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PubMedDate not supplied

Pressor hyperresponsiveness in saline-infused rabbits.

Conscious rabbits infused intravenously (i.v.) with isotonic saline at 1.5 to 1.8 ml/min for 24 hours had greater pressor responses to norepinephrine (NE) than did normal control rabbits. Infusion of the angiotension II (ANG II) antagonist [Sar1, Ile8] ANG II did not decrease the exaggerated pressor responses to NE in saline-infused rabbits. Measurements of cardiac output (CO) as well as the pressor responses to NE before and after saline infusion revealed that, although saline infusion increased the CO and decreased total peripheral resistance (TPR), CO did not change during NE infusion either before or after saline infusion, but NE produced significantly greater increases in mean arterial pressure (MAP) and TPR after saline infusion than before the saline infusion. The cross-circulation of blood at 10 ml/min for 5 minutes between saline-infused donor rabbits and normal recipient rabbits resulted in pressor hyperresponsiveness to NE in the normal recipients. Similar cross-circulation experiments between pairs of normal rabbits did not alter the pressor responses to NE. These studies provided direct evidence that expansion of body fluid volumes by saline infusion results in pressor and vascular hyperresponsiveness. There was no evidence to indicate that ANG II was involved in the mechanisms producing this pressor hyperresponsiveness. Some circulating hormonal factor, however, was involved in mediating the pressor hyperresponsiveness following saline infusion. The results of this study are compatible with the concept that natriuretic hormone may play a role in promoting pressor hyperresponsiveness in saline-expanded animals.

Angiotensin II↗
PubMed2001

Effects of prostaglandin E(1) on the efficacy of xenogeneic extracorporeal pig liver perfusion in a canine model of acute liver failure.

Xenogeneic extracorporeal liver perfusion (ECLP) has the potential to become an important tool in the management of patients with severe liver failure. We previously showed that xenogeneic pig liver perfusion may be prolonged for up to 9 hours by the administration of prostaglandin E(1) (PGE(1)). In this study, we used a canine model of acute liver failure to evaluate the effects of PGE(1) on the efficacy of ECLP as a liver-assist device. Liver failure was surgically induced in 12 beagle dogs, with a control group (group 1, n = 4) not connected to the ECLP circuit. Direct cross-circulation between the dogs and the ECLP circuit using a pig liver was performed without (group 2, n = 4) or with (group 3, n = 4) continuous administration of PGE(1) through the portal vein of the pig liver. The duration of cross-circulation in group 3 (9.4 +/- 1.2 hours) was significantly longer than in group 2 (4.3 +/- 1.0 hours). In addition, elevation of blood ammonia, total bile acid, and hyaluronic acid levels was less marked in group 3 compared with the other 2 groups. The ratio of branched-chain amino acids to aromatic amino acids was also improved in group 3. The mean survival time in group 3 (26.6 +/- 0.4 hours) was significantly longer than in group 1 (15.5 +/- 1.3 hours) or group 2 (17.1 +/- 2.9 hours). Continuous administration of PGE(1) to xenogeneic ECLP resulted in a significant improvement in both liver function and survival time of dogs with surgically induced liver failure.

Alprostadil↗
PubMed1981

Different cross-reacting circulating immune complexes in Behçet's syndrome and recurrent oral ulcers.

Circulating immune complexes were isolated by 2% polyethylene glycol precipitation from the sera of 15 out of 37 patients with Behçet's syndrome and 11 out of 23 patients with recurrent oral ulcers. The antigenic cross-reactions of the polyethylene glycol precipitates were studied by coating a plastic tube with one complex and adding another 125I-labeled complex in dissociating (acid) conditions. On neutralization, partial reassembly occurred with the complex coating the tube wall, thus indicating cross-reaction with it. In the first 30 complexes studied, the cross-reactions obtained were sorted by computer program into two mutually exclusive subsets of reactions. Two similar homologous subsets of reactions were found in the second group of 29 patients: in total, nine out of 16 ocular, four out of six herpetiform circulating immune complexes in one subset, and four out of seven neurological in the other. A wider pattern of reaction could be detected in addition, which induced most of the Behçet's syndrome and recurrent oral ulcers. Immune complexes from control sera did not cross-react. An exogenous agent could account for the circulating immune complexes' cross-reactions for the group as a whole, and two antigenic determinants of that agent or antigens from different damaged tissues explain the subsets.

Antigen-Antibody Complex↗
PubMed1977

Action of oleic acid on the exocrine pancreatic secretion of the conscious rat: evidence for an anti-cholecystokinin-pancreozymin factor.

