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PubMed1993

[Detection of circulating antigen in urine from mice infected with Toxoplasma tachyzoites].

Urine samples collected from three groups of mice infected experimentally with different numbers doses of Toxoplasma trophozoites were detected for the presence of Toxoplasma circulating antigen by using fast ELISA. The results showed that presence of circulating antigen in all three infected groups of mice in comparison with the normal control group. Toxoplasma circulating antigen was detected on days 5, 4 and 3 after infection in light-, moderate- and heavy-infection groups, respectively. The concentration of circulating antigen was on a parallel with the duration of infection. Western blot analysis of the Toxoplasma circulating antigen in urine revealed the existence of seven specific bands with molecular weights of 75, 67, 55, 43, 30, 28 and 22 kDa.

Animals↗
PubMed1993

The fate of circulating megakaryocytes during cardiopulmonary bypass.

Megakaryocytes with intact cytoplasm normally leave the bone marrow, enter central venous blood, and are filtered in the lungs. During cardiopulmonary bypass, large megakaryocytes are not filtered by the lungs and may not be removed in the extracorporeal circuit by arterial line filters. In such circumstances, they could enter the systemic circulation and block smaller cerebral vessels, resulting in neurologic impairment. To investigate the fate of circulating megakaryocytes during cardiopulmonary bypass, central venous blood and oxygenated blood samples before and after arterial line filtration (40 microns polyester screen filter) were obtained from 10 patients undergoing cardiopulmonary bypass. Megakaryocytes were isolated by whole blood filtration and identified by their characteristic structure after May-Grunwald-Giemsa staining. In preliminary studies, megakaryocyte identification was verified by immunolabeling. All samples contained megakaryocytes with copious cytoplasm. Their frequencies in central venous blood and oxygenated blood before and after the arterial line filtration (corrected for hemodilution) were 23.4 +/- 9.3 per milliliter (mean +/- standard error of the mean, range 3.1 to 89.7 per milliliter), 21.0 +/- 8.2 per milliliter (2.0 to 84.2 per milliliter) and 17.1 +/- 7.4 per milliliter (3.1 to 80.4 per milliliter), respectively. Megakaryocytes with scant or no visible cytoplasm were also observed. The results confirm that circulating megakaryocytes are a normal physiologic component. During cardiopulmonary bypass, megakaryocytes with copious cytoplasm (mean diameter 42.7 microns, range 22 to 78 microns) can pass through the extracorporeal circuit. In the absence of filtration by the lungs, these large cells have access to the systemic circulation. This study supports a possible role for circulating megakaryocytes in the development of cerebral dysfunction after cardiopulmonary bypass.

Adult↗
PubMed1996

Rapid clearance of human insulin-like growth factor binding protein-3 from the rat circulation and cellular localization in liver, kidney and stomach.

The gastrointestinal tract represents a major site for the trophic actions of insulin-like growth factors (IGFs), which may be derived in vivo from a large circulating pool. The high capacity binding protein for IGFs in blood is IGF binding protein-3 (IGFBP-3), which is largely complexed with an acid-labile subunit (ALS). However, we and others have shown that IGFBP-3 not complexed with ALS can rapidly leave the circulation, and may carry IGFs to peripheral tissues. In this study we investigated the transfer of recombinant, glycosylated human (h)IGFBP-3 from the rat circulation to the stomach and intestine, compared with liver and kidney. [125I]-labeled IGFBP-3 was administered into the tail vein of conscious male rats, which were killed between 5 min and 2 h later. Blood was taken for the preparation of plasma, and the liver, kidneys, stomach and intestine were removed either for estimation of the associated radioactivity, or fixed for autoradiographic analysis of histological sections. Following injection, [125I]-labeled IGFBP-3 was associated, in part, with a 150 kDa complex in plasma within 10 min when analyzed by gel filtration chromatography. However, 84% of the administered IGFBP-3 had already left the circulation, and 40% of the initial injected dose was accumulated in liver by 5 min, with a further 4% localized in the kidneys. Autoradiographic analysis showed that IGFBP-3 was selectively accumulated within Kupffer cells of the liver, and by the glomeruli and proximal tubules of the kidney. Little radiolabeled IGFBP-3 was recovered from the small intestine, but 14% of the initial injected dose was found within the stomach after 2 h, and a further 12% within the stomach contents. Autoradiographic localization within the stomach showed that the [125I]-labeled IGFBP-3 was primarily associated with the mucosal lining and gastric glands. Separation on sodium dodecyl sulphate polyacrylamide gel electrophoresis showed that the majority of the radioactivity associated with the stomach contents represented small, degraded peptides. These results suggest that while a rapid clearance of IGFBP-3 is achieved by the liver and kidney, a longer term accumulation occurs in the stomach with a luminal secretion. This may represent a delivery system by which circulating IGFs may reach gastric tissue.

