Hemodynarnics of Spontaneously Hypertensive Rats in Conscious State

Abstract

SUMMARYCardiac output of unanesthetized spontaneously hypertensive rats (SHR) and normotensive control rats (NCR) was measured by an aortic pressure pulse contour method. A catheter was introduced into the aortic arch under ether anesthesia and aortic pressure curves were recorded after the recovery from anesthesia. Stroke volume was calculated by reading required pressure and time data on the tracings and substituting them into a special equation. Cardiac output per min per body weight was not significantly different between SHR and NCR. Arterial pressure and total peripheral resistance were higher in SHR than in NCR. On ganglion blockade with hexamethonium bromide in the conscious state, arterial pressure decreased more markedly in SHR than in NCR. Though arterial pressure was still significantly (P< 0.05) higher in SHR after blockade, cardiac output was larger in SHR more than to account for the difference in arterial pressure. Total peripheral resistance was lower in SHR than in NCR after blockade. It is concluded that, even in the conscious state as in the anesthetized state, the major contribution to the hypertensive state in SHR is an increase in total peripheral resistance due to an elevation of the sympathetic tone.Additional Indexing Words: SHR Sympathetic hypertension Ganglion blockade Cardiac output Aortic compliance CUTE experiments on anesthetized spontaneously hypertensive rat or SHR (Okamoto and Aoki1)) have indicated that the hypertensive state is principally ascribable to an increase in total peripheral resistance due to an elevation of the sympathetic tone.2)-5) However, the question still remains unsettled as to whether this also holds for the unanesthetized, conscious state. Therefore, in the present study, aortic pressure was recorded in conscious SHR and control Wistar rats and cardiac output was calculated by a pulse contour method. This and other hemodynamic parameters were compared

Mechanism of elevation of hindquarter vascular resistance in spontaneously hypertensive rats.

“…Also in anesthetized SHR, the increase in efferent discharge in the splanchnic nerve was quantitated by IRIUCHI-JIMA (1973). That the sympathetic nerves, in the conscious state as well play an important role in hypertension in SHR was shown by NUMAO et al (1975), who observed normalization of total peripheral resistance by ganglion blockade with hexamethonium. Increased sympathetic discharge in conscious SHR was observed with the splanchnic nerve by JUDY et al (1976) and with the renal nerve by LUNDIN and THOREN (1982) and LUNDIN et al (1984).…”

“…However, this is due to a larger cardiac index in SHR than in NCR after ganglion blockade. Total peripheral resistance is somewhat lower in the former than the latter after blockade (NUMAO et al, 1975). The larger cardiac index may be ascribable to left ventricular hypertrophy and some possible change in the capacitance section of the circulatory system of SHR (NILSSON and FOLKOW, 1980;.…”

Central hemodynamics in the developmental stage of spontaneous hypertension in the unanesthetized rat.

“…50 Pentobarbital anesthesia and thoracotomy in the rat produce marked decreases in cardiac output in both SHR and Wistar rats, as well as decreases in aortic pressure in the SHR. 19 Thoracotomy alone can also reduce mean arterial pressure in the SHR up to 48%. 16 Indicator-dilution techniques as used in the study of spontaneous hypertension 11 ' 1J require anesthesia and are further limited by not being capable of measuring transient changes in cardiac output occurring over a short time period.…”

The measurement of heat production, mechanical power, and oxygen consumption of the isolated working rat heart

“…2). The in vivo compliance of the aortic segment of the arterial tree has been determined at 36 x 10 -3 cm 3 kPa -1 (27,31) which compares with the upper section of the model's compliance range (4.5 • 10-~36 • 10 -3 cm 3 kPa -1, Fig. 8).…”