, 1997.—We evaluated the ability of canine isolated nonperfused lung lobes to absorb fluid from their air spaces by simultaneously measuring alveolar liquid clearance (ALC) in three lobes removed from the same dog. Autologous plasma was instilled in the air spaces of each lobe, and the increase in plasma protein concentration resulting from fluid reabsorption was used to calculate ALC. ALC after 4 h was 16.5 ± 0.6% (SE) of the instilled fluid volume under baseline conditions and was 30.2 ± 1.3% after terbutaline (10−5 M) administration. These values were similar to those previously reported for intact dogs. Propranolol (10−4 M) and ouabain (10−3 M) reduced ALC in terbutaline-stimulated lobes to 20.4 ± 0.8 and 3.9 ± 1.4%, respectively. There was no significant difference in ALC among the three lobes under either baseline conditions or after terbutaline administration. These data indicate that the sodium and water transport mechanisms of the canine alveolar epithelium remain viable during 4 h of nonperfusion and that there are no intrinsic differences in the transport properties of individual lung lobes. The ability to study several lobes simultaneously without the need for perfusion will allow for the design of experiments in which multiple interventions can be studied by using lung lobes from the same animal.


1980 ◽  
Vol 49 (3) ◽  
pp. 516-520 ◽  
Author(s):  
K. L. Brigham ◽  
S. J. Padove ◽  
D. Bryant ◽  
C. R. McKeen ◽  
R. E. Bowers

Because, in sheep, histamine-induced increased lung vascular permeability is prevented by diphenhydramine, we tested the effects of diphenhydramine on the sheep lung vascular response to endotoxin. We infused E. coli endotoxin (0.40-1.00 micrograms/kg) with and without diphenhydramine (3.0 mg/kg bolus + 1.5 mg . kg-1 . h-1) in the same unanesthetized sheep while measuring pulmonary arterial (Ppa) and left atrial (Pla) pressures, lung lymph flow (Qlym) and lymph (L) and plasma (P) protein concentrations. Endotoxin caused pulmonary hypertension soon after infusion (base-line Ppa = 22 +/- 3 (SE) cmH2O; after endotoxin Ppa = 40 +/- 2; P less than 0.05, n = 6) and after several hours an increase in permeability reflected in high flow of protein-rich lymph (base-line; Qlym = 7.5 +/- 1.4 (SE) ml/h, L/P protein concentration = 0.60 +/- 0.02: after endotoxin; Qlym = 21.4 +/- 3.1, P less than 0.05; L/P = 0.66 +/- 0.03, P less than 0.05). In the presence of diphenhydramine, endotoxin caused identical pressure changes but Qlym was lower during the period of increased permeability (16.7 +/- 3.0 (SE) ml/h, P less than 0.05 compared to endotoxin alone) and L/P protein concentration was similar (0.68 +/- 0.04, P = NS). We conclude that endogenous histamine may be partly responsible for the increase in lung vascular permeability after endotoxemia, but that histamine probably is not the sole mediator of the permeability change.


1977 ◽  
Vol 146 (3) ◽  
pp. 641-652 ◽  
Author(s):  
J Fehr ◽  
HS Jacob

To study mechanisms and mediators regulating the distribution of intravascular granulocytes between circulating and marginated pools, a human model with extreme transient margination, the neutropenia of continuous flow filtration leukophoresis, was analyzed. Studies in animals demonstrated the existence of a complement (C)-derived granulocytopenia-inducing factor. Thus, autologous plasma, exposed to nylon fibers (NF) of the filtration system, produced an acute selective decrement of circulating granulocytes and monocytes. This phenomenon was blocked by decomplementing plasma, by pretreatment of plasma with EDTA or hydrazine, and by preheating at 56 degrees C, but did occur after recombination of heat-inactivated and hydrazine-treated plasma before NF exposure. Preheating plasma at 50 degrees C did not inhibit the neutropenic response, suggesting involvement of the classical pathway of C activation. Ultrafiltration studies indicated that the NF-provoked neutropenia-inducing factor has a mol wt in the range of 10,000-30,000, and is heat stable (56 degrees C). To analyze the hypothesis that C- induced neutrophil margination might be consequent to increased cell adhesiveness to endothelial surfaces, the role of C in promoting granulocyte adherence was evaluated in vitro. Measured with a plastic Petridish assay, granulocyte adherence was significantly reduced in heat- inactivated (56 degrees C) and hydrazine-treated plasma, but adherence promoting capacity was restored by mixing the two plasmas, or by adding purified C3 to hydrazine-treated plasma. After exposure to activated C, neutrophils showed significantly increased adhesiveness which was maintained when cells were resuspended in heat-inactivated plasma, but progressively lost when resuspended in fresh plasma. On the basis of these results we conclude that granulocyte adhesiveness in vitro and margination in vivo are closely associated, C-dependent phenomena.