Animals↗
PubMed1995

Temporal relationships between levels of circulating NO derivatives, vascular NO production and hyporeactivity to noradrenaline induced by endotoxin in rats.

OBJECTIVE: Lipopolysaccharide (LPS) induces early (within 1 h) and delayed (after several hours) impairment of vascular reactivity to catecholamines whose mechanisms are different, although they probably both involve nitric oxide (NO). Temporal and quantitative relationships between hyporeactivity to noradrenaline and NO production were investigated in a rat model of endotoxaemia allowing to clearly distinguish the two phases of hyporeactivity. METHODS: Anaesthetised rats were infused with LPS (14 mg kg-1 h-1) for 1 h. Pressure responses to noradrenaline (NA) and circulating NO derivatives (nitrosyl haemoglobin, NO2-, NO3-) were monitored for 5 h after the onset of infusion. Reactivity to NA and tissue cyclic GMP level were also assessed ex vivo, in aortic rings taken at different experimental times. RESULTS: LPS-induced early hyporeactivity to NA was associated with a moderate but significant increase in plasma NO3- level, without any significant change in concentration of the other circulating NO derivatives. Neither reactivity ex vivo nor cyclic GMP content were modified in aortae taken after 1 h of LPS infusion. By contrast, delayed hyporeactivity (5 h after the onset of LPS infusion) was associated with a large increase in all circulating NO derivatives (up to 2.5 fold), enhanced aortic cyclic GMP level and aortic hyporeactivity ex vivo. Pre-treatment of rats with NG-nitro-L-arginine methyl ester (1 mg kg-1 i.v.) entirely prevented early hyporeactivity and rise in NO3- concentration. In addition it attenuated in comparable proportion both delayed hyporeactivity to NA in vivo and circulating levels of NO derivatives. CONCLUSION: The results confirm the involvement of NO in the two phases of hyporeactivity to NA induced by LPS. They strongly support the view that a circulating factor is involved in triggering endothelial NO release during the early phase, whereas the delayed phase is associated with a high production of NO in vascular smooth muscle resulting from the induction of NO synthase.

Animals↗
PubMed1995

Taxol reduces circulating tumor cells to prevent bone metastases in SCID mice.

The correlative effects of taxol on the reduction of circulating PC-3 ML human prostatic tumor cells and bone metastasis have been examined in SCID mice. Normally, following injection of 2 x 10(5) cells i.v., the circulating levels in peripheral blood drop by about 50 and 100%, after 8 and 24 h, respectively. In contrast, in taxol-treated mice (40-60 mg/m2/injection given 0, 3, 7 and 23 h following injection of the cells) the numbers of circulating human prostatic PC-3 ML tumor cells were reduced by 100% at 8 h. In similar experiments were mice were injected with taxol 2 h prior to injecting the cells, dosages of 40 and 60 mg/m2/injection reduced circulating tumor cells about 91 and 100%, respectively, by 8 h. Alternatively, if PC-3 Ml cells were pretreated with taxol (0.5 and 1.0 microM for 8 and 24 h) prior to injection, tumor cell clearance by 7 h was also significantly increased (80-100%). Correlative studies showed that the incidence of bone metastases (observed after 40 days) was reduced significantly (a) in mice treated with 40 and 60 mg/m2/injection (i.e. from 73-80% in controls to 15-0% in treated mice) and (b) in mice injected with PC-3 ML cells pre-exposed to 0.5-1.0 microM taxol for 7 h. Immunofluorescence studies with tubulin antibodies showed that the microtubules were disrupted in cells exposed to taxol in vivo and in vitro under conditions that significantly increased cellular clearance from the blood. Taken together, the data suggests that taxol at nontoxic dosages (to mice) can prevent metastases by directly reducing the circulating levels of tumor cells.

