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Biomedical subjects

G Johnson

Publications and source records attributed to G Johnson.

At least 343 records · Page 19Linked to original sources
PubMed1990

Endothelial cell seeding of small diameter vascular grafts.

This study examines, under flow conditions, the adhesion of endothelial cells to 3 mm diameter fibronectin (Fn)-coated expanded polytetrafluoroethylene (PTFE) vascular grafts. Cultured ovine carotid artery endothelial cells were labelled with 35S-methionine. The grafts were seeded with endothelial cells (1.5 x 10(6)/ml) by rolling for 1 h at 37 degrees C and then either cultured to confluence for 48 h or flow tested immediately. Cell attachment to grafts (n = 5) was evaluated in an in vitro flow circuit, using flows of up to 330 ml/min. Ex vivo studies (n = 5 grafts) were conducted without anticoagulant using autologous cells in a sheep model. Grafts were inserted into an externalized carotid-jugular shunt and exposed to blood flows of approximately 150 ml/min for 3 h. One hour seeded and 48 h cultured grafts demonstrated greater than 95% cell retention following in vitro flow studies. Ex vivo studies of 48 h cultured grafts gave endothelial cell retention of 81% with no sign of thrombogenicity. Furthermore, a preliminary 24 h ex vivo study has shown greater than 95% retention. This study demonstrates the firm attachment of seeded endothelial cells to Fn-coated PTFE grafts in the sheep model.

Animals↗
PubMed1990

Beneficial effects of two forms of NO administration in feline splanchnic artery occlusion shock.

We studied the effects of nitric oxide (NO) solution and acidified sodium nitrite (NaNO2), which produces NO, in splanchnic artery occlusion (SAO) shock in cats. NO is thought to be endothelium-derived relaxing factor (EDRF), a labile substance having several potentially valuable biological effects. Anesthetized cats subjected to total occlusion of the celiac, superior mesenteric, and inferior mesenteric arteries for 120 min, followed by reperfusion, usually died approximately 60 min after reperfusion. NO infusion significantly improved survival time in SAO-shock cats compared with those receiving vehicle (P less than 0.005). Administration of NO also attenuated the increase in plasma activities of the lysosomal hydrolase cathepsin D (P less than 0.05), total amino-nitrogen (P less than 0.001), and of the cardiotoxic peptide, myocardial depressant factor (MDF) (P less than 0.001). SAO-shock cats treated with NaNO2 at pH 2.0 also exhibited lower plasma cathepsin D (P less than 0.001), amino-nitrogen (P less than 0.05), and MDF activities (P less than 0.01), and survival time was also significantly improved (P less than 0.02). The same dose of NaNO2 infused at pH 7.4 failed to exert any significant protective effect. These results indicate that NO exerts beneficial effects in SAO shock in cats and suggest that exogenously administered NO may be a potentially useful therapeutic agent in splanchnic ischemic shock, probably via a cytoprotective rather than a vasodilator effect.

Amines↗
PubMed1990

Transvenous defibrillation in humans via the coronary sinus.

A consistently effective transvenous defibrillation system for use in automatic defibrillators could significantly alter the approach to patients at risk of sudden death. Transvenous defibrillation systems that use a right ventricular (RV) electrode only or an RV electrode in combination with a chest patch are relatively inefficient at applying current to the posterolateral left ventricle. An RV electrode combined with a coronary sinus (CS) electrode, however, may improve current distribution to the posterolateral left ventricle. The purpose of this investigation, therefore, was to evaluate the effectiveness and safety of a specially designed transvenous lead system with a CS electrode capable of current delivery to this relatively inaccessible region of the heart. In 20 survivors of cardiac arrest, we determined defibrillation efficacy immediately before defibrillator surgery for monophasic pulses delivered between an RV catheter electrode and a CS catheter electrode system and compared these findings with an RV catheter electrode-thoracic patch defibrillation system. Subsequently, we referenced the efficacy of both transvenous systems to an epicardial patch electrode system at the time of defibrillator implantation. The mean delivered-energy defibrillation threshold for the CS-RV electrode system was 17.5 +/- 7.9 J, which was substantially lower than the RV electrode-thoracic patch system (25.6 +/- 11.4 J, p = 0.0016 [46% more]). Defibrillation threshold voltage was 529 +/- 123 V for the CS-RV electrode system and 647 +/- 164 V (22% more) for the RV electrode-thoracic patch system (p = 0.0013).(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Vessels↗
PubMed1990

Time course of endothelial dysfunction and myocardial injury during myocardial ischemia and reperfusion in the cat.