The effects on exocrine pancreatic secretion of an intraduodenal infusion of oleic acid (2 ml in 60 min) has been assessed in conscious rats provided with a new type of duodenal cannula permitting the normal flow of pancreatic juice, but not of bile, between experiments.1. Intraduodenal oleic acid infusion induces an increased secretion of water and bicarbonate which is still significantly above basal values 90 min after the end of infusion. Protein output increased during the infusion, but protein concentration and output significantly decreased under basal levels 120 min and 150 min after infusion (respectively -63 and -57% of basal values at 150 min).2. No inhibition was found when oleic acid was introduced into the caecum or into the first 20 cm of ileum isolated from the rest of small intestine. On the contrary, inhibition of protein secretion was induced immediately by intra-ileal oleic acid infusion.3. Inhibition of protein secretion secondary to intra-ileal oleic acid infusion was transmitted from a donor rat to a receiver rat by means of a cross-circulation.4. It is concluded that oleic acid induces an immediate and long lasting increase in water and bicarbonate secretion. During the infusion of oleic acid, protein output is increased, followed by an inhibition. This delayed inhibition stems from the second part of the small intestine and was transferred from one rat to another by cross-circulation: it is speculated that oleic acid releases in the conscious rat (from the distal part of the small intestine) a hormonal factor inhibiting pancreatic secretion.

Animals↗
PubMedDate not supplied

[The nature of the hypermetabolism and tachycardia in cold adaptation and experimental hyperthyroidism].

The cross circulation method has been used to study contribution of humoral and nonhumoral components to the origin of hypermetabolism (increased level of basal metabolism) and tachycardia under adaptation to cold and experimental hyperthyroidism. Consumption of oxygen, heart rate and rectal temperature have been studied in periods prior to and during the cross circulation. It is shown that under experimental hyperthyroidism contribution of humoral and nonhumoral factors to the origin of hypermetabolism equals 22 and 78%, while that to genesis of tachycardia--44 and 56%, respectively. Under cold adaptation an increase of the basal metabolism level depends on humoral agents by 77% and on changes of the stationary character only by 23%. The nature of adaptation tachycardia is mainly, of the humoral origin (65%).

Adaptation, Physiological↗
PubMed1990

C. Walton Lillehei and total correction of tetralogy of Fallot.

In March 1954, an operating team headed by C. Walton Lillehei introduced the technique of cross circulation for the first-ever total corrections of ventricular septal defect, tetralogy of Fallot, and atrioventricular canal. Ten of 45 patients operated on with this technique of cardiopulmonary bypass had correction of tetralogy of Fallot, and the results with these 10 patients were reported in a landmark article. The operative results achieved in 1954 and 1955 by Lillehei and his team using cross circulation were truly remarkable. In addition, the University of Minnesota team concomitantly developed a host of new techniques and biomedical devices that made subsequent cardiac operative procedures safer and simpler to perform. These techniques and devices included the first ventricular septal defect prosthetic patch, the first right ventricular outflow patch, the first clinically applicable bubble oxygenator, and the first intramyocardial electrode used in combination with an external pacemaker for a patient with complete heart block.

Cardiac Surgical Procedures↗
PubMed1980

Compensatory hypertrophy of the residual small intestine after partial enterectomy. A neurohumoral feedback?

Experiments were designed to test, using 76 pigs, 1) whether a humoral factor inducing compensatory hypertrophy is released after partial enterectomy or not, and 2) whether visceral sensitivity conducted to the central nervous system by the route of the vagus plays a role in the compensatory hypertrophy or not. Vascular parabiosis was established between pigs paired for an identical blood group and histocompatibility. A continuous blood cross circulation was maintained for 410 h either between two normal pigs or between a normal and a jejunectomized (30 per cent) pig. Their growth and food intake, and the tissue weight of their small intestine were checked. Both the jejunectomized pigs and their unoperated partners showed a significant hypertrophy of the small intestine, whether residual or intact, as compared to intact pigs cross circulated between them. The hypertrophy observed in the unoperated partners of the jejunectomized pigs was not the result of any hyperphagia. There was thus a true humoral mediation of the compensatory hypertrophy. Vagal deafferentation, i.e. a selective surgical suppression of the vagal afferent (sensory) pathways originating below the diaphragm, was performed in jejunectomized pigs. Their performances and small intestine morphology (whole tissue weight and dry weight of the mucosa) were compared to those measured in jejunectomized but vagally intact pigs. The dry weight of the mucosa of the residual small intestine in resected pigs was restored (after 28 days) at a value similar to that measured for the intact small intestine in controls. Opposite to that, the dry weight of the mucosa of the residual intestine of resected + deafferented pigs was significantly lower, due to the absence of any compensatory hypertrophy. This difference did not result from any change in the food intake level. Therefore it was concluded that vagal afferences from the digestive tract are necessary in eliciting the compensatory hypertrophy. From these results and some recent bibliographical data, it is tentatively concluded that compensatory hypertrophy of the residual small intestine after partial enterectomy might be mediated through a neuro-humoral feedback whose afferent way would be the vagal sensory pathway, and efferent way would be a hormonal one monitored by the hypothalamo-hypophyseal axis.