Animals↗
PubMed1996

Circulating burst-forming unit-erythroid (BFU-E) colonies as an early marker to measure the recombinant human erythropoietin response in peritoneal dialysis patients.

To evaluate circulating burst-forming unit-erythroid (BFU-E) cells after erythropoietin (EPO) treatment, 7 female continuous ambulatory peritoneal dialysis patients were studied [baseline hemoglobin (HB): 7-10.5 g/dL)]. EPO (4000 U subcutaneously) was administered twice weekly for two months. The control group consisted of 7 healthy women with similar demographic characteristics. Mononuclear cells (MC) (5 x 10(5)) were added to 1 mL of culture medium, supplemented with 30% fetal bovine serum, 2 U/mL of EPO, 1% bovine serum albumin, and 0.3% agar. To enumerate colonies derived from each circulating BFU-E, plates were examined by inverse light microscopy, identifying BFU-E as large aggregates with more than 100 hemoglobinized cells (HC). A remarkable individual response was observed, with Hb values ranging 8.4-13.6 g/dL at week 4 and 8.8-16.5 g/dL at week 8. Baseline levels of BFU-E in patients ranged 0-100/5 x 10(5) MC (0-358 mL of whole blood), and in controls they ranged 6-24/5 x 10(5) MC (29.6-101.3/mL) (NS). Hemoglobin levels after four and eight weeks of EPO showed a significant relationship with circulating BFU-E at baseline (r = -0.873, r = -0.928, respectively). The increment in Hb after eight weeks showed a significant relationship with baseline BFU-E (r = 0.812). Hemoglobin levels at the fourth to eighth week, and the increment in Hb after eight weeks, showed a significant, direct relationship with the increments in circulating BFU-E registered after one to two weeks of treatment. We conclude that, after the first week of EPO treatment, its effect on hemoglobin may be predieted by the increment in circulating BFU-E. Thus; a new tool to measure the earliest EPO effects has become available.

Adult↗
PubMedDate not supplied

Autoantibodies, immunoglobulins, complement and circulating immune complexes in acute malaria.

BACKGROUND: Malaria caused by Plasmodium vivax and Plasmodium falciparum is common in the Indian subcontinent. Studies conducted elsewhere have suggested that malarial infection causes intense immunostimulation. We screened patients with malarial infection for autoantibodies and measured the immunoglobulin, circulating immune complex and complement levels to determine the extent of immunological alterations in these patients. METHODS: One hundred adults with acute malarial infection confirmed by examination of the peripheral blood smear and 25 age- and sex-matched controls were studied. An autoantibody screen and serum immunoglobulin complement (C3 and C4) and circulating immune complex levels were measured at the time of admission and 4 weeks after they became afebrile. A direct Coomb's test was also done. RESULTS: Anti-ssDNA, anti-dsDNA and rheumatoid factor were positive at the time of admission in 51, 30 and 38 patients respectively. None of the controls were positive for these autoantibodies except for one who was positive for rheumatoid factor. The IgM, IgG and IgA levels were raised in 16, 25 and 36 patients respectively. Circulating immune complex levels were raised in 32 patients and complement C3 and C4 were low in 8 and 31 patients. Follow up studies at 4 weeks in 19 patients showed that the autoantibodies were negative. However, the immunoglobulin, C4 and circulating immune complex levels remained elevated. Six per cent of patients had a positive direct Coomb's test with reticulocytosis at the time of presentation. CONCLUSION: Acute malarial infection can cause false-positive results for anti-ssDNA, anti-dsDNA and rheumatoid factor and may also cause a rise in the serum immunoglobulin, complement and circulating immune complex levels.

Adolescent↗
PubMed1997

Differential pathogenesis of lethal mousepox in congenic DBA/2 mice implicates natural killer cell receptor NKR-P1 in necrotizing hepatitis and the fifth component of complement in recruitment of circulating leukocytes to spleen.