Myocardial ischemia and reperfusion have been shown to impair coronary vasorelaxation to endothelium-dependent vasodilators. To examine the time course of this dysfunction, occlusion of the left anterior descending (LAD) coronary artery (90 minutes) was followed by reperfusion for 0, 2.5, 5, 20, 180, or 270 minutes. Coronary arterial rings from the ischemic LAD and control left circumflex (LCx) arteries were tested for responsiveness to the endothelium-dependent receptor-mediated vasodilator, acetylcholine (ACh), and the endothelium-dependent nonreceptor-mediated vasodilator, A23187, as well as the endothelium-independent vasodilator, NaNO2. ACh relaxation was not impaired after 90 minutes of ischemia without reperfusion. However, 2.5 minutes of reperfusion resulted in depressed ACh responses (36 +/- 10% of control) that was further reduced to 16 +/- 6% at 20 minutes, and remained comparably depressed at every time thereafter. A23187 vasodilator responses were also attenuated after reperfusion, although the reduced response occurred later (that is, at 20 minutes). There was no significant decrease in response to NaNO2 in the LAD at any time or to any vasodilator in LCx control rings. Treatment with recombinant human superoxide dismutase (hSOD, 5 mg/kg/hr, that is, 15,545 SOD units/kg/hr), starting 10 minutes before reperfusion, preserved the vasodilator response to ACh (82 +/- 6%) and A23187, but treatment with the hydroxyl ion scavenger N-(2-mercapto proprionyl)-glycine (MPG) (8 mg/kg/hr) only protected the A23187 response. No damage to the surface of the endothelium was observed by scanning electron microscopy at any time point. Myocardial cell damage increased with time of reperfusion as assessed by increasing plasma CK activities and amounts of necrotic tissue indexed to area at risk. Significant myocardial injury occurred at 3 hours after reperfusion. These findings suggest that endothelial dysfunction resulting in reduced endothelium-derived relaxing factor release occurs before the development of myocardial cell necrosis and may be due to oxygen-derived free radicals produced rapidly on reperfusion.

Animals↗
PubMed1990

Endothelium and myocardial protecting actions of taprostene, a stable prostacyclin analogue, after acute myocardial ischemia and reperfusion in cats.

The effects of taprostene, a synthetic prostacyclin analogue, were investigated in a 6-hour model of myocardial ischemia (MI) with reperfusion in anesthetized cats. Taprostene (100 ng/kg/min) was infused intravenously starting 30 minutes postocclusion of the left anterior descending coronary artery followed by reperfusion 1 hour later, and the cats were observed for an additional 4.5 hours. Taprostene infusion resulted in significantly lower plasma creatine phosphokinase activities at every time from 3 to 6 hours for the MI + taprostene group compared with the MI + vehicle group and were not significantly different when compared with sham MI controls. The areas at risk, expressed as a percentage of the total left ventricular weights, were not significantly different between the MI groups. However, the necrotic area expressed as a percentage of the myocardial area at risk was significantly lower in the taprostene-treated cats compared with the untreated MI group (p less than 0.01). Cardiac myeloperoxidase activities indicated that significantly fewer neutrophils were attracted to the area at risk and to the ischemic zone of the MI + taprostene cats when compared with the MI cats given only the vehicle. Data from isolated left anterior descending coronary artery ring preparations removed from hearts after 6 hours of ischemia indicated that the endothelium was damaged by ischemia-reperfusion injury in the untreated cats. However, endothelial dysfunction was not observed in circumflex coronary arteries of ischemic cats or in coronary rings isolated from MI + taprostene cats. Thus, taprostene exerted a significant cardioprotection in cats subjected to ischemia and reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1990

Serum enhancement of human endothelial cell attachment to and spreading on collagens I and IV does not require serum fibronectin or vitronectin.

The initial attachment and spreading of endothelial cells from human umbilical artery onto type I collagen, type IV collagen or gelatin substrata was shown to be enhanced by inclusion of serum in the culture medium. To test whether this serum effect was mediated by adsorption of serum fibronectin or vitronectin onto the collagen, these adhesive glycoproteins were selectively removed from the serum prior to addition to the culture medium. The stimulatory effect of serum on human endothelial cell spreading on collagens I and IV was also observed with serum from which either fibronectin or vitronectin, or both, had been selectively removed. The stimulatory effect for cell spreading on gelatin was diminished by selective removal of serum fibronectin, but unaffected by removal of vitronectin. Human endothelial cell attachment and spreading onto tissue culture plastic was abolished by removal of vitronectin from the serum in the culture medium. These results emphasize that the native structure of collagens is required for serum-enhancement of human endothelial cell attachment and spreading on native collagen types I and IV, and show that on these substrata the stimulated adhesion and spreading are not dependent upon adsorption of serum fibronectin or vitronectin onto the collagen substratum.

