title: Preserved cerebral microcirculation during cardiogenic shock.
abstract: OBJECTIVE
  To hypothesize that in severe states of cardiogenic shock with profound decreases in buccal microcirculation, the cerebral microcirculation may be selectively protected. Decreases in buccal microcirculatory flow are closely associated with the severity and outcomes of circulatory shock.
  
  
  METHODS
  We investigated the concurrent changes in cerebral and buccal microcirculation, in a rat model of cardiogenic shock caused by left ventricular failure.
  
  
  METHODS
  Randomized prospective animal study.
  
  
  METHODS
  University-affiliated animal research laboratory.
  
  
  METHODS
  Sprague-Dawley rats.
  
  
  METHODS
  Studies were performed in ten male Sprague-Dawley rats, weighing between 450 and 550 g. After intraperitonial pentobarbital anesthesia and tracheostomy, a craniotomy exposed the parietal cortex for visualization of microcirculation. Animals then underwent thoracotomy and banding of ascending aorta producing left ventricular failure and cardiogenic shock.
  
  
  RESULTS
  Over a 4-hr interval, effects on arterial pressure, cardiac output, left ventricular end-diastolic volume, and ejection fractions were measured. The cerebral and buccal microcirculations were visualized concurrently with the aid of orthogonal polarization spectral imaging. Animals were randomized to identically treated controls in which the aorta was not ligated. Mean arterial pressure, cardiac output, and ejection fraction decreased strikingly and end-diastolic left ventricular volume more than doubled within 30 mins after aortic banding. The buccal microcirculation was concurrently reduced. However, cerebral microcirculatory flow was fully preserved.
  
  
  CONCLUSIONS
  In contrast to striking reduction in cardiac output and arterial pressures together with buccal microcirculatory flow, cerebral cortical microcirculatory flow was fully preserved during cardiogenic shock. These findings further document a dissociation between the systemic and cerebral circulations and potentially explain earlier clinical and experimental observations that the brain is selectively protected during severe states of cardiogenic shock in the absence of cardiac arrest.
authors.affiliation: Weil Institute of Critical Care Medicine, Rancho Mirage, CA, USA. drsheart@aol.com
authors.forename: Zhi
authors.initials: Z
authors.lastname: Wan
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Ristagno
authors.forename: Shijie
authors.initials: S
authors.lastname: Sun
authors.forename: Yongqin
authors.initials: Y
authors.lastname: Li
authors.forename: Max Harry
authors.initials: MH
authors.lastname: Weil
authors.forename: Wanchun
authors.initials: W
authors.lastname: Tang
mesh_terms: D000818:Animals; D002560:Cerebrovascular Circulation; D008297:Male; D008833:Microcirculation; D009061:Mouth Mucosa / Q000098:blood supply*; D010784:Photomicrography; D011446:Prospective Studies; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D012770:Shock, Cardiogenic / Q000503:physiopathology*