Adaptation, Physiological↗
PubMed1985

Alternations of liver pathophysiology in experimental hepatic failure treated by two forms of plasma purification procedure.

Plasma cross-circulation which resembles plasma exchange and plasma perfusion over charcoal and resin adsorbents were carried out using rats with galactosamine (GalN)-induced hepatic failure to investigate the effects of those plasma purification procedures on damaged liver function. Twenty-four hr after the injection of GalN, the plasma treatment procedures were performed at a plasma flow rate of 0.1 ml/min for 6 hr. Forty-eight hr after the injection of GalN, ATP synthesis in liver mitochondrial function, and ATP and total adenine nucleotide contents in the liver, which were markedly reduced by the GalN administration, were increased by both plasma cross-circulation and plasma perfusion over adsorbents. These results suggest that both plasma purification procedures improve the deterioration of mitochondrial phosphorylation activity and produce an augmented high energy status in the liver. In the histological study of the liver, volume ratio of hepatic parenchyma in the GalN-treated liver to that in the normal liver was significantly higher in rats treated with plasma perfusion than those with sham-perfusion. An efficient removal of the hepatotoxic metabolites from the plasma, therefore, decelerates the progress of GalN induced-liver tissue necrosis, if rats with GalN-induced hepatic failure are treated in an early stage.

Adenine Nucleotides↗
PubMed1979

Circulating natriuretic and kaliuretic factors in acute uremia: the role of the kidney.

The role of the kidney as a source or as the excretory route for natriuretic and kaliuretic factors present in acute uremia was studied using the technique of isovolemic cross-circulation in 49 pairs (eight groups) of anaesthetized rats. Marked and similar natriuresis, kaliuresis, and diuresis occurred in recipients undergoing cross-circulation with donors subjected to either bilateral nephrectomy or total intravenous urine reinfusion for 18 h previously, and were not seen with sham-operated donors. Similar and significant, but less marked, changes occurred in two groups with bilateral nephrectomy or urine reinfusion of only 3 h duration. Urea-loaded normal donors caused a natriuresis and kaliuresis which was similar to the two 18-h uremic donor groups. When donor animals were sodium depleted prior to bilateral nephrectomy the natriuretic response in the recipients was significantly reduced. The results indicate that the kidney is not necessary for the rapid appearance of natriuretic and kaliuretic activity in the blood of acutely uremic animals, and that such activity results from the retention of factors of extrarenal origin. Natriuresis and kaliuresis result from inhibition of tubular reabsorption and are not dependent on changes in glomerular filtration or renal hemodynamics. Pitressin or aldosterone levels. Urea appears to be a major component of the circulating natriuretic and kaliuretic activity in acute uremia but evidence of other factors was also obtained.

Acute Disease↗
PubMed2004

Effects of class I antiarrhythmic drugs on the digitalis-induced triggered activity arrhythmia model: a rationale for the short-term use of class I drugs against triggered arrhythmias.

Delayed afterdepolarization (DAD)-induced triggered activity has been considered to be one of the generation mechanisms of ventricular arrhythmias in the presence of intracellular Ca2+ overload. In this study, we analyzed the antiarrhythmic effects of class I antiarrhythmic drugs, namely, disopyramide, procainamide, mexiletine, and flecainide, on a recently developed DAD-induced triggered arrhythmia model, which consists of a canine ventricular septum preparation cross-circulated with a blood-donor dog. After intravenous administration of ouabain to the donor dog, triggered arrhythmias were consistently induced in the cross-circulated preparation by train stimulation (cycle length: 300 ms; train number: 15). Intracoronary administration of disopyramide, procainamide, mexiletine, and flecainide as well as lidocaine suppressed the triggered arrhythmias at clinically relevant doses. Similar doses have been demonstrated to suppress intraventricular conduction in the same experimental model. These results suggest that the Na+ channel inhibition by class I drugs is an effective pharmacological intervention for suppressing Ca2+ overload, which may provide a rationale for the short-term use of class I drugs against the triggered arrhythmias in clinical practice.

