Development of techniques for the continuous measurement of regional blood flow and vascular resistance in intact small animals has been impeded primarily by the bulkiness of flow probes. The availability of an ultrasonic pulsed Doppler flowmeter system enabled us to construct miniaturized probes using 1-mm-diameter piezoelectric crystals that emit a 20-mHz signal and receive the reflected sound waves from passing blood cells. The finished flow probe is approximately 2.5-4 mm long and 2 mm in cross-sectional diameter with lumen diameters appropriate for the rat, ranging from 0.7 to 1.2 mm. This report describes the materials and methods involved in constructing and implanting the probes in rats to monitor renal, mesenteric, and hindquarter blood flow velocity. The accuracy of the pulsed Doppler method in detecting changes in regional blood flow and vascular resistance was established by the demonstration of a highly significant correlation between velocity recorded from the Doppler unit and volume flow recorded simultaneously. These data indicate that the ultrasonic pulsed Doppler flowmeter provides the opportunity to measure changes in regional blood flow and vascular resistance in a conscious freely moving rat.
The results provide strong evidence that both the perceived odor and cognitive expectations about a chemical can significantly affect how individuals respond to it. Moreover, because naive control subjects appear to exhibit extreme variation in their cognitive evaluations of chemical effects, there may be limited value in using non-exposed controls to assess the irritancy of chemicals for worker populations.
A large body of evidence indicates that the central nervous system plays an essential role in the pathogenesis of hypertension. However, in many cases the specific brain regions involved and the mechanisms by which these regions promote hypertension are not known. In recent years, research in this and other laboratories has attempted to determine the mechanisms by which neural and humoral signals arising in response to pathological conditions (often occurring in the periphery) interact with the central nervous system to produce hypertension. In this article, we illustrate the coupling of peripheral and central factors in the pathogenesis of hypertension by examining the central actions of angiotensin II and mineralocorticoids in the expression of renal hypertension and mineralocorticoid-salt hypertension, respectively. We also review recent data from this laboratory illustrating the involvement of medullary vasomotor centers in the development of neurogenic hypertension after sinoaortic deafferentation and in the maintenance of hypertension in the spontaneously hypertensive rat.
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