Innate resistance of C57BL/6 (B6) mice to lethal mousepox is controlled by multiple genes. Previously, four resistance genes were localized to specific subchromosomal regions and transferred onto a susceptible DBA/2 (D2) background by serial backcrossing and intercrossing to produce congenic strains. Intraperitoneally inoculated ectromelia virus was uniformly lethal and achieved similar titers in B6 and D2 mice but elicited differential responses in liver, spleen, and circulating blood leukocytes. The distribution of these response phenotypes in congenic strains linked control of phenotypes with specific subchromosomal regions. D2.R1 mice, which carried a differential segment of chromosome 6, exhibited a B6 liver response and intermediate spleen and circulating leukocyte responses. D2.R2 and D2.R4 mice, which carried differential segments of chromosomes 2 and 1, respectively, exhibited a D2 liver response, a B6 spleen response, and an intermediate circulating leukocyte response. The localization of control of liver response phenotypes to chromosome 6 implicates cells that express natural killer (NK) cell receptor NKR-P1 alloantigens. The localization of control of spleen and circulating leukocyte responses to chromosomes 1, 2, and 6 implicates NK cells, the fifth component of complement, and a gene near the selectin gene complex in recruitment of circulating leukocytes to spleen.

Animals↗
PubMed1997

[Pattern of circulating eosinophils in allergic children suffering from infectious disease].

BACKGROUND AND AIM: Both bacterial and viral acute infections are accompanied by a typical fall in the number of circulating eosinophils followed, at remission, by a rapid return to starting values. The aim of this study was to check whether this typical pattern can be observed in atopical children. MATERIALS AND METHODS: A retrospective study was performed in a group of atopical subjects (mainly asthmatic) suffering from intercurrent infectious diseases (mainly bronchopneumonia); circulating eosinophils were assayed during the acute phase of disease and during remission. The control group consisted of 21 atopic children without signs or symptoms of infectious diseases. RESULTS: The mean number of circulating eosinophils was 412.6 +/- 199.8 in the control group of allergic children 25.1 +/- 39.7 in the group with acute infectious diseases and 241 +/- 137.5 in the group of children with infectious diseases during remission. The differences between the group of children with infectious diseases and that in remission were statistically significant. The typical pattern of the fall and rise of circulating eosinophils was observed in 9 out of 10 children with acute infections. The cut-off proposed as the discriminating factor between acute phase infection and subjects in remission or without infectious diseases was 100 eosinophils/mm3. CONCLUSIONS: During the course of infective pathologies in allergic subjects there is an abrupt and significant reduction in circulating eosinophils followed, during remission, by a return to levels comparable to those in controls. Eosinophil assay therefore appears to be a useful parameter to monitor acute infection in allergic subjects. In particular, increased eosinophil levels are an early indicator that the infection has been overcome and remission is in progress. The authors repropose the hypothesis that eosinophils play a double role that alternates between activating the allergic phlogosis and eliminating non-allergic phlogosis, depending on the cytokinic context in which this occurs.

Acute Disease↗
PubMed1998

Circulating neutrophils and liver injury in rat models of experimental alcoholic liver disease.

The present study examined the relationship between circulating neutrophils and liver injury in two widely used rat models of chronic ethanol administration. Hematological alterations, liver histopathology, and biochemical indices of liver injury were assessed in rats receiving chronic ethanol by oral liquid diet feeding (Lieber-DeCarli method) or by continuous intragastric infusion (Tsukamoto-French method). Oral administration of ethanol did not affect circulating neutrophil counts, but resulted in minimal liver injury characterized by elevated serum alanine aminotransferase (79%), increased liver mass (15%), and moderate steatosis. In contrast, rats receiving ethanol by continuous intragastric infusion showed an approximately 2-fold increase in circulating neutrophils, and a moderate degree of liver injury, indicated by a 169% elevation of serum alanine aminotransferase and a 2-fold increase in liver mass. Liver biopsies from these rats showed severe steatosis and scattered necrotic hepatocytes, and some neutrophil infiltrates. To determine whether an increase in the number of circulating neutrophils could potentiate liver injury induced by oral ethanol feeding, rats were treated with human recombinant granulocyte colony-stimulating factor at a dose of 100 microg/kg/day (s.c.) for 4 days. Treatment with granulocyte colony-stimulating factor resulted in a 6- to 9-fold increase in circulating neutrophil counts. Nevertheless, this change did not enhance the minor degree of ethanol-induced liver injury in this model. Our results indicate that, whereas neutrophil leukocytosis accompanies more severe manifestations of ethanol hepatotoxicity in rats, this condition per se does not directly induce or exacerbate ethanol-induced liver injury.

