Search PubMed⌕ Search

Biomedical subjects

L B Rowell

Publications and source records attributed to L B Rowell.

At least 37 records · Page 2Linked to original sources
PubMed1989

Hypoxemia raises muscle sympathetic activity but not norepinephrine in resting humans.

The experimental objective was to determine whether moderate to severe hypoxemia increases skeletal muscle sympathetic nervous activity (MSNA) in resting humans without increasing venous plasma concentrations of norepinephrine (NE) and epinephrine (E). In nine healthy subjects (20-34 yr), we measured MSNA (peroneal nerve), venous plasma levels of NE and E, arterial blood pressure, heart rate, and end-tidal O2 and CO2 before (control) and during breathing of 1) 12% O2 for 20 min, 2) 10% O2 for 20 min, and 3) 8% O2 for 10 min--in random order. MSNA increased above control in five, six, and all nine subjects during 12, 10, and 8% O2, respectively (P less than 0.01), but only after delays of 12 (12% O2) and 4 min (8 and 10% O2). MSNA (total activity) rose 83 +/- 20, 260 +/- 146, and 298 +/- 109% (SE) above control by the final minute of breathing 12, 10, and 8% O2, respectively. NE did not rise above control at any level of hypoxemia; E rose slightly (P less than 0.05) at one time only with both 10 and 8% O2. Individual changes in MSNA during hypoxemia were unrelated to elevations in heart rate or decrements in blood pressure and end-tidal CO2--neither of which always fell. We conclude that in contrast to some other sympathoexcitatory stimuli such as exercise or cold stress, moderate to severe hypoxemia increases leg MSNA without raising plasma NE in resting humans.

Adult↗
PubMed1988

Venomotor responses during central and local hypoxia.

Venomotor responses, measured as the pressure rise in occluded forearm veins, were used in a two-part experiment to test presence or absence of sympathetic neuroeffector mechanisms in 10 men made moderately to severely hypoxemic. In part I, forearm venoconstriction was induced by ice water on the contralateral forearm (a spinal reflex) in eight supine, resting men who breathed air, 10.3% oxygen or 7.7% oxygen. Large reflex venoconstrictions persisted during hypoxia. In part II (seven men), venoconstriction was centrally induced by exercise while subjects were 1) normoxic; 2) arm hypoxic, body normoxic; 3) arm hyperoxic (or normoxic), body hypoxic; or 4) both arm and body hypoxic. Arm vs. body oxygen tensions were separated by occluding the arm as one gas mixture was breathed, then switching the subject to another mixture as the arm remained occluded. Strong venoconstrictor responses to moderate exercise (100-150 W) persisted during both local and central hypoxemia. We conclude that moderate to severe hypoxemia does not block, pre- or postjunctionally, sympathetic venoconstriction that originates from spinal reflexes (cold). Venoconstriction in exercise (presumably originating in higher centers) was not blocked by moderate hypoxemia; severe hypoxemia was not studied.

Adult↗
PubMed1988

Muscle blood flow in humans: how high can it go?

The question is whether skeletal muscle blood flow (MBF) in humans can reach the peak values of 300-400 ml.100 g-1.min-1 seen in dogs, ponies, and rats. The answer depends on the total mass of active muscle. Total MBF has a fixed upper limit or maximal value set by maximal cardiac output--normally about 25 1.min-1. In a 75-kg man with 30 kg of muscle, total MBF is 22 1.min-1 or 73 ml.100 g-1.min-1. As the mass of active muscle decreases, MBF available per 100 g of muscle increases, but a "maximal" value can no longer be defined because it becomes a function of blood pressure and muscle vascular conductance (and not maximal cardiac output) for which "maximal" values are also undefined. This paper emphasizes three key points. First, pumping capacity of the human heart is much smaller per kg body weight than in many other species. Second, human cardiac pumping capacity is exceeded by the vasodilator capacity of skeletal muscle; thus, so-called "peak MBF" often occurs when metabolic vasodilator and blood pressure-regulating vasoconstrictor mechanisms are competing. Third, in order to observe a peak MBF, one must maximally activate a mass of muscle that is too small to overwhelm cardiac pumping capacity. This experimental approach has revealed that MBF can exceed 300 ml.100 g-1.min-1 in small masses of active human muscle. The upper limit for flow, which depends on pressure, and for vascular conductance is still unknown.

