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PubMed1987

The effect of antihypertensive treatment on the circulating hypertensive factor in the spontaneously hypertensive rat.

To elucidate the role of circulating hypertensive factors in the spontaneously hypertensive rat and the effects of antihypertensive treatment on the circulating hypertensive factor, cross circulation was performed in 54 couples of spontaneously hypertensive and normotensive rats. 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). Increases in mean arterial pressure were also obtained by cross-circulation with spontaneously hypertensive rats pretreated with propranolol, furosemide, and nifedipine. Mean arterial pressure was not changed by cross circulation after pretreatment of the spontaneously hypertensive rats with alpha methyldopa. It is concluded that in this strain of spontaneously hypertensive rats a circulating hypertensive factor exists, the secretion of which can be suppressed by the centrally acting drug, alpha methyldopa. Therefore either the central nervous system may take part in the regulation of the factor or the factor may be synthetized in the central nervous system.

Animals↗
PubMed1977

Influence of intestinal inhibitory reflex on mesenteric blood flow through an intestinal segment of the dog.

The variations in both tonus and rhythmical motility of the intestinal musculature are known to affect profoundly intestinal blood flow. In the present study, the influence of marked reflex inhibition of intestinal tone on the blood flow through an intestinal segment was investigated in the dog. Experiments were performed under conditions of both normal circulation and cross-circulation. Inhibitory reflex was elicited by elevating the intraluminal pressure of a loop or by electrical stimulation of the intestinal wall. Fluctuations of blood flow during the intestinal inhibitory reflex were observed with normal circulation. Arterial and venous blood flows decreased in the initial period of intestinal relaxation, and recovered within 30 sec although reflex inhibition still remained. This is an autoregulatory escape phenomenon. In successive periods, arterial and venous blood flows decreased again due to "the venous-arteriolar response" and then recovered to the quiescent level. The decrease in venous blood flow corresponded to an increase of the degree of oxygen saturation in the venous blood. The decreases in arterial and venous blood flows were observed during the inhibitory reflex even when the intestinal circulation was maintained by the cross-circulation. Two different patterns, i.e., the parallel and reversed patterns, were distinguished in correlation with venous blood flow and oxygen saturation. The autoregulatory escape phenomenon could not be elicited in the experiments in the cross-circulation system because variation of the systemic blood pressure during inhibitory reflex was limited to +/-4%.

Animals↗
PubMed1994

Postextrasystolic transient contractile alternans in canine hearts.

We found that postextrasystolic potentiated contractility after a spontaneous extrasystole most frequently decayed as a transient alternans over several beats in excised, cross-circulated, atrially paced canine hearts. This type of heart preparation; which we have been using consistently in mechanoenergetic studies, had normal coronary blood perfusion pressure as well as flow and mechanoenergetic performance. Spontaneous atrial and ventricular extrasystoles occurred occasionally in every heart. Arrhythmic changes in left ventricular (LV) pressure at a fixed volume reflected corresponding changes in contractility. We analyzed nearly 3,600 cases of postextrasystolic potentiation in 68 hearts; 84% decayed as transient alternans, 6% decayed exponentially, and 10% belonged to neither type. We found that a postextrasystolic compensatory pause always preceded the transient alternans after either an atrial or ventricular extrasystole at any constant atrial pacing rate (85-188 beats/min). The decay was either exponential or nonalternating when the pause did not exist after an atrial extrasystole during occasional pacing failure. Therefore, the compensatory pause after either an atrial or ventricular extrasystole seems essential for the postextrasystolic transient alternans of LV contractility in the type of canine heart preparation we have been using.

Animals↗
PubMed1983

Cigarette smoking behavior in conjoined twins.

A study of cigarette smoking was undertaken in a pair of craniopagus twins to determine how a transfer of products of smoking is occurring between the twins. Alternately and independently, one twin smoked a nicotine-free cigarette, then the second twin smoked a nicotine-containing cigarette. The procedure enabled the investigators to study the migration of nicotine and carbon monoxide from one twin to the other. Salivary determination provided a noninvasive method of measuring cross circulation in conjoined twins. Measurements of salivary nicotine, however, indicated that, although the nicotine levels rose following smoking, there was relatively little transfer from one twin to the other through the circulation.

Adult↗
PubMed1994

Utilization of an isolated, blood-perfused canine papillary muscle preparation as a model to assess efficacy and adversity of class I antiarrhythmic drugs.

