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Biomedical subjects

L B Rowell

Publications and source records attributed to L B Rowell.

At least 73 records · Page 4Linked to original sources

Renal vascular response to heat stress in baboons--role of renin-angiotensin.

To determine if hyperthermia in the baboon caused a reduction of renal blood flow (RBF) similar to that reported in man, we repeatedly exposed six unanesthetized male baboons (Papio cynocephalus) to ambient temperatures of 42.5-49.0 degrees C for 55-175 min. Internal temperatures rose 1.0-2.0 degrees C. On the average, RBF fell 23.7% per degrees C, renal vascular resistance (RVR) rose 34.0% per degrees C, and mean arterial pressure (MAP) fell by only 2.9 Torr. Plasma renin activity (PRA), measured in four baboons, rose 97.5% per degrees C. To investigate the role of the renin-angiotensin system in this renal response, we infused propranolol or saralasin (1-sar-8-ala-angiotensin II), an angiotensin II antagonist, systemically in 14 experiments on three baboons. Both propranolol and saralasin infusions prevented most of the reduction in RBF during hyperthermia. Propranolol prevented the increase in PRA. We conclude that renal vasoconstriction accompanies moderate hyperthermia in the awake baboon, and much of this response is mediated by a beta-adrenergic release of renin.

Angiotensin II↗

Altered control of skin blood flow during exercise at high internal temperatures.

We have investigated further the behavior of skin blood flow (SkBF) as internal temperature (measured as esophageal temperature (Tes)) rises in a heated exercising man. A previous study showed that when skin temperature (Tsk) is driven up in exercising men, the increase in SkBF is less than that found for the same Tes and Tsk in a resting man. In this study, we extended our observations into the range of higher Tes to see if SkBF (measured plethysmographically as changes in forearm blood flow) could be driven to higher levels despite competition with skeletal muscle for cardiac output. After Tsk was elevated to 38 degrees C by means of water-perfused suits, subjects exercised at 525-900 kp.m/min (86-147 W) for 17-30 min while Tsk was held at 38 degrees C. We found that SkBF increase per unit increase in Tes is attenuated at higher Tes. In seven men, the average slope obtained from linear regression of FBF on Tes below 38 degrees C was 7.6 flow units/degrees C. Above 38 degrees C, the average was 2.12 flow units/degrees C. In some subjects, the FBF response appeared virtually saturated at a plateau despite a steady rate of increase in Tes with time. Clearly, SkBF does not increase in direct proportion to Tes without bound. Other stimuli (presumably related to blood pressure regulation) interact either to reduce the rate of SkBF increase or to prevent any further increase after Tes exceeds 38 degrees C.

Adult↗

Control of baboon limb blood flow and heart rate-role of skin vs. core temperature.

To discover the relative importance of body core temperature versus bodyskin temperature in raising limb blood flow and heart rate, we exposed seven unanesthetized, chaired baboons (Papio anubis) to a variety of heating protocols. First, the baboons were exposed to a 40-45 degrees C environment for 0.75-1.5 h. Arterial or right atrial blood temperature (Tbl), skin temperature (Tsk), mean right iliac blood flow (MRIF), and heart rate (HR) all increased gradually during heating. On the average, HR increased from 106 to 160 beats/min and MRIF rose to 286% of control level. To separate influences of Tbl and Tsk on cardiovascular changes, we manipulated Tbl and Tsk independently via a heat exchanger incorporated into a chronic femoral arteriovenous shunt. In most baboons, the MRIF and HR response to a hot environment could be essentially duplicated by elevation of bTbl with Tsk held neutral, while elevation of Tsk with Tbl held neutral had little effect. One baboon exhibited significant response to Tsk elevation with Tbl held neutral, although subsequent manipulation of Tbl overrode this response. We conclude that the normal response to heating in baboons is mainly attributable to drives from internal temperature-sensitive mechanisms. Elevated Tsk shows large effects only in exceptional cases.

Animals↗

Lack of humanlike active vasodilation in skin of heat-stressed baboons.

To discover whether humanlike active skin vasodilation occurs in a sweating, subhuman primate, four unanesthetized male baboons (Papio anubis) were heated (blood temp = 39-39.5 degrees C) before and after arterial administration of the alpha-adrenergic blocking agent phenoxybenzamine HCl. Hcat stress alone increased common iliac vascular conductance (CIVC) from 1.2 to 3.7 ml-min-1-mmHg-1 (averages). alpha-Blockade alone increased CIVC from 1.2 to 3.3 ml-min-1-mmHg-1. Heat stress subsequent to alpha-blockade further increased CIVC by only 0.4 ml-min-1-mmHg-1. Thus, most of the rise in CIVC caused by heat stress could be mimicked by alpha-blockade. If, as in man, the dominant means of raising skin blood flow were nonadrenergic active vasodilation, the response of CIVC to heating would far exceed that due to alpha-blockade. We conclude that, in baboons, humanlike active vasodilation of skin plays no significant role in CIVC response to heat stress. Thus, the baboon is not an appropriate model for investigation of control of human skin circulation during hyperthermia.

