title: Protection of the renal artery in nephron-sparing surgery. II. Arterial contractility investigations.
abstract: It has been well known that reperfusion following ischaemia may cause functional and structural damage to not only the organ involved but also the blood vessels supplying that organ. As in organ-sparing renal surgery it is inevitable to clamp the renal artery for some time, it is expected that reperfusion, following the removing of clamping, causes structural changes in the vessel wall which may result in a decrease in arterial function. In our model experiments on animals, the left renal arteries were atraumatically clamped for 30, 45 and 60 minutes. Simultaneously with clamping, perfusion regional renal venous cooling was applied to some of the animals, together with nephrotomy. In some cases cooling was performed in combination with antioxidant treatment. On the 3rd postoperative day renal arteries from both sides were removed, the right, intact ones serving as control. Noradrenaline dose effect curves characterizing vessel contractility were determined to demonstrate functional changes. It was established that cooling the renal artery for only 30 minutes was enough to rule out the damage due to ischaemia-reperfusion. If clamping lasted for 45 minutes, venous cooling of the kidney in combination with antioxidant treatment was necessary to spare arterial function. Clamping for 60 minutes resulted in irreversible/permanent decrease in contractility even if hypothermia and antioxidant treatment were given simultaneously.
authors.affiliation: Department of Experimental Surgery, Medical University School of Debrecen, Hungary.
authors.forename: I
authors.initials: I
authors.lastname: Mikó
authors.forename: S
authors.initials: S
authors.lastname: Csabina
authors.forename: M
authors.initials: M
authors.lastname: Hauck
authors.forename: J
authors.initials: J
authors.lastname: Kovács
authors.forename: E
authors.initials: E
authors.lastname: Schmidt
authors.forename: K
authors.initials: K
authors.lastname: Petö
authors.forename: I
authors.initials: I
authors.lastname: Furka
authors.forename: A
authors.initials: A
authors.lastname: Varga
authors.forename: G
authors.initials: G
authors.lastname: Tóth
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000627:therapeutic use; D003250:Constriction; D004195:Disease Models, Animal; D004285:Dogs; D004305:Dose-Response Relationship, Drug; D005260:Female; D005500:Follow-Up Studies; D006982:Hypertonic Solutions / Q000627:therapeutic use; D007036:Hypothermia, Induced; D007511:Ischemia / Q000473:pathology / Q000503:physiopathology; D007668:Kidney / Q000601:surgery*; D008297:Male; D009399:Nephrons / Q000601:surgery*; D009638:Norepinephrine / Q000008:administration & dosage / Q000494:pharmacology; D019188:Organ Preservation Solutions / Q000627:therapeutic use; D011804:Quinolines / Q000627:therapeutic use; D012077:Renal Artery / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology*; D015427:Reperfusion Injury / Q000473:pathology / Q000503:physiopathology; D013997:Time Factors; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology*; D014662:Vasoconstrictor Agents / Q000008:administration & dosage / Q000494:pharmacology
chemical_list: D000975:Antioxidants; C037096:Euro-Collins' solution; D006982:Hypertonic Solutions; D019188:Organ Preservation Solutions; D011804:Quinolines; C027821:Sack's solution; D014662:Vasoconstrictor Agents; C044964:6,6'-methylenebis(2,2-dimethyl-4-methanesulfonic acid-1,2-dihydroquinoline); D009638:Norepinephrine