Regional distribution of blood flow during arterial hypertension produced by lesions of the nucleus tractus solitarii in rats.

Abstract

SUMMARY Changes in the fractional distribution of cardiac output (FF), organ blood flow, and regional vascular resistance were measured by the isotope dilution technique of Sapirstein using 86 Rb as indicator in unanesthetized rats during acute arterial hypertension produced by bilateral lesions of the nucleus tractus solitarii (NTS). After NTS lesions, the FF was significantly reduced in skin, muscle, and colon, increased in ventricular myocardium, spleen, and adrenal glands, and was unchanged elsewhere. Because of a marked reduction in cardiac output (CO) during hypertension, the absolute organ blood flow (FF x CO) was reduced in lesioned rats to 30-40% of control in skin, muscle, and colon and between 60% and 75% of control in most of the remainder of the gastrointestinal tract and renal cortex; it was unchanged in myocardium and endocrine glands. Resistance was substantially increased (4-to 6-fold) in skin, muscle and colon but was only moderately increased (1.5-to 2.5-fold) in the remaining organs. The results indicate that, while NTS lesions will increase resistance in most vascular beds, the response is unequally distributed, influencing skin, muscle, and colon disproportionately to other tissues. Because of an interaction between a reduction in CO and little autoregulation, blood flow is reduced primarily in skin, muscle, and colon. The pattern of redistribution of CO was consistent with the interpretation that NTS hypertension results from interrupting baroreceptor reflexes centrally. The pattern of redistribution of blood flow in rats with NTS lesions differs from that produced by deoxycorticosterone acetate-salt and renal ischemia. IN RATS, bilateral lesions of the nucleus tractus solitarii (NTS) results in the rapid development of arterial hypertension.1 In this model, termed NTS hypertension, the rise of blood pressure is presumed to be due to increased vasoconstrictor discharge resulting from central deafferentation of arterial baroreceptors by destruction of their primary synapse within NTS. As a result, the total peripheral resistance is markedly increased, leading to ventricular overload, reduction in cardiac output, progressive heart failure, and death associated with pulmonary edema within 3-4 hours.1 ' 2In the present study, we measured the changes in regional blood flow and in vascular resistances after lesions of NTS. Our objective has been 2-fold. First, we sought to determine whether the increase in total peripheral resistance produced by the lesion could be attributed to changes in vascular resistances within specific vascular beds reflecting, in turn, a differential activation of sympathetic neurons. Second, NTS lesions abolish arterial baroreceptor reflexes, 3 -4 and arterial baroreceptor activity is not uniformly distributed to all vascular beds, since vasoconstrictor activity in skeletal muscle is under greater baroreceptor control than that in kidney, skin, or the gastrointestinal tract. "10 Evidence of appropriate changes in resistance and flows in vascular beds after NTS lesions ...

Production of sustained hypertension by lesions in the nucleus tractus solitarii of the American foxhound.

“…Nevertheless, studies of regional blood flow by the isotope dilution technique in rats with NTS hypertension suggest that the maximum vasoconstriction occurs in skin, skeletal muscle and lower bowel, and that blood flow to the kidneys is normal in these animals. 29 The present data in dogs with NTS hypertension are similar to previous results in dogs with chronic norepinephrine infusion in that acute sodium retention was demonstrated in both studies. However, in dogs with intrarenal norepinephrine infusion, a consistent 25% reduction in renal plasma flow was demonstrated at 1, 5 and 11 days of infusion of this sympathetic neurotransmitter."…”

Abnormal oxygen homeostasis in the nucleus tractus solitarii of the spontaneously hypertensive rat

“…Electrolytic lesions of cardiovascular control areas in the NTS produce dramatic increases in ABP, leading to sustained arterial hypertension, suggesting that damage to the NTS may play an important role in the development of arterial hypertension (Doba & Reis, 1973; Nathan & Reis, 1977; Snyder et al . 1978). We have recently shown that in anaesthetized SHRs, resting local tissue $P_{{\mathrm{normalO}}_2}$ ($P_{\mathrm{normalt}{\mathrm{O}}_2}$) in the brainstem is significantly lower compared with normotensive Wistar rats, despite normal values of arterial $P_{{\mathrm{normalO}}_2}$ (Marina et al .…”

Role of the Medulla Oblongata in Hypertension

“…The vasoconstriction is regionally differentiated, being more intense in skin, muscle, and portions of the gastrointestinal tract. 13 The increase in total peripheral resistance leads to ventricular overload, reduction in cardiac output, progressive heart failure, and pulmonary edema, and ends in death within 3 to 4 hours. 12 The same response can be elicited by destroying NTS neurons with a high dose of kainic acid, 14 an analogue of L-glutamate.…”