Cell Adhesion↗
PubMed1990

Building undergraduate nursing students' knowledge of the research process in nursing.

This article describes a simple approach to teaching a nursing research course to undergraduate nursing students which was received with enthusiasm by both students and faculty. Through short answer progressive assignments throughout the semester involving students in the thinking processes required at each stage of the research process, student knowledge of the research process was progressively developed. Students chose a topic of personal interest for a proposed study and carried this topic through the various phases of the research process. Students positively evaluated this approach frequently commenting that the approach helped them to "think in different ways than before" and strongly recommended continuance of the approach in future course presentations.

Curriculum↗
PubMed1990

Protective effects of the specific thromboxane receptor antagonist (+)-S145Na in splanchnic artery occlusion shock in rats.

We studied the effects of a new potent thromboxane A2 receptor antagonist as a protective measure in circulatory shock induced by splanchnic artery occlusion and reperfusion. The celiac and superior mesenteric arteries of anesthetized rats were occluded for 40 min followed by reperfusion, resulting in a large decrease in mean arterial blood pressure usually leading to a fatal outcome within 60 to 90 min. Rats were treated with the specific thromboxane A2 receptor antagonist, (+)-S145Na, at one of three doses (50, 200 or 500 micrograms/kg) or with its vehicle (0.9% NaCl). In isolated rat aortic rings, (+)-S145Na was found to be a highly specific and potent thromboxane receptor antagonist having an IC50 of 1 ng/ml. The highest dose of the drug exhibited protection characterized by an attenuation in the increases in hematocrit (P less than .05), plasma cathepsin D activity (P less than .05), plasma aminonitrogen concentration (P less than .05), and plasma myocardial depressant factor activity (P less than .01) as well as increased survival rate and time (P less than .01), compared to the splanchnic artery occlusion shock group given the vehicle. The lowest dose of (+)-S145Na failed to provide protection, whereas the intermediate dose (i.e., 200 micrograms/kg) exerted less dramatic protective effects than the 500 micrograms/kg dose. These findings suggest an important role of thromboxane A2 in the pathogenesis of splanchnic artery occlusion shock, and that (+)-S145Na may be a useful agent in the treatment of bowel ischemia and its complications.

Animals↗
PubMed1990

Cardioprotective effects of acidified sodium nitrite in myocardial ischemia with reperfusion.

The effects of acidified sodium nitrite (NaNO2) which releases nitric oxide, a substance which is thought to be indistinguishable from endothelium-derived relaxing factor, were investigated in a 6-h model of myocardial ischemia (MI) with reperfusion in open-chest, anesthetized cats. Acidified NaNO2 (12.5-50 mmol/kg/hr) was infused i.v., starting 30 min postocclusion followed by reperfusion 1 hr later, in cats subjected to MI by occlusion of the left anterior descending coronary artery. Acidified NaNO2 infusion (25 and 50 mmol/kg/hr) resulted in significantly lower plasma creatine kinase activities at every time beyond 1 hr for the MI + vehicle group, and was not significantly different when compared to sham MI + NaNO2 controls. The areas at risk expressed as percentage of the total left ventricular weights were not significantly different between the MI + vehicle and MI + acidified NaNO2 groups. However, the necrotic area expressed as a percentage of the myocardial area at risk was significantly lower in the 25 and 50 mmol/kg/hr NaNO2-treated cats. Cardiac myeloperoxidase activities indicated that significantly fewer neutrophils were attracted to the ischemic zone of the NaNO2-treated MI cats when compared to the vehicle-infused MI cats. Acidified NaNO2 significantly inhibited platelet aggregation in a dose-dependent manner in cat platelet-rich plasma. Thus, acidified NaNO2 exerts a significant protective action during ischemia and reperfusion injury, which suggests that endothelium-derived relaxing factor has a cardioprotective effect in MI.

Animals↗
PubMed1990

Transformation of early erythroid precursor cells (BFU-E) by a recombinant murine retrovirus containing v-erb-B.

