The accuracy of transit-time ultrasonic flow probes for measurement of regional blood flow and cardiac output was evaluated after long-term implantation in sheep. Transit-time flow probes (3, 4, 6, and 20 mm) accurately measured flow in vitro. Recalibration in vivo demonstrated that this accuracy was maintained after 1-9 mo of implantation on the left circumflex coronary (3-mm probe), cranial mesenteric (6-mm probe), left renal (4-mm probe), and left external iliac (6-mm probe) arteries of sheep. The flow probes also showed good zero stability. However, a transit-time flow probe (20 mm) chronically implanted on the pulmonary trunk significantly underestimated cardiac output compared with thermodilution or timed collection of blood. Although this flow probe underestimated flow, the response was linear. Bilateral carotid occlusion caused mesenteric, renal, and iliac vasoconstrictions, confirming that innervation of these vascular beds was undamaged. For experimental purposes, regional blood flow was measured with transit-time flow probes and cardiac output was measured with electromagnetic flow probes calibrated against thermodilution. In summary, transit-time flow probes reliably and accurately measure regional blood flow over many months in adult sheep, but, to measure cardiac output in sheep, the probes must be calibrated in vivo against another reference technique.
The regional hemodynamic effects of 5 days of intravenous infusion of corticotropin (ACTH) (5 /xg/kg per day) were examined in conscious sheep (n=8). Mean arterial pressure increased from 81 ±2 to 93±3 mm Hg (/><.001) on day 2 of ACTH and remained at this level during the infusion. Cardiac output increased from 5.13±0.19 to 6.06±0.33 L/min (/ ) <.O1) because of an increase in stroke volume from 65±4 to 79±8 mL per beat (P<.01); heart rate remained unchanged. ACTH did not alter total peripheral conductance but had differential effects on regional conductances. Mesenteric conductance fell from 5.8±0.2 to a minimum of 4.9±0.3 (mL/min)/mm Hg (P<.05), and renal conductance increased from 3.5±0.3 to 4.6±0.3 (mL/min)/ mm Hg (P<.001). There was a small increase in iliac conductance (f<.05) and no change in coronary conductance. Mesenteric and iliac conductances fell progressively over 24 to 48 hours, whereas renal conductance increased rapidly after 3 hours of ACTH, reaching a maximum after 6 hours. Renal blood flow was increased during ACTH infusion from 278±18 to 403±23 mL/min (P<.001); mesenteric C orticotropin (ACTH) administration increases blood pressure in both humans 1 -3 and experimental animals. 46 In conscious sheep intravenous infusion of ACTH results in an increase in arterial blood pressure within 24 hours, which is sustained as long as ACTH is infused over a 5-to 10-day period. 7 ACTH hypertension can be reproduced by infusion of a combination of adrenocortical steroids and is dependent on the presence of the adrenal glands but not on intact adrenal innervation. 48 The hypertension is associated with an increase in plasma volume, without a significant change in extracellular fluid volume.9 A volume component of the hypertension is also suggested by the finding that the ACTH-induced rise in blood pressure can be modulated by alterations in sodium status. Long-term sodium loading magnifies the pressure rise produced by ACTH, and long-term dietary sodium restriction blunts the rise.10 " The hemodynamic profile of ACTH hypertension in conscious sheep is characterized by an elevated cardiac output (CO), with no change in total peripheral resistance. peripheral resistance to remain constant in the presence of renal vasodilatation, vasoconstriction must be occurring in other vascular beds. In the present study the effect of ACTH infusion on regional hemodynamics was examined in conscious sheep instrumented with electromagnetic flow probes to measure CO and with transittime flow probes to measure regional arterial blood flows. The aim of the study was to examine the regional hemodynamic effects of ACTH and to determine whether ACTH acts selectively to cause vasoconstriction in one vascular bed or whether the vasoconstriction is a more generalized phenomenon. MethodsMerino cross ewes (35-to 45-kg body weight), oophorectomized and with carotid artery loops, were housed in metabolism cages in association with other sheep. They were not used for at least 4 weeks after surgery until they were accustomed to ...
We studied the cardiovascular responses to 5 days' infusion of aldosterone (10 micrograms/h) and cortisol (5 mg/h) to determine the possible contribution of mineralocorticoid and glucocorticoid actions to the regional hemodynamic changes caused by corticotropin. These infusion rates produce plasma levels similar to those seen during corticotropin stimulation. In five conscious sheep aldosterone progressively increased mean arterial pressure (P < .001) to a maximum of 11 mm Hg on day 5, whereas cortisol increased pressure by 5 mm Hg (P < .01) within 24 hours. Cardiac outputs on the control day and on day 5 of infusion were 4.4 +/- 0.3 and 4.9 +/- 0.3 L/min, respectively, for aldosterone and 4.3 +/- 0.4 and 5.0 +/- 0.4 L/min for cortisol. Neither steroid significantly altered total peripheral conductance, but they had different, nonuniform regional hemodynamic effects. Mesenteric conductance fell progressively with aldosterone from 7.14 +/- 0.35 (mL/min)/mm Hg to a minimum of 6.17 +/- 0.38 (P < .01) on day 5 of infusion. Mesenteric conductance was transiently reduced with cortisol, but this was not significant over the 5 days. Renal conductance was unchanged with aldosterone, but cortisol caused a rapid, sustained increase in renal conductance from 2.9 +/- 0.3 to 4.0 +/- 0.4 (mL/min) / mm Hg (P < .001) within 24 hours, similar to the increase caused by corticotropin. As with corticotropin there were only minor changes in the coronary and iliac vascular beds. In summary, these two endogenous steroids had contrasting, nonuniform regional hemodynamic effects, aldosterone causing mesenteric vasoconstriction, and cortisol causing renal vasodilatation.(ABSTRACT TRUNCATED AT 250 WORDS)
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