Animals↗
PubMed1976

Studies on platelet plasma membranes. II. Characterization of surface proteins of rabbit platelets in vitro and during circulation in vivo using diazotized (125i)-diiodosulfanilic acid as a label.

Diazotized (125I)-diiodosulfanilic acid (DD125ISA) binds specifically to the exposed proteins on the surface of the rabbit platelet plasma membrane. This was demonstrated by the following observations with the use of sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) of whole platelets and the isolated plasma membrane fraction: (1) the specific activity of isolated membrane protein was sevenfold that of whole platelet protein, (2) no proteins of intact platelets were labeled which were not represented in the isolated plasma membrane, (3) DD125ISA-labeled proteins were altered by trypsin treatment of intact, labeled platelets, and (4) the pattern of labeling produced by reaction of isolated membranes with DD125ISA differed from that produced by the labeling of intact platelets. Reaction of DD125ISA with intact platelets produced labeling of only the three membrane glycoproteins (molecular weights: 180,000, 125,000, and 92,000 daltons) with greatest labeling of the largest glycoprotein and least labeling of the smallest glycoprotein. When rabbit platelets were labeled simultaneously with DD125ISA and 51Cr, the two isotopes were similarly distributed in various density populations of platelets. Some DD125ISA was solubilized from labeled and washed platelets by sonication, but all platelet DD125ISA was recovered in the plasma membrane fraction after 30 minutes' circulation in vivo. In vivo 51Cr recovery and survival were not altered by simultaneous labeling of platelets with DD125ISA. The disappearance of DD125ISA from circulating platelets (T 1/2 = 17 hours) was more rapid than 51Cr (T 1/2 = 30 hours) and appeared exponential in contrast to the linear 51Cr disappearance. On the other hand, DD125ISA did not disappear from platelets faster than 51Cr when doubly labeled platelets were harvested after 3 hours' circulation and incubated in autologous plasma (T 1/2 of DD125ISA elution = 43 hours, 51Cr = 33 hours). SDS-PAGE analysis of DD125ISA-labeled platelets after 14 to 20 hours' circulation in vivo demonstrated the same pattern of DD125ISA distribution on membrane glycoproteins as on the platelets prior to infusion. We interpret this symmetrical loss of the membrane label to indicate symmetrical loss of membrane proteins, suggesting that the platelet may lose pieces of membrane and not specific surface proteins during circulation. This could occur during reversible adhesion encounters during the process of hemostasis and cause the smaller size and decreased effectiveness of older platelets.

Animals↗
PubMedDate not supplied

[Longitudinal observations on the circulation of rotaviruses in Nizhny Novgorod using molecular-genetic methods].

1370 natural strains of human rotaviruses which circulated on the territory of Nizhny Novgorod during the period of 1984-1996 were differentiated with the use of electrophoretic typing of RNA. 58 electrophoretic types of RNA were detected; of these, 8 types dominated in the populations. The specific features of the circulation of strains with different electrophoretic types of RNA were characterized: co-circulation, time of domination, the change of the dominating genetic variant of the virus consecutively between seasons and during seasons. The change of domination during seasons, connected with the specific features of the circulation of rotaviruses having RNA of electrophoretic type 3, determined the winter-spring dynamics of the monthly detection rate of rotaviruses and was accompanied by an rise in the level of their detection. Such change was supposedly be caused by the biological properties of rotavirus with RNA of electrophoretic type 3, virulence constituting one of these properties. The study revealed that a change in the domination of the electrophoretic type of rotavirus, reflecting the change of the antigenic variant between seasons, occurred gradually during 5 seasons of the active circulation of strains.

Adolescent↗
PubMed1999

Increased circulating leptin in alcoholic cirrhosis: relation to release and disposal.