Animals↗
PubMed2000

Myocardial performance after brain death: studies in isolated hearts.

OBJECTIVES AND METHODS: Brain death related hemodynamic instability and/or cardiac dysfunction is frequently described in the potential organ donor which may lead to exclusion of the heart from transplantation. The underlying mechanisms are controversely discussed. Therefore, in the present study, potential brain death associated cardiodepressant factors were evaluated separately in cross-circulated canine heart models. Brain death was induced by inflation of a subdural balloon catheter. Loading conditions and coronary perfusion pressure were kept identical in all cross-circulated hearts throughout the experiment. RESULTS: Induction of brain death led to a significant hyperdynamic response in all groups, with a maximal effect by the combination of neural and humoral pathways. After the initial reaction all hemodynamic parameters returned to baseline and remained stable until the end of experiments. Even if the hearts were explanted from brain dead donors with typical hemodynamic deterioration in vivo, they showed no significant differences in comparison to the other groups including healthy controls ex vivo. CONCLUSIONS: Therefore we conclude, that hemodynamic instability in the potential donor may rather reflect altered loading conditions and impaired coronary perfusion than neuro-humorally mediated direct myocardial injury.

Animals↗
PubMed1988

No significant increase in O2 consumption of KCl-arrested dog heart with filling and dobutamine.

In the cross-circulated dog hearts arrested with KCl, we examined the effects of left ventricular volume and dobutamine on the resting oxygen consumption (MVO2). The perfusion pressure of the excised heart was stable under the cross-circulation for 1-1.5 h with a dialyzer to normalize coronary venous KCl despite continuous coronary arterial injection of KCl. The resting MVO2 declined gradually during the first 10 min of cardiac arrest but changed little thereafter. The resting MVO2 at 5 min and 30 min of arrest were 30.5 +/- 9.3 (SD) and 23.8 +/- 12.9%, respectively, of unloaded MVO2 before arrest. The resting MVO2 after its stabilization was 1.02 +/- 0.42 ml O2.min-1.100 g ventricle-1 in the control. It was 1.12 +/- 0.48 ml O2.min-1.100 g ventricle-1 under a continuous infusion of dobutamine at rate of 10-25 micrograms/min. This change with dobutamine was statistically insignificant. The resting MVO2 was not affected by changes in left ventricular volume both before and under dobutamine. The present result implies that MVO2 for basal metabolism in a working dog heart is virtually constant regardless of ventricular volume and contractility.

Animals↗
PubMed1998

Effects of explosive brain death on cytokine activation of peripheral organs in the rat.

BACKGROUND: The success rate of transplanted organs from brain-dead cadaver donors is consistently inferior to that of living sources. As cadaver and living unrelated donors are equally genetically disparate with a given recipient, the difference must lie within the donor himself and/or the effects of organ preservation and storage. We have hypothesized that irreversible central nervous system injury may up-regulate proinflammatory mediators and cell surface molecules in peripheral organs to be engrafted, making them more prone to host inflammatory and immunological responses. METHODS: Rats undergoing surgically induced acutely increased intracranial pressure (explosive brain death) were followed for 6 hr. Their peripheral tissues were examined by reverse transcriptase polymerase chain reaction and immunohistology, serum factors were assessed by enzyme-linked immunosorbent assay, and the influence of inflammatory molecules in the blood stream was determined by cross-circulation experiments with normal animals. RESULTS: mRNA expression of both lymphocyte- and macrophage-associated products increased dramatically in all tissues. Similar factors in serum were coincidentally increased; these were shown to be active in vivo by cross-circulation with normal animals. The organs of all control groups, including animals with important ischemic injury and with hemorrhagic shock, were negative. Up-regulation of MHC class I and II antigens and the co-stimulatory molecule B7 suggests increased immunogenicity of the peripheral organs. These changes could be inhibited by: (i) administration of a recombinant soluble P-selectin glycoprotein ligand-Ig, a P- and E-selectin antagonist; and (ii) a fusion protein, cytotoxic T lymphocyte antigen 4-Ig, which blocks B7-mediated T-cell co-stimulation. CONCLUSIONS: Activation of peripheral organs following explosive brain death may be caused by various interrelated events, including the effects of massive acute central injury, hypotension, and circulating factors. Almost complete suppression of these changes could be produced by biological agents. Such interventions, if reproducible in humans, could improve the quality of organs from "marginal" donors, broadening the criteria for donor acceptance.

Animals↗
PubMed1997

Mechanoenergetics of rat left ventricles in in situ and excised blood-perfused hearts and in unloaded rat left ventricular slices.

