Effects of stretch or distention on phenylephrine-induced constriction of human coronary artery bypass grafts.

OBJECTIVE: To determine the effects of grafting saphenous veins into the arterial circulation and to compare the responsiveness of saphenous veins and mammary arteries to vasoconstrictors (phenylephrine or potassium) and a vasodilator (the calcium antagonist isradipine). DESIGN: Prospective, controlled, in vitro study. SETTING: Laboratory facility in a university teaching hospital. PARTICIPANTS: Small excess segments of internal mammary arteries or saphenous veins obtained from patients undergoing coronary artery bypass graft surgery. INTERVENTIONS: Vessel segments were cut into rings to measure isometric tension development in isolated tissue chambers. The law of LaPlace for a cylinder was applied to determine tensions in vitro corresponding with arterial or venous tensions in vivo or distending pressures ex vivo. MEASUREMENTS AND MAIN RESULTS: Stretching saphenous vein rings from venous to arterial tensions reduced maximal phenylephrine-induced constriction but did not alter their dose response to phenylephrine, potassium, or isradipine. At arterial tensions, potassium, but not phenylephrine, was more potent in constricting mammary artery than saphenous vein; isradipine was more potent as a vasodilator of potassium-constricted mammary artery than saphenous vein. Maximal phenylephrine-induced or potassium-induced constriction was no different for either vessel at arterial tensions; however, prior distention of veins to tensions corresponding with pressures of 200 or 300 mmHg significantly (p < 0.01, Dunnett's test) reduced subsequent constriction. CONCLUSION: Phenylephrine may be more likely to constrict native internal mammary arteries than distended autogenous saphenous vein grafts in vivo because high-pressure distention of veins markedly inhibits their vasoreactivity.

Direct effects of triiodothyronine on human internal mammary artery and saphenous veins.

OBJECTIVE: Thyroid hormone (3,5,3'-triiodo-L-thyronine is under investigation as a positive inotrope and vasodilator for patients undergoing cardiac surgery. This study determined the direct effects of triiodothyronine on human blood vessels. DESIGN: Prospective, controlled, in vitro study. SETTING: Laboratory facility in a university teaching hospital. PARTICIPANTS: Small excess segments of internal mammary arteries or saphenous veins were obtained from patients undergoing coronary artery bypass surgery. INTERVENTIONS: Vessel segments were cut into rings to measure isometric tension development in isolated tissue baths containing Krebs-Ringer bicarbonate solution at 37 degrees C. Rings were prestretched in vitro to resting tensions analogous to mean arterial or central venous pressures in vivo and then constricted with potassium or phenylephrine. Rings were exposed to increasing concentrations of triiodothyronine (4 x 10(-12) to 1 x 10(-4) mol/L) to obtain dose-response curves. MEASUREMENTS AND MAIN RESULTS: High concentrations (> or = 3.3 x 10(-5) mol/L) of trilodothyronine produced dose-dependent relaxation of preconstricted rings. The relaxation was not selective for arteries or veins at arterial resting tensions, and with either potassium or phenylephrine as a vasoconstrictor. Propranolol had little effect on subsequent triiodothyronine-induced relaxation of potassium-constricted rings at resting arterial tensions. CONCLUSIONS: Triiodothyronine, in supraphysiological and suprapharmacological concentrations, dilates preconstricted rings of human blood vessels in vitro; however, triiodothyronine had no demonstrable vasomotor effects on human internal mammary artery or saphenous vein in clinically relevant concentrations (10(-9) to 10(-8) mol/L). Triiodothyronine administration in vivo most likely has little direct effect on the tone of human vascular smooth muscle, particularly coronary artery bypass conduits.

Antigen-specific inhibition of the IL-2-driven proliferation of myelin basic protein-reactive, human T cells.

This report examines the antigen-specific inhibition of the IL-2-driven proliferation of autoantigen-reactive, human T cells. Human, myelin basic protein (MBP)-reactive CD4+ cell lines and clones were isolated and maintained in culture by use of IL-2 and periodic antigen stimulation. When freshly isolated antigen-presenting cells (APC) were present, MBP induced proliferation of MBP-reactive T cell populations. However, under different culture conditions, MBP reduced the IL-2-driven proliferation of some MBP-reactive T cell populations. The inhibition of IL-2-driven proliferation did not appear to require CD8+ or OKM 1+ cells since these were not detected when inhibition studies were performed at least 9 days after the last restimulation by irradiated APC and MBP. Supraoptimal concentrations of MBP were not required for inhibition of proliferation. Some heterogeneity of response was apparent since MBP inhibited the IL-2-driven proliferation of some T cell clones while for others MBP had either no effect or produced slight enhancement of proliferation. These results demonstrate an antigen-specific, in vitro immune mechanism that reduces the IL-2-dependent proliferation of autoantigen-reactive, human T cells.

Effects of intravenous perfluorocarbon and oxygen breathing on acute decompression sickness in the hamster.

Anesthetized female hamsters (Mesocricetus auratus) were divided into 3 experimental groups with 16 animals in each group. After control arterial blood pressure and ECG recordings, the animals were placed in a hyperbaric chamber for 30 min at 7 ATA and then decompressed directly to the surface at a rate of 60 fsw/min. After their removal from the chamber, animals were either not treated (group 1); given i.v. saline while breathing 100% oxygen (group 2), or given i.v. oxypherolperfluorochemical (Fluosol-43) perfusion emulsion while breathing 100% oxygen (group 3). Thirty minutes after decompression, all but one of group 1 had died (a 6% survival rate). Group 2 had a 62% survival rate and group 3 had a 94% survival rate. Perfluorochemicals were observed to reduce the number of bubbles formed, enhance bubble disappearance, and reduce dysrhythmias.

Isolation of P2 protein--reactive T-cell lines from human blood.

Human T-cell lines reactive with the peripheral nerve myelin protein, P2 protein, were isolated from the peripheral blood of 4 normal persons and 1 patient with Guillain-Barré syndrome. These predominantly helper phenotype T-cell lines were isolated and maintained in vitro by antigen stimulation followed by culture with interleukin 2. Myelin basic protein-reactive T cells were also isolated in parallel from the same subjects as antigen specificity controls. T cells recognizing myelin basic protein did not respond to P2 protein, nor did P2-reactive cells respond to myelin basic protein. These findings suggest that a potential for autoimmune reactivity with peripheral nervous system myelin antigens may exist for both normal persons and some patients with neurological disease.

Human cellular immune response to copolymer I and myelin basic protein.

Copolymer I (Cop I) is being tested as a treatment for MS because it protects animals against experimental allergic encephalomyelitis, and because there is immunologic cross-reactivity reported between Cop I and myelin basic protein (MBP). From the peripheral blood mononuclear cells of four normal individuals, we isolated helper-phenotype T-cell lines that reacted in vitro with Cop I or MBP. Cop I-reactive cell lines did not respond to MBP, nor did MBP-reactive T-cell lines respond to Cop I. Antigen-specific immune tolerance was induced in MBP-reactive cell lines by exposure to MBP in vitro, but similar exposure to Cop I did not induce tolerance in the MBP-reactive cell lines. We found no evidence of immunologic cross-reactivity between Cop I and MBP.