Cardiac Output↗
PubMed1987

Human cardiovascular adjustments to acute hypoxaemia.

Traditionally, cardiovascular adjustments to hypoxaemia are viewed as resultants of competing local vasodilation and vasoconstriction via arterial chemoreflexes with net effects of increased cerebral and coronary blood flows (local) and reduced flow to visceral organs and muscle (reflex). Although true in asphyxia, breathing activates lung mechanoreceptors which reduce vagal outflow and apparently, in humans, abolishes sympathetic vasomotor activity (SNA). During rest, moderate to severe hypoxaemia (PaO2 = 35 to 27 mmHg) caused no splanchnic, cutaneous or muscle vasoconstriction. Local vasodilator effects of hypoxaemia were not sufficient to overwhelm vasoconstriction; splanchnic arterioles responded normally to infused noradrenalin (NA) during hypoxaemia. Possibly, central effects of hypoxaemia blunt SNA or peripheral, prejunctional effects impair neuronal release of NA. Persistent orthostatic tolerance with normal skeletal muscle vasoconstriction and retained spinal venomotor reflexes during hypoxaemia argue against prejunctional inhibition of NA release. Results so far suggest that beyond a certain threshold, hypoxaemia centrally inhibits SNA. In contrast to rest, even moderate hypoxaemia during exercise markedly increases plasma NA concentration (and SNA), but the usual relationship among splanchnic blood flow, plasma NA and heart rate was not observed--NA and heart rate rose together, whereas the predicted splanchnic vasoconstriction was not observed. In moderate hypoxaemia, muscle blood flow and cardiac output are greater than in normoxia at a given submaximal oxygen uptake; but at maximal oxygen uptake, blood pressure, total vascular conductance and maximal cardiac output are unaffected. Given the fixed upper limit to cardiac output and the greater capacity of active muscle to vasodilate and exceed cardiac pumping capacity during hypoxaemia, we conclude that blood pressure is maintained by baroreflex- (not chemoreflex-) mediated vasoconstriction in the active muscle which must be the primary target of increased SNA and the source of NA.

Adaptation, Physiological↗
PubMed1987

Does inadequate oxygen delivery trigger pressor response to muscle hypoperfusion during exercise?

In dogs running on a treadmill at 2 or 4 mph or 4 mph plus 10% incline, graded reductions in hindlimb perfusion reflexly elicited pressor responses. To test the idea that systemic arterial pressure (SAP) is raised by accumulation in muscle of a nerve-activating "pressor substance" release when O2 delivery becomes inadequate, arterial O2 content (CaO2) was reduced 29.1% by carbon monoxide (CO) inhalation before repeating exercise at 2 mph. We reasoned that the pressor substance, or related substances, should appear in femoral venous blood and be correlated to SAP. [K+] behaved inappropriately as a signal to raise SAP, i.e., when flow was reduced, SAP rose markedly with little or no change in [K+]. SAP was well correlated to pH and [lactate] over the three work loads. Compared with the same work load with normal CaO2, CO shifted the relation between SAP and terminal aortic flow rightward 0.30 l/min (34.5%) and the relation between SAP and PO2 leftward 7.7 mmHg. CO did not affect the relation of SAP to terminal aortic O2 delivery, hindlimb O2 uptake index, pH, or [lactate]. Thus pressor responses are apparently generated when O2 delivery falls below some critical level causing accumulation of a pressor substance the release of which is linked to a metabolic event that precipitates lactate accumulation.

Animals↗
PubMed1987

Unaltered norepinephrine-heart rate relationship in exercise with exogenous heat.