Avian erythroblastosis virus (AEV) is a replication-defective retrovirus that transforms erythroid and fibroblast cells in vitro and in vivo. The transforming ability of AEV is due primarily to the oncogene v-erb-B. A recombinant murine retrovirus has been constructed by inserting a chimeric gag-v-erb-B gene into a Moloney murine leukemia virus based vector. This retrovirus was used to examine v-erb-B-induced transformation of murine hematopoietic cells. Infection of murine primary fetal liver, adult bone marrow or adult spleen cells with the recombinant virus generated large hemoglobinized erythroid colonies in the absence of exogenous growth factors. Generation of such colonies usually requires the presence of erythropoietin (Epo) and interleukin-3 (IL-3). These growth-factor independent colonies were shown to be derived from early (BFU-E) and not late (CFU-E) erythroid progenitor cells, and the effect was not attributable to growth factors elicited by the virus-producing cell lines. In order to confirm that the recombinant virus was responsible for this transformation of BFU-E to growth factor independence, bone marrow cells from post 5-fluorouracil treated mice were infected and used to repopulate lethally-irradiated mice. Growth factor-independent BFU-E were obtained in up to 30% of day-13 spleen colonies and it was shown by DNA analysis that cells from these colonies contained integrated provirus. Our results indicate that v-erb-B transforms early erythroid progenitors to growth factor independent growth and subsequent differentiation to erythrocytes -a process that normally requires Epo plus either IL-3 or granulocyte-macrophage colony stimulating factor (GM-CSF).

Alpharetrovirus↗
PubMed1990

Endothelial cells can synthesize leukotriene B4.

Leukotriene B4 (LTB4) from vascular endothelium may play a key role in the genesis of atherosclerotic lesions. However, the ability of this tissue to synthesize LTB4 is controversial. To resolve this issue arachidonic acid metabolism was characterized in cultures of confluent monolayers of a rabbit aortic endothelial cell line by use of both high-pressure liquid chromatography and radioimmunoassay. Cells were grown to confluence in Dulbecco's modified Eagle's medium/Ham's F12 with 5% fetal bovine serum. Lipoxygenase activity was studied by placing the cells in Hank's balanced salt solution with 2 mumol/L indomethacin. After 30 minutes preincubation with indomethacin cells were exposed to either arachidonic acid (10 mumol/L) or arachidonic acid labeled with radioactive carbon (14C) (1 microCi; SA 58 mCi/mmol) and then stimulated with 9.5 mumol/L calcium ionophore A23187 for 55 minutes. Studies of the cyclooxygenase activity were performed without preincubating with indomethacin. Samples were prepared for high-pressure liquid chromatography by evaporation to dryness under a vacuum and resuspending in 2 ml of 1:1 methanol/water. Tritium-labeled standards were added before loading the 14C-labeled samples on the column. Radiolabeled arachidonic acid metabolites were separated by high-pressure liquid chromatography and detected by means of a dual channel flow-through radiodetector that monitors both 14C and 3H. Based on coelution with authentic standards three lipoxygenase metabolites of arachidonic acid have been identified: LTB4, 12- and 5-hydroxyeicosatetraneoic acid. Leukotriene B4 was further characterized by ultraviolet spectral analysis and inhibition studies with use of nordihydroguaiaretic acid. Quantitation was facilitated by commercially available radioimmunoassay kits. An average of 600 pg LTB4/10(6) cells was measured from separate experiments.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Bioavailability and the mechanisms of intestinal absorption of iron from ferrous ascorbate and ferric polymaltose in experimental animals.

The comparative bioavailability from matching quantities of iron in the form of ferrous ascorbate or ferric polymaltose was defined in rats. Studies were carried out in the intact animals under basal conditions and also when requirements for this metal were either increased or decreased by manipulating stores or erythropoietic activity. No significant difference was found in the total quantity of iron absorbed from either salt or complex under any of these circumstances, suggesting that the mucosal mechanism regulating the overall process was common to both. However, the rate of transfer from the lumen into portal blood was distinctive, reaching a maximum with salt at 30 min compared to 24 h for the complex. To explore the possibility that iron from the two sources was initially handled by different subcellular pathways, the radiolabeled compounds were instilled into loops of bowel that had been isolated between ligatures in vivo. Enterocytes were harvested and fractionated, and incorporation into ferritin and transferrin was determined using RIA. From salt, iron appeared rapidly in duodenal but not ileal ferritin, whereas mucosal transferrin increased under conditions of stimulated absorption, suggesting that this protein may act as a shuttle for the metal. In contrast, iron from polymaltose showed a cumulative incorporation into duodenal ferritin over time that correlated with iron absorption, defined by the appearance of radiolabel in the serum and in the carcass; a similar pattern was demonstrable in ileal mucosal cells. Conversely, binding of iron to transferrin was minimal. No iron polymaltose was found within the mucosal cells. It is suggested that the low rate of iron transfer from this ferric complex may reflect its extracellular breakdown in the lumen of the gastrointestinal tract.