We investigated rat left ventricular (LV) mechanoenergetics in three different preparations. We obtained an upward convex curvilinear end-systolic pressure-volume relation (ESPVR) regardless of left ventricular (LV) contractility in in situ and excised cross-circulated rat hearts. We also obtained a linear myocardial O2 consumption per beat (VO2)-end-systolic pressure-volume area (PVA; a measure of ventricular total mechanical energy) relation regardless of the curvilinear LV ESPVR in the excised cross-circulated heart. The slope and the VO2 intercept of the VO2-PVA relation was similar to those in other species. The basal metabolism obtained by KCl arrest was higher than those in other species. In the whole heart preparation, the VO2 intercept may include O2 consumption for residual crossbridge cycling as well as O2 consumption for excitation-contraction (E-C) coupling and basal metabolism. Therefore, we established a new system for measuring myocardial O2 consumption of mechanically unloaded (zero PVA) rat LV slices. The increment in O2 consumption by stimulation of the slices represents O2 consumption for E-C coupling (but not for crossbridge cycling). Most O2 consumption for E-C coupling seems consist of O2 consumption for the sarcoplasmic reticulum Ca2+ pump.

Animals↗
PubMed1995

Suppression of myocardial mitochondrial respiratory function in acute failing hearts made by a short-term Ca2+ free, high Ca2+ coronary perfusion.

We made acute cardiac failure in excised cross-circulated canine hearts by a new coronary perfusion protocol consisting of Ca2+ free Tyrode perfusion for the first 10 min, high Ca2+ (16 mmol/l) Tyrode perfusion for the next 5 min, and normal Tyrode perfusion for the last 5 min interrupting blood cross circulation. After 50 min from the blood recirculation, left ventricular contractility was stably depressed to 60% of control. We studied mechanoenergetics of these acute failing hearts for the next 1-3 h. Then, we prepared mitochondria from these excised failing hearts and the support dogs' normal hearts to examine their mitochondrial respiratory function by the respiratory control index (RCI) and the oxygen consumption rate in state III (State III O2). RCI and State III O2 were significantly smaller in the failing hearts than in the normal hearts. However, sham protocol consisting of normal Tyrode coronary perfusion for 20 min did not affect RCI and State III O2. These results revealed that the mitochondrial respiratory function was moderately impaired in these acute failing hearts made by the new short-term Ca2+ intervention. However, no ultrastructural injuries of mitochondria were detected in these failing hearts.

Animals↗
PubMed1998

Scintigraphic evaluation of craniopagus twins.

Craniopagus twinning is a rare congenital abnormality, occurring at a frequency of 4-6 per 10 million births. A case is reported in which separation was successful for both twins. The importance of pre-operative radionuclide assessment of crucial organ function (liver, kidneys, heart, brain) and crossed circulation is stressed. The scintigraphic results were in keeping with radiographic, operative, and clinical findings. The routine use of radionuclide studies in the investigation of conjoined twins is recommended in order to delineate individual organ function, degree of fusion and measurement of cross-circulation.

Brain↗
PubMed1988

The humoral renal antihypertensive system: nervous and hemodynamic effects in normotensive and unclipped renal hypertensive rats.

A series of studies of the humoral renal antihypertensive system in normotensive and 2K 1C-renal antihypertensive rats is outlined. The rapid structural upward resetting of the cardiovascular system in renal hypertensive rats was associated with a structural downward resetting in the vasculature of the hypotensive clipped kidney. Unclipping of this kidney caused a pronounced release of renomedullary depressor agents, explaining the rapid normalization of pressure seen after unclipping. This normalization of pressure masks a state of pronounced functional hypotension in a structurally still hypertensive cardiovascular system, characterized by marked splanchnic vasodilatation and a lack of neurogenic counter-regulation. Only when this state has lasted long enough to normalize the structural upward resettings, characteristic of hypertension does the cardiovascular system return to normal. Further, cross-circulation techniques have shown that the humoral antihypertensive agents suppress tonic sympathetic activity, thereby inhibiting normal reflex counter-regulation of their vasodilator effects. Presumably this occurs via both vagal cardiac afferents and central actions. Further, behavior and awareness become depressed during intense and prolonged renomedullary release. Finally, experiments for which a normotensive kidney is cross-circulated from a normotensive rat suggest that the humoral renomedullary antihypertensive system has its threshold of release set so low as to contribute to normal blood pressure regulation, presumably in reciprocal balance with the renocortical renin-angiotensin system. Stepwise pressure elevations increasingly enhance release of the depressor agents from the cross-perfused kidney.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