1991 ◽  
Vol 70 (4) ◽  
pp. 1827-1835 ◽  
Author(s):  
N. Smedira ◽  
L. Gates ◽  
R. Hastings ◽  
C. Jayr ◽  
T. Sakuma ◽  
...  

Alveolar and lung liquid clearance were studied over 8 h in intact anesthetized ventilated rabbits by instillation of either isosmolar Ringer lactate (2 ml/kg) or autologous plasma (2 or 3 ml/kg) into one lower lobe. The half time for lung liquid clearance of the isosmolar Ringer lactate was 3.3 h and that for plasma clearance was 6 h. In the plasma experiments, the alveolar protein concentration after 1 h was 5.2 +/- 0.8 g/dl, which was significantly greater than the initial instilled protein concentration of 4.3 +/- 0.7 g/dl (P less than 0.05). Thus alveolar protein concentration increased by 21 +/- 12% over 1 h, which matched clearance from the entire lung of 19 +/- 11% of the instilled volume. Overall the rate of alveolar and lung liquid clearance in rabbits was significantly faster than in prior studies in dogs and sheep. The fast alveolar liquid clearance rate in rabbits was not due to higher endogenous catecholamine release, because intravenous and alveolar (5 x 10(-5) M) propranolol did not slow the clearance. Also, beta-adrenergic therapy with alveolar terbutaline (10(-5) or 10(-4) M) did not increase the alveolar or lung liquid clearance rates. Phloridzin (10(-3) M) did not slow alveolar liquid clearance. However, amiloride (10(-4) M) inhibited 75% of the basal alveolar liquid clearance in rabbits, thus providing evidence that alveolar liquid clearance in rabbits depends primarily on sodium-dependent transport. This rabbit study provides further evidence for important species differences in the basal rates of alveolar liquid and solute clearance as well as the response to beta-adrenergic agonists and ion transport inhibitors.


1992 ◽  
Vol 262 (4) ◽  
pp. H937-H941 ◽  
Author(s):  
R. D. Manning

The long-term effects of hyperproteinemia on blood volume and lymph protein concentration were studied in six conscious dogs over a 17-day period. Plasma protein concentration (PPC) was increased by daily intravenous infusion of approximately 300 ml of previously collected autologous plasma. By day 17 PPC had increased 2.4 g/dl, and plasma colloid osmotic pressure had increased 51%; however, blood volume was not changed. Also, at this time sulfate space, an index of extracellular fluid volume, had increased 12%, prenodal lymph protein concentration had increased from 1.6 to 5.1 g/dl, mean arterial pressure was unchanged, circulating protein mass was increased, and plasma sodium concentration was decreased slightly. In conclusion, the increase in lymph protein concentration during hyperproteinemia may indicate that interstitial fluid protein concentration also increased. This, in turn, would help to prevent any increase in the transcapillary colloid osmotic pressure gradient and thus attenuate any changes in blood volume.


1997 ◽  
Vol 20 (11) ◽  
pp. 603-609 ◽  
Author(s):  
S. Mandolfo ◽  
C. Tetta ◽  
S. David ◽  
R. Gervasio ◽  
D. Ognibene ◽  
...  

Regenerated cellulosic membranes are held as bioincompatible due to their high complement - and leukopenia - inducing properties. Adherence of polymorphonuclear neutrophils and monocyte purified from normal human blood to the three membranes were evaluated in an in vitro recirculation circuit in the presence or absence of fresh, autologous plasma after recirculation in an in vitro circuit using minimodules with each of the three membranes. In in vivo studies, 9 patients were treated with conventional haemodialysis for 2 weeks with each membrane and 1 week for wash-out using haemodialysers with the following surface: 1.95 m2 for benzyl-cellulose, 1.8 m2 for acetate-cellulose and low-flux polysulfone. Measurement of leukopenia, plasma C3a des Arg and elastase-α 1 proteinase inhibitor complex levels as well as urea, creatinine, phosphate and uric acid clearances was performed. Plasma-free neutrophils adhered maximally to acetate-cellulose (65% remaining in the circulation), while there was no significant difference between low-flux polysulfone and benzyl-cellulose (80% circulating neutrophils, at 15 min, p<0.001 vs acetate cellulose). In the presence of fresh plasma, as source of complement, the differences between acetate cellulose vs polysulfone and benzyl-cellulose were even more evident, suggesting the role of complement-activated products in neutrophil adherence. A similar trend was observed for monocyte adherence with the three membranes in the absence or presence of plasma. In vivo studies showed that the nadir of leukopenia was at 15 and 30 min with acetate-cellulose (79%) and benzyl-cellulose (50%) (p<0.05 acetate- vs benzyl-cellulose) and at 15 min with polysulfone (24%) (p<0.01 vs acetate- and benzyl-cellulose). Plasma C3a des Arg levels arose to 2037 ± 120 ng/ml, 1216 + 434 ng/ml and 46 ± 55 ng/ml with acetate-, benzyl-cellulose and polysulfone, respectively. No pre- vs post-dialysis increase in the intracellular content of TNF-α was detected with any of three membranes. Clearance values of urea, creatinine and uric acid were superimposable for all the three membranes. However, benzyl cellulose had a significantly higher clearance for phosphorus (normalized for surface area) (p<0.01 vs acetate-cellulose, 0.001 vs polysulfone). These results implicate that synthetic modification of the cellulose polymer as for the benzyl-cellulose significantly reduces the in vitro adherence, delays the in vivo activation of “classic” biocompatibility parameters and notably improves the removal of inorganic phosphorus.