Anemia, Hemolytic↗
PubMed1990

Protective effects of a novel 21-aminosteroid during splanchnic artery occlusion shock.

We investigated the effects of a novel, non-glucocorticoid 21-aminosteroid, U74006F, in the pathogenesis of splanchnic artery occlusion (SAO) shock in rats. Pentobarbital-anesthetized (40 mg/kg) rats were subjected to 40 min of occlusion of both the celiac and superior mesenteric arteries followed by reperfusion, which resulted in a severe shock state characterized by a markedly lower mean arterial blood pressure (MABP) and a survival time of 40-80 min post-reperfusion. In contrast, infusion of U74006F (22.5 mg/kg) during the occlusion period resulted in a significantly higher MABP following reperfusion which prolonged survival (117 +/- 3 min vs. 66 +/- 10, P less than .01) compared to those rats receiving only the vehicle for U74006F (0.002 N HCl). Hematocrits measured at the end of each experiment were significantly lower in the treated shock rats compared to the untreated group (55.7 +/- 1.8 vs. 63.0 +/- 1.7, P less than .01). SAO shock rats treated with U74006F also exhibited significantly attenuated plasma accumulation of cathepsin D (P less than .05) and myocardial depressant factor (MDF) (P less than .01). Six of 7 SAO shock rats treated with U74006F survived for 120 min following reperfusion, while none of 7 SAO shock rats given the vehicle survived for 120 min (P less than .01). These results suggest that U74006F has therapeutic utility in SAO shock.

Animals↗
PubMed1990

Heart failure with normal ejection fraction. The V-HeFT Study. Veterans Administration Cooperative Study Group.

In patients with clinical heart failure entered into the Veterans Administration Cooperative Study (V-HeFT) trial, 83 of 623 who had a baseline radionuclide measurement of left ventricular ejection fraction exhibited an ejection fraction of at least 0.45. When compared with the patients with an ejection fraction of less than 0.45, these subjects with apparent predominant diastolic dysfunction had a lower incidence of coronary artery disease (26.5% vs. 47.2%, p less than 0.001) and a higher incidence of preexisting hypertension (53.0% vs. 39.4%, p less than 0.02). In the normal ejection fraction group, systolic blood pressure was higher (129.7 vs. 117.7 mm Hg, p = 0.0001), heart rate slower (75.0 vs. 83.2 beats/min, p = 0.0001), cardiothoracic ratio smaller (0.512 vs. 0.536, p = 0.002), echocardiographic left ventricular dimension smaller in diastole (61.7 vs. 69.2 mm, p = 0.0001) and in systole (47.4 vs. 58.1 mm, p = 0.0001), and posterior wall thickness greater (9.0 vs. 7.9 mm, p = 0.004). Exercise tolerance was only slightly better in the normal ejection fraction group (peak oxygen consumption, 15.5 vs. 14.6 ml/kg/min, p = 0.04). Prognosis in the normal ejection fraction patients (annual mortality rate, 8.0%) was significantly better than in the low ejection fraction group (annual mortality rate, 19.0%) (p = 0.0001). Ventricular tachycardia on Holter monitor was a poor prognostic sign in these patients, and severe reduction in exercise tolerance also tended to predict poor outcome.(ABSTRACT TRUNCATED AT 250 WORDS)

Exercise Test↗
PubMed1989

In vitro immunologic features of Weimaraner dogs with neutrophil abnormalities and recurrent infections.

In vitro evaluation of cellular and humoral immunity in Weimaraner dogs with recurrent infections and abnormal neutrophil function revealed significantly lower serum immunoglobulin (Ig) G and M concentrations than control dogs. Lymphocyte blastogenesis in response to three different mitogens, interleukin-1 and -2 production, natural killer (NK) cell activity, and in vitro IgG and IgM production were similar to those of control dogs.

Animals↗