Ventrolateral medullary lesions and fastigial cardiovascular response in beagles.

Abstract

These studies were designed to verify that the putative vasomotor center in the rostral ventrolateral medulla (RVLM) contained the outflow paths for the fastigial nucleus (FN) sympathoexcitatory cardiovascular response. If so, then lesions placed by radiofrequency heating (75 degrees C) or application of kainic acid (40 mM) pledgets would reduce or ablate the pressor-tachycardia response after electrical stimulation of FN. Anesthetized beagles (alpha-chloralose, 115 mg/kg) were used in this study to maintain consistency in medullary brain stem anatomy. A ventral brain stem approach exposed the three chemosensitive zones of Mitchell, Schlaefke, and Loeschcke. In other species the intermediate zone and a portion of the rostral zone underlie the Hokfelt C1 cell group and the putative RVLM vasomotor center. Heart rate, arterial and left ventricular (LV) pressures, and maximal rate of pressure development (LV dp/dt) increased 14-84% above control levels in response to stimulating FN 5-10 times the stimulation threshold. The cardiovascular response was abolished in four of six dogs that received bilateral radiofrequency lesions at a depth of 1-2 mm. In five of seven dogs that received kainate surface lesions, the response was substantially reduced but not abolished. These lesions were effective only in the RVLM, above the corresponding intermediate, but not adjacent rostral or caudal chemosensitive areas. The data support the hypotheses of others that an epinphrine-containing cell group in this region is a final common pathway of sympathoexcitation. Expression of the FN cardiovascular response is primarily mediated through this vasomotor region previously identified by others in the rat, cat, rabbit, and primate.(ABSTRACT TRUNCATED AT 250 WORDS)