Leptin is a cytokine peptide that decreases appetite and thereby food intake and increases energy expenditure. It is produced in fat cells, but recent animal experiments have shown expression of leptin in modified stellate hepatic cells. Because a change in circulating leptin in cirrhosis could be caused by an altered production rate, altered disposal rate, or both, the present study was undertaken to identify regions of leptin overflow into the blood stream and regions of leptin extraction. Patients with alcoholic cirrhosis (n = 16) and control patients without liver disease (n = 12) were studied during catheterization with elective blood sampling from different vascular beds. Blood samples for leptin determination (radioimmunoassay) were taken simultaneously from artery/hepatic vein, artery/renal vein, artery/iliac vein, and artery/cubital vein. Patients with cirrhosis had significantly increased circulating leptin (7.3 vs. control 2.6 ng/mL, P <.002) that correlated directly to ascitic-free body mass index (r = 0.71, P <.005). A significant renal extraction ratio of leptin was observed in control patients (0. 16) and in patients with cirrhosis (0.07), but the latter value was significantly lower than in the control patients (-44%, P <.05) and inversely correlated to serum creatinine (r = -0.60, P <.05). A significant, but equal, hepatosplanchnic extraction of leptin was observed in cirrhotic patients and control patients (0.08 vs. 0.07). In patients with cirrhosis a significant cubital venous-arterial difference in leptin was observed, but not in control patients. The iliac venous/arterial leptin ratio was significantly above 1.0 in both groups and of similar size (1.16 vs. 1.15), but a higher difference in concentration was found in the cirrhotic patients (+33%, P <.05). The spillover rates of leptin in cirrhotic patients may be even higher than estimated from the increased systemic veno-arterial gradients. In conclusion, the elevated circulating leptin in patients with cirrhosis is most likely caused by a combination of decreased renal extraction and increased release from subcutaneous abdominal, femoral, gluteal, retroperitoneal pelvic, and upper limb fat tissue areas. The hepatosplanchnic bed drained through hepatic veins could not be identified as a source of increased circulating leptin in cirrhosis, but a contribution by the portosystemic collateral flow cannot be excluded.

Adult↗
PubMed1978

The behavior of collateral circulation after coronary artery bypass surgery.

The changes in coronary collateral circulation after bypass surgery were analyzed in 50 patients with coronary disease. The demonstration of collateral circulation was found to be dependent upon the severity of the coronary heart disease and the patency of the bypass. When the graft was patent, it was usually not possible to visualize the collateral circulation demonstrated preoperatively. When the bypass was occluded, the same collateral circulation as before surgery was frequently found.

Collateral Circulation↗
PubMed2002

[Prevalence and significance of coronary collateral circulation in patients with acute myocardial infarct].

UNLABELLED: Angiograms from consecutive and unselected patients with acute myocardial infarction were studied with respect to the prevalence as well as the significance of coronary collateral circulation to myocardium distal to the acute coronary occlusion. METHODS: Coronary angiograms were obtained from 700 consecutive and unselected patients with an acute transmural infarction within 3.7 +/- 3 hours (0.5-12) of symptom onset. No patient had undergone i.v. thrombolysis prior to angiography. Complete and acute vessel occlusion was found in 626/700 patients (89%). Coronary collaterals were detected and graded using Rentrop's classification. The grade of collateral circulation was related to the clinical course after 30 days and to the global and regional left ventricular wall motion. RESULTS: Collaterals were found in 334 patients (69%); 242 patients (38%) had collateral flow grade 2 or 3. Collaterals were demonstrated more frequently in women vs men and in patients with multivessel disease. The prevalence of collaterals was unrelated to age and the presence of diabetes mellitus. Patients who had angiography within 3 hours of symptom onset had collaterals detected less frequently than patients who had angiography beyond 6 hours (66% vs 75%, p < 0.05). No collaterals were found in 17/37 patients (47%) in cardiogenic shock and inferior MI but in only 30/164 patients (18%, p < 0.01) without shock. Global and regional left ventricular wall motion after 2 weeks was unrelated to the degree of coronary collateral circulation during acute myocardial infarction. CONCLUSION: Collateral circulation to myocardium distal to an acutely occluded coronary artery is detected in 2/3 patients during the acute infarct phase. The absence of collaterals is related to the early occurrence of cardiogenic shock in patients with inferior MI but not to the presence of diabetes mellitus. After direct angioplasty of the infarct vessel, the protective effects of coronary collaterals on chronic LV function remain uncertain.