To develop a model to predict the efficacy and adversity of class I antiarrhythmic drugs, intraventricular conduction time (IVCT), coronary blood flow (CBF), developed tension of papillary muscle (DT) and idioventricular automaticity rate (VR) were measured following drug administration in an isolated canine papillary muscle preparation cross-circulated with the heparinized blood of a donor dog. Tetrodotoxin, the prototypic fast Na+ channel blocker, and class I drugs increased IVCT and CBF, but decreased DT and VR, in a dose-dependent manner. The profiles of known class I drugs, procainamide, disopyramide, lidocaine, mexiletine and flecainide were similar, but the potencies of each drug were different. Two new class I drugs, ME3202 and AN-132, were also tested and found to have effects that were similar to that of tetrodotoxin. There was a good correlation between the doses of drugs prolonging IVCT by 50% and the canine antiarrhythmic plasma concentrations in our previous study. This model can also be used to estimate the use-dependency and the kinetics of use-dependent sodium channel block; however, it is not suitable for extensive investigation of cellular and molecular mechanisms. Thus, the use of this model facilitates the comparison of multiple cardiac effects of class I drugs and may be an effective way to better assess new antiarrhythmic drugs.

Animals↗
PubMed1979

[Mechanisms of blood deposition in dogs with a cytotoxic heart lesion].

The reactions of capacitance blood vessels of the abdominal cavity and pelvis were studied in vagotomized dogs during cytotoxic heart injury. The same reactions were investigated in recipient dogs during cross circulation with cardiac damage in the donors. A certain role of the neuroreflex and humoral cardiogenic factors involved in the development of increased capacity of blood vessels is shown.

Animals↗
PubMed1994

The effects of dynamic cardiac compression on ventricular mechanics and energetics. Role of ventricular size and contractility.

The purpose of this study was to determine the role of ventricular size or contractility in the effectiveness of dynamic cardiac compression in terms of the pressure-volume relationship and myocardial oxygen consumption. In 10 isolated cross-circulated dog hearts, the ventricle was directly compressed during systole. For the volume run, measurements for slope of the end-systolic pressure-volume relation, pressure-volume area, external work, coronary blood flow, and myocardial oxygen consumption were achieved before and during a fixed amount of dynamic cardiac compression. Left ventricular volume was then increased while stroke volume was kept constant, and measurements were repeated. For the contractility run, after the control measurements were taken, left ventricular contractility was significantly increased or decreased by infusion of either dobutamine or propranolol into the coronary circulation. Measurements were repeated before and during dynamic cardiac compression at the control level of end-diastolic and stroke volumes. Dynamic cardiac compression significantly increased slope of the end-systolic pressure-volume relation, pressure-volume area, and external work (p < 0.01), whereas coronary blood flow and myocardial oxygen consumption were not affected. The increase in pressure-volume area caused by dynamic cardiac compression was greater with the larger volume. Despite the significant differences in the native left ventricular contractility, the increases in slope of the end-systolic pressure-volume relation, pressure-volume area, and external work did not differ among the three groups. We conclude that dynamic cardiac compression enhances left ventricular systolic function independent of ventricular contractility and without affecting coronary blood flow or myocardial oxygen consumption. Mechanical enhancement is more effective in the dilated heart.

Animals↗
PubMed1985

Humoral factors in the pathogenesis of primary hypertension.

In 42 spontaneously hypertensive rats of the Münster strain either parabiosis or cross circulation with normotensive Wistar Kyoto rats was performed. Cross circulation was made through the common carotid arteries and external jugular veins using a peristaltic pump. In parabiosis and in cross circulation experiments hypertension was transmitted from the spontaneously hypertensive rats to normotensive rats. Nephrectomy or adrenalectomy in the spontaneously hypertensive rat before cross circulation abolished this effect. After volume depletion in the hypertensive animals hypertension was not transmitted either. It is concluded that humoral factors causing vasoconstriction play an essential role in the development of hypertension in the spontaneously hypertensive rat.

Adrenal Glands↗
PubMed1970

Current concepts in viral hepatitis.