Animals↗

Human cardiovascular and respiratory responses to graded muscle ischemia.

Responses of heart rate (HR), mean arterial blood pressure (MAP) ventilation (VE), and forearm blood flow (FBF) to different degrees of leg muscle ischemia were measured in eight subjects in a four-part experiment. Part I. Total circulatory occlusion (OCCL) of resting legs for 15 min had little or no effect on HR, MAP, VE, or FBF. Part II. OCCL of the legs for 3 min immediately after exercise at 50-250 W did not affect HR or end-tidal CO2; it lowered VO2 and VE and prevented recovery of MAP. Part III. OCCL beginning at end and 10, 20, 30 s before end of 7-min exercise (100-150 W) and continuing 3 min into recovery period produced sustained and graded increments (5-10 mmHg) in MAP, only small changes in HR, and accelerated recovery of VE while end-tidal CO2 remained constant. Part IV. OCCL at end and 30 s before end of exercise increased FBF 2.5-3.5 times; both skin and muscle vasodilated. Thus muscle ischemia preceded by exercise can raise MAP without affecting VE, whereas baroreflexes may lower HR and raise FBF. The results suggest the presence of muscle chemoreceptors whose major effect is on MAP.

Adult↗

Interactions between local and reflex influences on human forearm skin blood flow.

A three-part experiment was designed to examine interactions between local and reflex influences on forearm skin blood flow (SkBF). In part I locally increasing arm skin temperature (Tsk) to 42.5 degrees C was not associated with increases in underlying forearm muscle blood flow, esophageal temperature (Tes), or forearm blood flow in the contralateral cool arm. In part II whole-body Tsk was held at 38 or 40 degrees C and the surface temperature of one arm held at 38 or 42 degrees C for prolonged periods. SkBF in the heated arm rose rapidly with the elevation in body Tsk and arm Tsk continued to rise as Tes rose. SkBF in the arm kept at 32 degrees C paralleled rising Tes. In six studies, SkBF in the cool arm ultimately converged with SkBF in the heated arm. In eight other studies, heated arm SkBF maintained an offset above cool arm SkBF throughout the period of whole-body heating. In part III, local arm Tsk of 42.5 degrees C did not abolish skin vasoconstrictor response to lower body negative pressure. We conclude that local and reflex influences to skin interact so as to modify the degree but not the pattern of skin vasomotor response.

Adult↗

Altered control of skin blood flow at high skin and core temperatures.

Five subjects were studied during periods of controlled increases and decreases in skin temperature (Ts) over the Ts range of 34-40 degrees C. One protocol was designed to observe changes in forearm blood flow (FBF) and heart rate (HR) with changes in core temperature (Tc; right atrial blood temperature and esophageal temperature were measured) with Ts held constant at two levels. FBF and HR changed linearly with Tc in the Tc range of 37-38 degrees C with Ts constant at 38 degrees C. A second protocol imposed Ts changes at two levels of Ts and Tc; this protocol also included a prolonged cooling period. The influence of Ts on FBF and HR was reduced when Ts changes occurred at an elevated Ts and Tc, and FBF showed considerable hysteresis during cooling. We conclude that a linear model for the control of FBF or HR is inadequate as a tool for predicting the control of these variables.

Adult↗

Forearm skin and muscle vascular responses to prolonged leg exercise in man.

To determine the cutaneous and resting skeletal muscle vascular responses to prolonged exercise, total forearm blood flow (FBF-plethysmography) (5 men) and forearm muscle blood flow (MBF-[125I]antipyrine clearance) (4 men) were measured throughout 55-60 min of bicycle exercise (600-750 kpm/min). Heart rate (HR) and esophageal temperature (Tes) were also measured throughout exercise. FBF showed only small changes during the first 10 min followed by progressive increments during the 10-40 min interval and smaller rises thereafter. For the full 60 min of exercise, there was an average increase in FBF of 8.26 ml/100 ml-min. MBF showed an initial fall with the onset of exercise (on the average from 3.84 to 2.13 ml/100 ml-min) which was sustained or fell further as exercise continued, indicating that increments in FBF were confined to skin. Much of the increase in FBF occurred despite essentially constant Tes. Results suggest that the progressive decrements in central venous pressure, stroke volume, and arterial pressure previously seen during prolonged exercise are due in part to progressive increments in cutaneous blood flow and volume.

Adult↗