David G. Cable, MD, James A. Caccitolo, MD, Eric A

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Presentation transcript:

Endothelial regulation of vascular contraction in radial and internal mammary arteries David G. Cable, MD, James A. Caccitolo, MD, Eric A. Pfeifer, MD, Richard C. Daly, MD, Joseph A. Dearani, MD, Charles J. Mullany, MD, Timothy O’Brien, MD, Thomas A. Orszulak, MD, Hartzell V. Schaff, MD The Annals of Thoracic Surgery Volume 67, Issue 4, Pages 1083-1090 (April 1999) DOI: 10.1016/S0003-4975(99)00130-7

Fig 1 Histology. (A) Human internal mammary and (B) radial arteries were stained to highlight the elastic tissue in each artery. The medial thickness of the radial artery is greater than that of the internal mammary artery. (Verhoeff–van Gieson; ×40 before 50.5% reduction.) The Annals of Thoracic Surgery 1999 67, 1083-1090DOI: (10.1016/S0003-4975(99)00130-7)

Fig 2 Receptor-dependent smooth muscle contraction. Human radial and internal mammary (IMA) arteries demonstrated concentration-dependent increases in tension with prostaglandin F2α (10−9 to 10−5 mol/L). The radial artery segments generated significantly more tension at a given concentration of prostaglandin F2α than the IMAs. Data are expressed as the mean ± the standard error of the mean. The Annals of Thoracic Surgery 1999 67, 1083-1090DOI: (10.1016/S0003-4975(99)00130-7)

Fig 3 Relaxation to sodium nitroprusside. Human radial and internal mammary (IMA) arteries were contracted with a submaximal concentration of prostaglandin F2α and stimulated with increasing concentrations of sodium nitroprusside (10−9 to 10−4 mol/L), an endothelium-independent agonist. No significant difference in relaxations was noted between the two types of arteries. Data are shown as the mean ± the standard error of the mean. The Annals of Thoracic Surgery 1999 67, 1083-1090DOI: (10.1016/S0003-4975(99)00130-7)

Fig 4 Relaxation to acetylcholine. Human radial and internal mammary (IMA) arteries were contracted with a submaximal concentration of prostaglandin F2α and stimulated with increasing concentrations of acetylcholine (10−9 to 10−6 mol/L). Internal mammary arteries demonstrated significantly greater relaxations than radial arteries. Data are shown as the mean ± the standard error of the mean. The Annals of Thoracic Surgery 1999 67, 1083-1090DOI: (10.1016/S0003-4975(99)00130-7)

Fig 5 Relaxation to calcium ionophore. Human radial and internal mammary (IMA) arteries were contracted with a submaximal concentration of prostaglandin F2α and stimulated with increasing concentrations of calcium ionophore A23187 (10−9 to 10−6 mol/L). Internal mammary arteries demonstrated significantly greater relaxations than radial arteries. Data are shown as the mean ± the standard error of the mean. The Annals of Thoracic Surgery 1999 67, 1083-1090DOI: (10.1016/S0003-4975(99)00130-7)

Fig 6 Superfusion bioassay. The bioassay rings were contracted with a submaximal concentration of prostaglandin F2α. Relaxations of the detector rings were documented before (Basal) and after stimulation with acetylcholine (ACH) or calcium ionophore (A23187) proximal to the arterial segments. (IMA = internal mammary artery.) The Annals of Thoracic Surgery 1999 67, 1083-1090DOI: (10.1016/S0003-4975(99)00130-7)

Fig 7 Nitric oxide synthase (NOS) immunohistochemistry. Immunohistochemistry with a monoclonal antibody specific for endothelial nitric oxide synthase (eNOS) demonstrated that endogenous endothelial production of this enzyme was greater in (A) internal mammary arteries than in (B) radial arteries. Overexpression of NOS by adenovirus-mediated gene transfer of eNOS was localized to both (C) endothelial and (D) adventitial layers of human radial arteries (×200 before 44.9% reduction.) The Annals of Thoracic Surgery 1999 67, 1083-1090DOI: (10.1016/S0003-4975(99)00130-7)

Fig 8 Relaxation to acetylcholine after adenovirus-mediated gene transfer. Human radial arteries were exposed to vehicle (phosphate-buffered saline solution with 0.1% albumin [PBSA]) or adenovirus-encoding β-galactosidase (Ad.CMVLacZ) or endothelial nitric oxide synthase (Ad.CMVeNOS) for 2 hours. After a 40-hour ex vivo incubation, paired segments were contracted with a submaximal concentration of prostaglandin F2α and stimulated with acetylcholine (10−9 to 10−6 mol/L). Maximum relaxation to acetylcholine was similar in vehicle (PBSA) and virus (Ad.CMVLacZ) controls. In contrast, overexpression of recombinant nitric oxide synthase (Ad.CMVeNOS) significantly increased relaxations compared with controls. The Annals of Thoracic Surgery 1999 67, 1083-1090DOI: (10.1016/S0003-4975(99)00130-7)