A great deal of interest and speculation has arisen from the discovery of a specific antigen, Australia antigen, in the serum of a high proportion of patients with viral hepatitis. This antigen has been found also in the serum of some patients with other conditions, including Down's syndrome, leukemia, leprosy, chronic renal disorders, and chronic active liver disease. It is not found in the serum of normal persons. Australia antigen has been postulated as the causative agent of viral hepatitis. In most patients the antigen can be detected for less than two weeks during the acute phase of the disease. Its persistence in other conditions may be due to an impairment of the immune response. The course of acute viral hepatitis is usually uncomplicated, full recovery of liver function taking place within four to six weeks, with restoration of normal liver histology within three to four months. Follow-up studies of patients in whom hepatitis has developed during epidemics have failed to reveal evidence of subsequent chronic progressive liver disease. This suggests that most cases of chronic active hepatitis are not the result of preceding acute viral hepatitis. However, the recent finding of Australia antigen in the serum of a small number of patients raises the possibility that sporadic viral hepatitis may be one of the causes of the chronic active hepatitis. Alternatively, the presence of the antigen may be interpreted as being due to an altered immune response. The treatment of acute hepatic coma remains unsatisfactory. Several new forms of therapy have been tried in recent years in an uncontrolled way. These include multiple exchange blood transfusions, isolated pig liver perfusion, human cross-circulation, and cross-circulation with baboons. Transient improvement may follow any of these procedures, but evidence that they influence the final outcome of the disease is lacking. The rapid fluctuations in the neurological status of individual patients makes it difficult to interpret the effects of therapy. Also, until satisfactory objective criteria of degrees of coma are universally accepted it will be impossible to compare one mode of therapy with another.

Adolescent↗
PubMed1985

Humoral factors in primary hypertension.

In 56 spontaneously hypertensive rats of the Muenster strain, either parabiosis or cross circulation was performed with normotensive Wistar Kyoto rats. Crossed circulation was made through the common carotid arteries and external jugular veins using a peristaltic pump. In parabiosis and in cross-circulation experiments, hypertension was transmitted from spontaneously hypertensive to normotensive rats. Nephrectomy or adrenalectomy in the spontaneously hypertensive rat before cross circulation abolished this effect. After volume depletion in the hypertensive animals, hypertension was not transmitted either. Furthermore, the effect of plasma fractions from essential hypertensives (n = 20) on blood pressure of normotensive rats was studied. Substances with molecular weights higher than 6000-8000 and lower than 500 were removed from 60-ml plasma by ultrafiltration and dialysis. After chromatography on a Bio-Gel P-4 or P-2 column, three to four fractions were formed according to the results of UV spectrophotometry and concentrated to 0.5 ml. One fraction from hypertensive plasma containing substances with molecular weights between 1000 and 2000 increased blood pressure in the rat by 16.3 +/- 8.2 mmHg within 10 minutes when injected intravenously. The respective fractions from normotensive rat plasma increased blood pressure by 3.6 +/- 2.1 mmHg (p less than 0.01). The results demonstrate a circulating hypertensive factor both in spontaneously hypertensive rats and in essential hypertensives, which may be crucial for the pathogenesis of essential hypertension.

Animals↗
PubMed1994

[The central mechanism of pressor response induced by infusing 7.5% sodium chloride solution in hemorrhagic hypotension dog].

Nine pairs of dogs were operated with head cross circulation and four pairs of dogs with brain cross circulation. Bleeding of formoral artery decreased the mean arterial pressure to 5.33 kPa and maintained for 30 min. In each pair of A dog 10% of total blood lose was infused intravenously by 7.5% NaCl solution (as test) or normal saline (as control), but B dog was not treated. The results showed that in the test group the arterial blood pressure recovered immediately in both A and B dogs and lasted for more than 60 min after infusion. The recovery value of systolic pressure was higher than diastolic pressure and pulse pressure increased. In the control group the blood pressure recovered slightly but of no statistical significance. There was no remarkable difference in heart rate between the two groups. A marked decrease in hematocrit appeared after bleeding and infusion, but there was no significant difference between the two groups (P > 0.05). Plasma sodium increased significantly after infusion in A dogs of the test group (P < 0.01), but the change in B dogs was the same in the control group. These results mentioned above indicate that the central nervous system plays important role on the mechanism of pressor response induced by infusing 7.5% NaCl solution in the hemorrhagic hypotension dog.

Animals↗
PubMed2001

Influence of extracorporeal porcine liver perfusion on nonhuman primates: minimizing hemolysis improves subsequent survival.

The aim of this study is to detect and analyze risk factors of direct cross-circulation between porcine liver and nonhuman primates before a clinical application of extracorporeal liver perfusion (ECLP) as a liver-assist method. Porcine livers were perfused with baboon blood in an ECLP system. Six healthy baboons were directly connected to the ECLP system with continuous prostaglandin E(1) administration. Cross-circulation was terminated in the following circumstances: (1) hepatic arterial or portal perfusion pressures elevated to 200 or 60 mm Hg, respectively; (2) massive exudative bleeding from the graft surface; or (3) bile output decreased to less than 5 microL/h/g of liver weight. In case 1, cross-circulation was continued for 10 hours. Severe macroscopic hemolysis occurred, and serum hemoglobin (s-Hb) concentration reached a peak of 47 mg/dL. The baboon died of acute renal failure 2 days later. Histological study of the perfused porcine liver showed marked microthrombi formation. In 3 of the later 5 cases, cross-circulation was discontinued when mild macroscopic hemolysis was observed. The duration of the 5 cross-circulations was maximally 6 hours (mean, 4.4 +/- 1.2 [SD] hours). Mean s-Hb concentration in the 5 cases was elevated to 14.8 +/- 5.8 mg/dL at the end of cross-circulation and decreased to the baseline level within 24 hours. These 5 baboons survived without organ dysfunction or immunologic disturbance. When severe hemolysis is avoided, direct cross-circulation using the ECLP system can be achieved without serious complications in nonhuman primates.

