title: [Significance of therapy timing for the effects of systemic and local therapy with the ACE inhibitor captopril on intestinal microcirculation in manifest mesenteric ischemia. An animal experiment study in the swine].
abstract: We present the results of a study based on an animal model concurring whether captopril can improve microcirculation in the small intestine in nonocclusive mesenteric ischemia dependent on when therapy is begun. Cardiogenic shock was produced by pericardial tamponade with starch solution. The flow in the carotid artery could be reduced to 43% of the preshock value. In four therapy groups and a control group the intestinal microcirculation was examined by laser Doppler flowmetry in the serosa and mucosa. The measurements were taken at regular intervals during the 4 h of the experiments. Captopril was either given systemically or locoregionally through the upper mesenteric artery. Therapy was given at the beginning of the shock or 1 h after induction of shock at a dosage of 0.25 mg/kg body weight as a bolus and continuous application of 10 micrograms/kg body wt. Concerning the hemodynamic changes during shock the group receiving captopril systemically at the beginning of shock showed a significant (P = 0.05) improvement in microcirculation compared to the controls and other therapy groups. Flow reduction was seen in the controls (156-32 relative flow units = RFU) in group Ia (systemic therapy 1 h after shock), as well as the controls (129 to 12 RFU) and, in group Ib (systemic therapy beginning with shock) a flow rise could be seen (307 to 481 RFU). In group IIa (local therapy 1 h after shock) (a steady flow was seen (168-170 RFU) and in group IIb (local therapy beginning with shock) and group Ib an increase in flow was also measured (226-303 RFU). This positive effect of captopril on the intestinal perfusion was observed when applied 1 h after the induction of shock.
authors.affiliation: Chirurgische Universitätsklink und Poliklinik, Bonn Venusberg.
authors.forename: J
authors.initials: J
authors.lastname: Jakschik
authors.forename: P
authors.initials: P
authors.lastname: Decker
authors.forename: A
authors.initials: A
authors.lastname: Hirner
mesh_terms: D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology*; D000818:Animals; D001783:Blood Flow Velocity / Q000187:drug effects / Q000502:physiology; D002216:Captopril / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D004334:Drug Administration Schedule; D006439:Hemodynamics / Q000187:drug effects* / Q000502:physiology; D007262:Infusions, Intravenous; D007269:Injections, Intra-Arterial; D007413:Intestinal Mucosa / Q000098:blood supply; D007421:Intestine, Small / Q000098:blood supply*; D007511:Ischemia / Q000503:physiopathology*; D017078:Laser-Doppler Flowmetry; D017538:Mesenteric Artery, Superior / Q000187:drug effects / Q000503:physiopathology; D008643:Mesentery / Q000098:blood supply*; D008833:Microcirculation / Q000187:drug effects / Q000502:physiology; D012039:Regional Blood Flow / Q000187:drug effects / Q000502:physiology; D012770:Shock, Cardiogenic / Q000503:physiopathology; D013552:Swine
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D002216:Captopril