Aged↗
PubMed1993

The role of the coronary collateral circulation in limiting myocardial ischemia and infarct size.

The role of coronary collateral circulation in limiting ischemia and infarction has been studied prospectively. Transient occlusion of a coronary artery angioplasty has provided evidence that collateral circulation decreases wall motion abnormalities, ST segment changes, and lactate production. Patients who have collateral flow also have a better outcome after coronary artery dissection and acute closure than patients without collateral flow. Collateral circulation also limits infarct size during acute myocardial infarction with and without thrombolysis. Although collateral flow may decrease coronary artery bypass graft patency in certain subgroups of patients, the perioperative infarct rate and mortality is decreased. Growth factors have been identified that increase the development collateral circulation and may improve ventricular function in the setting of myocardial infarction.

Acute Disease↗
PubMedDate not supplied

Use of artificial circulation in resuscitation of drowned dogs.

The effectiveness of artificial circulation by the method of Bryukhonenko and his colleagues in the resuscitation of dogs that had died from drowning in fresh- or salt-water was studied. Eight out of ten dogs were revived after freshwater drowning 'death' lasting from 10.5 to 21 min, when a variant of the artificial circulation method, dog donor with a venous pump of the artificial heart, was used. Resuscitated dogs remained alive from 3 to 72 h and died from pulmonary oedema. Artificial circulation appeared to be more effective in resuscitation of dogs drowned in saltwater. Their clinical 'death' lasted up to 31.5 min; clinically signs of pulmonary oedema were not observed in any of them, though some signs of oedema were revealed by histological studies. Of the 42 dogs in this series, all the main functions of the central nervous system were restored in 18 with clinical 'death' for up to 25 min. Resuscitation was performed by one of two methods, either the dog donor plus venous pump of the artificial heart, or the method of Bryukhonenko. The effectiveness of artificial circulation for resuscitation of dogs from drowning was demonstrated.

Animals↗
PubMed2006

Rapid decline of collateral circulation increases susceptibility to myocardial ischemia: the trade-off of successful percutaneous recanalization of chronic total occlusions.

OBJECTIVES: We evaluated the time-behavior of changes in collateral circulation after successful percutaneous coronary intervention (PCI) with drug-eluting stents (DES) in chronic (>1 month) total occlusions (CTO), and assessed their relationship with myocardial ischemia. BACKGROUND: It has been hypothesized that the immediate reduction of collateral flow after PCI of CTO could expose the patients to a higher risk of future ischemic events in the case of vessel reocclusion. METHODS: In 42 patients with CTO, two consecutive balloon inflations and final DES deployment were performed after positioning of a pressure guidewire. Minimal lumen diameter (MLD), diameter stenosis (DS), angiographic collateral grading (Rentrop score), myocardial (FFRmyo), coronary (FFRcor), and collateral fractional flow reserve (FFRcoll) were evaluated. Chest pain and the sum of ST-segment elevation (SigmaST) were analyzed to document the occurrence and extent of myocardial ischemia. RESULTS: Percutaneous coronary intervention induced a progressive improvement of indexes of stenosis severity (MLD, DS, Thrombolysis in Myocardial Infarction flow, FFRmyo, and FFRcor) and a rapid reduction in collateral circulation (FFRcoll and Rentrop score). A progressive worsening of ischemia at each balloon inflation occurred, concomitant with the reduction of collateral circulation. At linear regression analysis, an inverse relationship of FFRcoll with SigmaST (R2 = 0.352, p < 0.001) and angina pain score (R(2) = 0.247, p < 0.001) was observed. CONCLUSIONS: In CTO, collateral circulation, which provides most coronary flow at baseline, rapidly declines after successful stent implantation and the restoration of an antegrade flow. This rapid de-recruitment of collaterals is likely to put such patients at risk of future ischemic events.

Aged↗