We measured plasma norepinephrine (NE) concentration, an index of sympathetic nervous activity, and epinephrine (E), an index of adrenal medulla activity, in six normal young men during mild to severe exercise, with and without superimposed heat stress. The primary objective was to observe whether the normally close relationship between heart rate and log NE concentration in upset when heart rate at a given work load is increased by heat stress. Exercise, beginning at 50 W, was graded in 50-W increments lasting 10 min each up to 200 W, which lasted 5-10 min. Each subject went through the protocol twice, once with skin temperature kept low by a water-perfused suit and then with skin temperature raised to 38 degrees C. Exogenous heart stress raised log circulating NE concentration in proportion to the rise in heart rate at a given work load so that the usual relationship between these variables, previously observed during other stresses, was preserved. In contrast to some other stresses, heat stress had no added effect on E concentration, indicating that this stress during exercise raises sympathetic neural activity (as reflected in the rise in NE) without stimulating additional adrenal release of E.

Adult↗
PubMed1986

Lack of effect of moderate hypoxaemia on human postural reflexes to skeletal muscle.

The effect of moderate hypoxemia upon postural sympathetic vasoconstrictor reflexes in skeletal muscle was studied in five healthy young students, aged 20-30 years. The vasoconstrictor response to head-up tilt was studied in brachio radial muscle kept at heart level and in the anterior tibial muscle. The local sympathetic veno-arteriolar axon reflex was studied in the anterior tibial muscle placed at heart level and lowered 30-50 cm below heart level. Muscle blood flow was measured by the local 133Xe wash-out technique. The measurements were carried out with the subject breathing atmospheric air and with the subject breathing 10-11% oxygen. No sign of orthostatic intolerance was seen during hypoxaemia as arterial blood pressure remained constant in the tilted position. Hypoxaemia did not alter the head-up tilt induced vasoconstriction in brachio-radial and anterior tibial muscles. The vasoconstriction elicited by the local veno-arteriolar reflex was slightly reduced during hypoxaemia. The results suggest that central orthostatic vasoconstrictor reflexes to muscle are essentially normal during moderate hypoxaemia, but local veno-arteriolar reflexes are slightly attenuated. This does not, however, significantly alter blood pressure control during head-up tilt.

Adult↗
PubMed1986

Lack of sympathetic vasoconstriction in hypoxemic humans at rest.

A three-part experiment was designed to show whether hypoxemia alters splanchnic vasomotor responses to other stresses by vasodilating splanchnic organs, preventing norepinephrine (NE)-induced vasoconstriction, or altering total sympathetic nervous activity (SNA) assessed by plasma levels of NE and epinephrine (Epi). Splanchnic blood flow (SBF) was measured by plasma clearance and hepatic extraction of indocyanine green (constant infusion). Part I: two degrees of hypoxemia [fractional concn of inspired O2 (FIO2) = 10.4 and 7.6%, arterial PO2 (PaO2) = 34.8 and 27 Torr] caused a small splanchnic vasodilation; resistance fell 16 and 26%, respectively, in five men; and SBF rose from 1.78 to 2.04 (10.4% O2) and to 2.02 1 X min-1 (7.6% O2). Plasma NE was unaffected by hypoxemia and by a fall in mean arterial pressure from 82 to 63 Torr at FIO2 = 7.6%. Part II: NE infused intravenously to raise pressure by 20 Torr in five subjects breathing air and 10.3% O2 caused splanchnic vasoconstriction irrespective of PaO2. Part III: in six subjects, two levels of hypoxemia (FIO2 = 10.4 and 7.7%) did not increase NE levels in five men, and Epi increased in two men only at FIO2 = 7.7%. We conclude that hypoxemia caused only a small splanchnic vasodilation not mediated by Epi, did not prevent transient NE-induced vasoconstriction, and either did not significantly increase SNA or prejunctionally inhibited NE release. Severe hypoxemia abolished the rise in NE and heart rate in response to falling pressure.

Adult↗
PubMed1986

Is peak quadriceps blood flow in humans even higher during exercise with hypoxemia?

