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At least 19 recordsLinked to original sources
PubMed1989

Transmission of hypertension in rats by cross circulation.

Cross circulation was performed in 54 couples of spontaneously hypertensive and normotensive rats. Blood was pumped through two anastomoses between the carotid arteries and external jugular veins in both directions with equal flow rate. In normotensive rats cross-circulated with untreated spontaneously hypertensive rats mean arterial pressure increased by 20.9 +/- 12.2 mm Hg (p less than 0.01). Administration of digoxin antibody in a dose binding 0.25 mg digoxin to the spontaneously hypertensive rats before cross circulation prevented the transmission of hypertension to the normotensive rat, whereas chemical sympathectomy with 6-hydroxydopamine and intravenous injection of inactive Fab fragments had no inhibitory effect. It is concluded that, in this strain of spontaneously hypertensive rats, a circulating hypertensive factor exists. The factor binds to digoxin antibody and is not produced in sympathetic nervous tissue.

Animals↗
PubMed1986

The first open-heart repairs of ventricular septal defect, atrioventricular communis, and tetralogy of Fallot using extracorporeal circulation by cross-circulation: a 30-year follow-up.

From March 26, 1954, to July 19, 1955, 45 patients with major cardiac malformations not previously correctable underwent open repair utilizing cross-circulation between patient and donor without donor deaths. All operations were carried out at normothermia with lowered flow rates based on azygos flow studies. Twenty-seven patients, more than half of them infants, had ventricular septal defects closed. There were 8 hospital deaths, and there have been only 2 late deaths in 30 years. Fourteen (87.5%) of 16 who underwent recatheterization have closed defects. The 17 30-year-survivors are all in New York Heart Association Functional Class I. Five patients 4 months to 10 years old were operated on for atrioventricular canal (complete form). All had intractable failure, and 4 had pulmonary hypertension. Two of the 3 hospital deaths were due to heart block. The long-term survivor, a 15-month-old infant at the time of operation (severe pulmonary hypertension, 90/50 mm Hg), underwent repair 31 years ago and is now married with 3 children. Recatheterization disclosed normal pulmonary pressure (20/4 mm Hg), no shunts, and mild mitral regurgitation. Ten cyanotic tetrads 13 months to 14 years old were operated on with 5 hospital deaths. Of the 3 late deaths, 1 was accidental at 17 years, 1 occurred suddenly at home 13 years after operation in infancy for atresia, and the third occurred at reoperation 10 years later. The 2 remaining patients (1 the first patient operated on) are in excellent health. The surgical methods used and the physiological advantages of cross-circulation (temporary placenta) that made these results possible at a time when surgical knowledge was primitive are described.

Cardiac Catheterization↗
PubMed1999

Influence of brain death and cardiac preservation on systolic and diastolic function and coronary circulation in the cross-circulated canine heart.

Previous studies have demonstrated hemodynamic instability and cardiac dysfunction in the brain-dead organ donor. It remains unclear if primary cardiac dysfunction is responsible for hemodynamic deterioration or decreased cardiac function is secondary to brain death-associated altered loading conditions. Therefore in the present study the effects of brain death on hemodynamics and cardiac function were analyzed in vivo in an open chest model and ex vivo in a cross-circulated heart preparation. In a second protocol, the impact of brain death-associated hemodynamic changes on postischemic graft function was investigated. Brain death was induced injecting saline in a subdural Foley catheter. Induction of brain death led to a hyperdynamic reaction followed by hemodynamic deterioration with a decrease of systemic vascular resistance and myocardial contractility. If the hearts were explanted and assessed ex vivo, no differences were found between control and brain-dead hearts. Furthermore, both control and brain-dead hearts showed full functional recovery after 4 hours of hypothermic ischemic storage. Despite hemodynamic deterioration in situ after brain death, there were no differences between the postischemic function of control and brain-dead hearts. These results indicate that myocardial dysfunction is not irreversible and may be secondary to altered loading conditions, and that the recovery of cardiac function after long-term hypothermic storage is not impaired by the hemodynamic changes observed in situ after brain death induction. These data may also indicate that potential donor hearts might not be excluded from transplantation on the basis of impaired hemodynamic characteristics, especially if they are evaluated by load-dependent parameters.

Analysis of Variance↗
PubMed1984

[Long-term cross-circulation on galactosamine induced hepatic failure rats].

Cross-circulation was carried out in between galactosamine treated hepatic failure rats and normal rats and its efficacy was mainly evaluated by measuring mitochondrial respiratory function of the liver. Twenty-four hours after the injection of galactosamine, cross-circulation was performed at a blood flow rate of 1 ml/min for 8 hours. Survival rate of the rats in 48 hours and 60 hours after the injection of galactosamine was 86% and 57% in a cross-circulation group and 66% and 23% in a sham-circulation group, respectively. In a cross-circulation group, there showed significant increases of ATP synthesis per 100 gr. body weight, turnover number of phosphorylation and Cyt a (+a3) which were markedly reduced in a sham-circulation group. These appear to suggest that cross-circulation provides augmented mitochondrial energy supply in the liver and contributes higher survival rate of the rats.

Animals↗
PubMed1967

Regeneration of rat liver: transfer of humoral agent by cross circulation.

Carotid-to-jugular cross circulation between partially hepatectomized and normal rats, via polyethylene cannulas, stimulated incorporation of (14)C-thymidine into hepatic DNA in the normal partners when it was maintained for 19 hours at a flow rate of about 2 milliliters per minute. Cross circulation for 7 hours or less was ineffective.

