title: Systemic hypertension induced by aortic cross-clamping: detrimental effects of direct smooth muscle relaxation compared with ganglionic blockade.
abstract: OBJECTIVE
  Infrarenal aortic cross-clamping performed during vascular reconstructive procedures is often accompanied by systemic supraclamp hypertension. Much of the disease and death that attend aortic cross-clamping centers around hypertension. Many different strategies have been developed to attenuate intraoperative hypertension, and a host of pharmacologic agents are regularly used to lessen the heart-related, cerebral, and systemic effects of clamp-induced hypertension. This study was performed to evaluate two such strategies; the intravenous administration of either trimethaphan camsylate or nitroprusside.
  
  
  METHODS
  We used a highly controllable and reproducible model of aortic cross-clamping in which we have previously shown the hypertension associated with clamping to be an active process mediated by means of a reflex arc. Ten dogs, five treated with nitroprusside (NP group) and five treated with trimethaphan camsylate (TC group), underwent 90 minutes of aortic cross-clamping. During this 90-minute period each group received 30 minutes of antihypertensive therapy.
  
  
  RESULTS
  Control mean arterial pressure +/- SEM was 80 +/- 5 mm Hg for both groups and increased to 140 +/- 5 mm Hg with clamp application. With antihypertensive treatment the elevation in mean arterial pressure produced by cross-clamping was reduced to preclamp levels in the TC group and only partially (52%) in the NP group, despite very high doses of nitroprusside. Cardiac output (CO) increased in the NP group by 115% and decreased by 36% in the TC group. This increase in CO translates into a large (101%) increase in cardiac minute work for the NP group.
  
  
  CONCLUSIONS
  The attenuation of clamp-induced hypertension by nitroprusside is associated with a dramatic increase in CO and cardiac work whereas the use of trimethaphan camsylate is not. The use of this ganglionic blocker may be more appropriate in this setting.
authors.affiliation: Department of Surgery, University of Michigan Medical School, Ann Arbor 48109.
authors.forename: M M
authors.initials: MM
authors.lastname: Moursi
authors.forename: M A
authors.initials: MA
authors.lastname: Facktor
authors.forename: G B
authors.initials: GB
authors.lastname: Zelenock
authors.forename: L G
authors.initials: LG
authors.lastname: D'Alecy
mesh_terms: D000818:Animals; D001012:Aorta, Abdominal / Q000502:physiology*; D002302:Cardiac Output / Q000502:physiology; D003250:Constriction; D004285:Dogs; D005730:Ganglionic Blockers / Q000627:therapeutic use*; D006439:Hemodynamics / Q000187:drug effects* / Q000502:physiology; D006973:Hypertension / Q000209:etiology / Q000517:prevention & control*; D007431:Intraoperative Complications / Q000517:prevention & control*; D008297:Male; D009599:Nitroprusside / Q000627:therapeutic use*; D013997:Time Factors; D014294:Trimethaphan / Q000627:therapeutic use*; D014665:Vasodilator Agents / Q000627:therapeutic use*
chemical_list: D005730:Ganglionic Blockers; D014665:Vasodilator Agents; D009599:Nitroprusside; D014294:Trimethaphan; C017774:trimethaphan camsylate