Preserved cerebral microcirculation during cardiogenic shock.

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.

DESIGN

We investigated the concurrent changes in cerebral and buccal microcirculation, in a rat model of cardiogenic shock caused by left ventricular failure.

DESIGN

Randomized prospective animal study.

SETTING

University-affiliated animal research laboratory.

SUBJECTS: Sprague-Dawley rats.

INTERVENTIONS: 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.

MEASUREMENTS AND MAIN

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.