Animals↗
PubMed1984

[Homologous plasma cross-circulation on galactosamine induced hepatic failure rats].

Plasma cross-circulation which resembles plasma exchange clinically was carried out in between galactosamine (GalN) treated hepatic failure rats and normal rats. Twenty-four hours after the injection of GalN, plasma cross-circulation was performed at a plasma flow rate of 0.1 ml/min for 6 hours. In eighteen hours after the completion of a procedure, survival rate was 75% (6 out of 8 survived) in GalN injected rats treated with plasma cross-circulation, as compared to 40% (4 out of 10 survived) in GalN injected rats treated with sham-circulation. State 3 oxygen consumption and ATP synthesis in the liver mitochondrial respiratory function, and ATP and total adenine nucleotide contents in the liver in the former group were significantly higher than those in the latter group at the time of sacrifice of the survived animals. These appear to suggest that plasma cross-circulation enhances mitochondrial phosphorylative activity in the liver and may contribute higher survival rate of the rats. Plasma exchange using a large amount of fresh plasma, therefore, would be effective for the treatment of acute liver failure in its early stage.

Animals↗
PubMed1986

Cerebral metabolism during cross-circulation in experimental hepatic failure in the pig.

The effect of hepatic assistance on cerebral metabolism was evaluated in a series using cross-circulation, anticipating increased efficiency of hepatic support. The experimental model for liver failure was pigs with totally devascularized liver. Cross-circulation with a normal sibling pig, cross-circulation with inflow in the donor directly into the portal vein and cross-perfusion with isolated perfused liver starting 20 h after elimination of liver function in the recipient and lasting for 3 h did not increase survival. Before cross-circulation in these three groups, the cerebral flow and oxygen uptake were decreased; during the cross-circulation a significant but temporary increase was found. In experiments with early and prolonged perfusion with isolated perfused liver no changes in cerebral flow, oxygen or glucose uptake were found, and these variables were still normal 6 h after termination of the perfusion. The survival time was significantly increased. In the control group a significant rise in blood and CSF ammonia was found with a mean CSF/blood ratio of 0.92. After cross-circulation, the CSF/blood ratio was 0.52 and 0.62, respectively, indicating a proportionally greater elimination of ammonia from the cerebrospinal fluid than from the blood. Cross-circulation did not significantly change the alpha-ketoglutarate, glutamate or glutamine CSF concentrations. After prolonged cross-perfusion, the ammonia blood/CSF ratio was 0.24. It is concluded that by extended extracorporeal hepatic assistance it is possible to increase survival and to prevent changes in cerebral metabolism and ammonia accumulating in the cerebrospinal fluid.

Ammonia↗
PubMed1985

[Significance of cross-circulation on obstructive jaundice in rats with special reference to the mitochondrial function of the liver and kidney].

Cross-circulation was performed to investigate the mitochondrial respiratory function of the liver and kidney in rats after 1, 2 and 3 weeks of biliary obstruction. Serum bilirubin and total bile acids concentration in blood in rats with biliary obstruction markedly decreased with 3 hours cross-circulation. There demonstrated, however, no significant change in mitochondrial function in the liver after cross-circulation. In contrast, mitochondrial function in the kidney showed significant improvement after 3 hours cross-circulation. Mitochondrial respiratory function in normal partner rats cross-circulation with jaundiced rats demonstrated temporal deterioration in the kidney and prolonged deterioration in the liver. It can be concluded that cross-circulation or plasma exchange might be useful for the prevention of renal failure in obstructive jaundice, since cross-circulation induced persistent improvement of the mitochondrial respiratory function in the kidney deteriorated by biliary obstruction.

Animals↗
PubMed2003

Suppressed complement activation in human decay accelerating factor transgenic porcine liver cross-circulated with nonhuman primates.

BACKGROUND: We developed an extracorporeal liver perfusion (ECLP) system as a liver-assist device. In this study, we evaluated the safety of the ECLP using human decay accelerating factor (hDAF) transgenic porcine livers in healthy baboons. METHODS: Livers were isolated from five hDAF transgenic pigs and five nontransgenic pigs for the ECLP. Ten cross-circulations between the ECLP and healthy baboons were performed without immunosuppressive agents. Cross-circulation was discontinued in any of the following circumstances: elevated hepatic arterial (>200 mm Hg) or portal (>60 mm Hg) perfusion pressure, massive exudate from the graft liver, mild macroscopic hemolysis, thrombocytopenia, or 24-hr well-conditioned cross-circulation. RESULTS: The cross-circulations with nontransgenic porcine livers were discontinued at 4.4+/-1.2 hr (mean+/-standard deviation) because of high perfusion pressure (n=2) or hemolysis (n=3). Three cross-circulations with hDAF transgenic porcine livers were performed for 24 hr; the other two cross-circulations were discontinued at 13 and 17 hr because of massive exudate and thrombocytopenia, respectively. The duration was 20.4+/-5.1 hr. Deposition of membrane attack complex in the hDAF transgenic porcine liver was less than that in the nontransgenic liver, although immunoglobulin-M deposition was comparable. The porcine livers showed no apparent interlobular bleeding or lobular necrosis. All porcine livers maintained bile production during the cross-circulation. No baboons showed any serious complications after the cross-circulation. CONCLUSION: The hDAF transgenic porcine liver reduced complement activation in xenoperfusion with healthy nonhuman primate blood and led to extended duration of cross-circulation.

Animals↗