1959 ◽  
Vol 197 (1) ◽  
pp. 193-200 ◽  
Author(s):  
John W. Remington ◽  
Carleton H. Baker

Splenectomized dogs were infused serially with 5–10 cc/kg of blood or plasma. There was a high incidence of reactions to the homologous plasma or blood, marked by a fall in arterial pressure, urticaria, cutaneous edema, a prolonged bleeding time, labored respiration and some fatalities. The pressure fall was not seen in anesthetized dogs. The urticaria and skin edema were largely prevented by injections of antihistaminic drugs, but the other reactions were not reduced. In the majority of dogs given homologous blood, the hematocrit showed a steep rise, indicating a disappearance of plasma. The reduced plasma volume was confirmed by T-1824 injections, although the agreement between hematocrit change and plasma volume change by dye was not always quantitative. These changes were not clearly affected by the antihistaminic drugs. However, when dogs were given their own (autologous) plasma, the blood volume increase as measured by dye or calculated from hematocrit change was the same as that expected from the known amount of plasma transfused, corrected for ultrafiltrate shifts. The infusion reactions were also greatly curtailed.


1998 ◽  
Vol 275 (1) ◽  
pp. R135-R140 ◽  
Author(s):  
R. Davis Manning

The long-term responses of lymph flow, lymph protein transport, and the permeability-surface area (PS) product to hyperproteinemia have been studied in conscious dogs. Plasma protein concentration (PPC) was increased by daily intravenous infusion of previously collected autologous plasma for 9 days. Lymph flow was determined by collecting lymph chronically from a lymphatic afferent to the popliteal node in the hind leg. Compared with the average value during the normal-PPC period, the following changes occurred during 10 days of high PPC: lymph flow decreased from 12.3 ± 1.1 to 3.8 ± 0.6 μl/min, lymph protein transport decreased from 241 ± 24 to 141 ± 21 μg/min, PS product decreased from 4.7 ± 0.5 to 3.0 ± 0.5 μl/min, PPC increased from 7.1 ± 0.1 to 8.8 ± 0.4 g/dl, lymph protein concentration increased from 1.9 ± 0.1 to 3.8 ± 0.1 g/dl, plasma colloid osmotic pressure increased from 18.6 ± 0.8 to 24.2 ± 2.1 mmHg, and lymph colloid osmotic pressure increased from 4.8 ± 0.2 to 10.4 ± 0.7 mmHg. In conclusion, long-term hyperproteinemia in dogs resulted in chronic decreases in lymph flow, lymph protein transport, and the PS product and chronic increases in lymph protein concentration and lymph colloid osmotic pressure. The marked decrease in lymph flow during hyperproteinemia decreased lymph protein transport and thus contributed to the increase in lymph protein concentration. In addition, the decreases in PS product and lymph protein transport suggest that transcapillary protein flux decreases during hyperproteinemia.


2000 ◽  
Vol 89 (2) ◽  
pp. 644-648 ◽  
Author(s):  
Machiko Ikegami ◽  
Alan H. Jobe ◽  
Jeffrey Whitsett ◽  
Thomas Korfhagen

Mice carrying a null mutation of the surfactant-associated protein A (SP-A) gene have normal respiratory function, but their surfactant lacks tubular myelin, is sensitive to protein inactivation in vitro, and contains decreased pool sizes of the biophysically active large-aggregate surfactant. We hypothesized that SP-A-deficient mice would be more susceptible to exercise-induced stress and O2-induced lung injury. SP-A-(−/−) and SP-A-(+/+) mice tolerated 1 h of swimming or 45 min of running on a treadmill at 15 m/min equivalently, without alterations of the amount of alveolar saturated phosphatidylcholine. After 3 days of hyperoxia, SP-A-(−/−) mice had increased alveolar protein, but pressure-volume curves were not different between groups. Alveolar protein concentration was similarly increased in SP-A-(−/−) and SP-A-(+/+) mice after 4 days of exposure to hyperoxia. Survival rates were similar after 4 days of hyperoxia. SP-A-(−/−) mice were equally tolerant to exercise and 4 days of hyperoxia, indicating that the SP-A-dependent alterations in surfactant did not result in functional deficits.


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