Animals↗
PubMed1975

Time course of onset and decay of humoral natriuretic activity in the rat.

The natriuretic mechanism.tic activity shown in earlier cross-circulation experiments to develop in the blood of rats undergoing sustained vascular expansion has been further characterized. Following whole blood infusion and urine reinfusion of the donor rat, a cross-circulated isovolaemic partner exhibits a natriuresis of gradual onset, requiring 60-80 min to reach a peak (0.04-3.24 muequiv./min per gram kidney weight). The gradual feature of recipient natriuresis was unchanged by infusing the donor rat 1 h prior to cross-circulation. Once developed, the recipient natriuresis was sustained when fluid depletion by the renal response was prevented, but was reversible with a half-life of about 30 min on interruption of the cross-circulation; reconnection of cross-circulation promptly restored recipient natriuresis. No significant natriuresis (0.04-0.16 muequiv/min per gram kidney weight) occurred in the recipients if the donors in comparable cross-circulations were not infused. These findings confirm that a natriuretic activity develops in the blood as a consequence of vascular expansion, and reveal that the activity has a slowly developing and reversible action on the renal natriure

Animals↗
PubMed1985

Contribution of circulating formed elements to prostanoid production in complement-mediated lung injury in sheep.

Incubation of plasma with zymosan results in complement activation. Infusion of this "zymosan-activated plasma" (ZAP) into the superior vena cava in sheep results in pulmonary leukostasis, pulmonary hypertension with generation of thromboxane (TXB), and hypoxemia. To examine the contribution of circulating formed elements to TXB generated when ZAP is infused, we studied four pairs of sheep in a cross-circulation model. Acetylsalicylic acid (ASA) irreversibly acetylates cyclooxygenase and blocks TXB production. Four hours after an intravenous dose of ASA (10 mg/kg), no circulating ASA was detectable by high-pressure liquid chromatography. Infusion of ZAP in ASA-treated animals resulted in no pulmonary hypertension and no rise in serum TXB levels. Treated animals were then cross-circulated with untreated sheep through cannulas that attached a carotid artery of each animal to a jugular vein of the other, creating simultaneous arteriovenous fistulas between the animals. A roller pump maintained cross-circulation flow at 450 ml/min for 15 minutes. This resulted in greater than 80% mixing of the circulating blood volumes of each pair of animals, verified by measurement of an intravascular marker. After cross-circulation the ASA-treated animals were still unable to generate TXB in response to ZAP infusion. Untreated animals had a typical response when infused with ZAP after cross-circulation, with elaboration of large amounts of TXB. Since the treated animals with circulating, nonaspirinated formed elements showed no response and the untreated animals with similar blood composition had a normal response, we conclude that circulating formed elements do not contribute significantly to the TXB recovered from sheep infused with activated complement components.

Animals↗
PubMedDate not supplied

Humoral factor in pressor hyperresponsiveness in renal prehypertensive rabbits.

Prehypertensive rabbits with renal artery stenosis of 3 days' duration (one-kidney, one clip) are known to have increased pressor responses to norepinephrine and vasopressin; this pressor hyperresponsiveness is restored to normal by the angiotensin II (AII) antagonist, [ Sar1, Ile8 ] AII, even though plasma renin activity (PRA) and plasma AII concentrations are not elevated. In the present study, the cross-circulation of blood between conscious one-kidney, 3-day renal artery stenosis rabbits and conscious normal rabbits resulted in the transfer of pressor hyperresponsiveness to the normal rabbits, although both groups of rabbits had normal values for PRA. A similar cross-circulation of blood between one-kidney rabbits without renal artery stenosis and normal rabbits did not alter the pressor responsiveness of the normal rabbits to norepinephrine. It was concluded that a circulating humoral factor is involved in mediating pressor hyperresponsiveness in 3-day renal artery stenosis rabbits. To evaluate the interrelationship between AII and the hormonal hyperresponsiveness factor, an additional experiment was performed in which blood was cross-circulated between one-kidney, 3-day renal artery stenosis rabbits and normal rabbits, with the normal rabbits receiving [ Sar1, Ile8 ] AII immediately following cross-circulation. Administration of this AII antagonist to the normal rabbits prevented them from showing pressor hyperresponsiveness following the cross-circulation of blood. It is concluded that in this prehypertensive renal artery stenosis model the humoral hyperresponsiveness factor exerts its effect through AII mechanisms, rather than AII acting to increase the release or secretion of the hyperresponsiveness factor.

1-Sarcosine-8-Isoleucine Angiotensin II↗
PubMed1989

Stimulation of protooncogene expression by partial hepatectomy is not tissue-specific.

We have characterized the early protooncogene response and the later cell proliferative response in the kidneys and livers of normal rats cross-circulated with partially hepatectomized animals. Increase c-myc and C-Ha-ras expression was observed in the kidneys of totally hepatectomized rats, as well as those of their cross-circulated partners. This indicates that the initial response to hepatectomy is not organ-specific, although the later DNA synthetic response of the kidney is only approximately one-tenth that of regenerating liver. Expression of c-myc and c-Ha-ras is dramatically increased in the livers of both hepatectomized and nonhepatectomized, parabiotic (cross-circulated) rats within 1 hr of partial hepatectomy, confirming the presence of a circulating factor which stimulates protooncogene expression early in regeneration. DNA synthesis was also stimulated in the livers of the cross-circulated animals between 20 and 26 hr following hepatectomy, but only to a level one-eighth that of the livers of hepatectomized animals. Normal rats cross-circulated with totally hepatectomized animals also demonstrated an early increase in hepatic c-myc and c-Ha-ras expression, indicating that regeneration must be stimulated by an extrahepatic signal. Our data suggest that the early increase in protooncogene expression is a non-organ-specific response to partial hepatectomy which does not insure subsequent cellular proliferation. The organ specificity of liver regeneration must involve an event separate from the early stimulation of protooncogene expression.

Animals↗
PubMed1985

Pressor responsiveness to norepinephrine in rabbits with adrenal perturbations.

The purpose of this study was to examine pressor responsiveness in a rabbit model with adrenal perturbation. Adrenals in rabbits were stabbed with a needle, and the rabbits were given water (adrenal-water group) or 0.9% NaCl (adrenal-salt) to drink; additional rabbits were sham-operated and given water (sham-water group) or 0.9% NaCl (sham-salt group) to drink. Acute experiments were performed two weeks later on conscious rabbits. All four groups of rabbits had the same body weights, mean arterial pressures, heart rates, and plasma concentrations of Na+ and K+. Intravenous norepinephrine infusions at several doses produced greater pressor responses in the adrenal-water and adrenal-salt groups than in the sham-water or sham-salt groups. Administration 1-sarcosine-8-isoleucine angiotensin II ([Sar1, Ile8]Ang II) did not alter the pressor responses to norepinephrine in either the sham-water or the adrenal-salt groups. Cross-circulation of blood between adrenal-salt donor rabbits and normal recipient rabbits at 10 ml/min for 5 min resulted in enhanced pressor responses to norepinephrine in the recipients at 5 min after the cross-circulation. Similar cross-circulation experiments between sham-water donors and normal recipients did not alter the pressor responses to norepinephrine in the recipients. These studies demonstrated that rabbits with adrenal perturbations have pressor hyper-responsiveness to norepinephrine, which does not involve angiotensin II mechanisms, but is mediated by a fast-acting blood-borne factor.

Adrenal Glands↗
PubMed1979

The nonportal origin of the factors initiating hepatic regeneration.

To determine the site of origin of the factors that initiate deoxyribonucleic acid (DNA) synthesis in the liver after partial hepatectomy, normal rats were cross-circulated with totally hepatectomized rats. Half of the hepatectomized rats had also undergone excision of all of the portal organs. After 48 hours of cross-circulation, active DNA synthesis and other evidences of hepatic regeneration were found in normal rats cross-circulated with the hepatectomized portally eviscerated rats. This demonstrates that a blood-borne factor that does not arise from the portal organs is capable of initiating hepatic regeneration. When a normal rat was cross-circulated with a hepatectomized rat with the portal organs still present, hepatic regeneration occurred but was significantly less than when the portal organs had been removed. It is postulated that under these experimental conditions portal factors from the normal rat have a permissive role that allows active regeneration when initiating factors are furnished from the hepatectomized rat. Additional portal organs in the hepatectomized rat decreased DNA synthesis, possibly by alterations of the insulin/glucagon ratio.

Animals↗