Blood flow (Q) to quadriceps muscles was measured by thermal dilution in six men during rest and dynamic exercise [20, 38, and 42.5-60 W (peak load)] restricted to quadriceps of one leg in normoxia (N) and hypoxemia (H; 10-11% O2). Without exception Q and quadriceps vascular conductance were higher in H. Arterial mean pressure, lactate, norepinephrine, and epinephrine all rose when work exceeded 20 W. Q in N was 0.25, 3.28, 4.27, and 5.81 l/min (rest to peak exercise) and in H was 0.25, 4.08, 5.24, and 6.58 l/min. Peak Q per 100 grams of muscle (quadriceps mass = 2.2 kg) was 273.3 (N) and 308.8 ml/min (H). Quadriceps VO2 (Q X femoral A-VO2 difference) was 25, 388, 556, and 771 ml/min (N) and 25, 390, 556, and 743 (lower peak load in H)-net mechanical efficiency was 23%. Muscle O2 delivery (Q X arterial O2 content) was unaffected by H; O2 extraction fell in H but femoral venous O2 content remained near 6 (N) and 5 ml/100 ml (H) at all workloads, in contrast to much lower values in whole body exercise. In H muscle Q can rise to even higher peak values, without apparent limit, when the mass of active muscle is too small to overwhelm the pumping capacity of the heart.

Adult↗
PubMed1986

Hepatic splanchnic function in acutely hypoxemic humans at rest.

Splanchnic metabolism of O2, glucose, and lactate was studied in five normal men during rest while breathing air, 10.4% O2 [arterial O2 partial pressure (PaO2) = 34.8 Torr], and in four men breathing 7.6% O2 (PaO2 = 27.0 Torr). Despite reduction in arterial O2 content to 10.7 ml/100 ml, splanchnic O2 uptake (VO2) and arteriovenous O2 difference remained constant through a fall in hepatic venous O2 content to 7.3 ml/100 ml. Hepatic release of glucose and uptake of lactate were unaffected by either moderate or severe hypoxemia. In five other men hepatic extraction efficiency, removal rate, and clearance of norepinephrine (NE) and epinephrine (E) (radioenzymatic assay) were determined, while air and 10.27% O2 were breathed, and while NE was infused over widely ranging rates (constant in a given subject). Over arterial concentrations of 1.8-17 ng/ml for NE and 0.03-0.3 ng/ml for E, splanchnic removal was closely related to arterial concentration and was unaffected by hypoxemia. NE extraction efficiency rose from 60 (control) to 94% (during infusion in normoxia and hypoxemia); E extraction efficiency remained constant at 85% under all conditions. Hepatic clearances of both NE (556-824 ml/min) and E (630-804 ml/min) were unaffected by hypoxemia. The only observed deficiency in hepatic function was a significant decrease in extraction of indocyanine green in all 10 subjects at both levels of hypoxemia.

Acute Disease↗
PubMed1986

The nature of the exercise stimulus.

The two foremost hypotheses concerning the nature of the exercise stimulus are: Central Command. Centrally generated signals activate in parallel cardiovascular and skeletal muscle motor systems; Muscle Chemoreflex. Chemosensitive nerves within the skeletal muscle detect local accumulations of metabolites which reflect disparities between muscle blood flow and metabolism. The focus is mainly on the second hypothesis. The neurophysiological basis for this reflex is well established. Accumulations of metabolites within ischemic muscle reflexly trigger pressor responses that are abolished by blockade of sensory nerves from muscle. However, such blockade does not abolish circulatory responses to static or mild dynamic exercise. To assess the importance of muscle chemoreflexes, stepwise partial occlusions of the terminal aorta were made in exercising dogs. The rise in arterial pressure was related to reductions in terminal aortic flow and arterial pressure below the occluder. In mild exercise sensitivity of the reflex was low until flow was substantially reduced to a threshold. In heavier exercise sensitivity of the reflex was high (no threshold) and could provide a tonically active exercise stimulus. The nature of the metabolic signal is unknown. The pressor response was most closely related to femoral venous lactate concentration and unrelated to femoral venous K+ or PO2.

Animals↗
PubMed1985

Stability of heterogeneity of myocardial blood flow in normal awake baboons.

Regional myocardial blood flow has been thought to be relatively uniform, in accord with the singular function of myocardial cells. However, considerable spatial heterogeneity has been observed in the hearts of anesthetized animals and in isolated hearts. Studies were undertaken in a total of 13 baboons. Eleven were awake, healthy animals sitting in chairs at rest or feeding, some performed mild leg exercise (wheel turning), and others were subjected to whole body heating; two were anesthetized, methodological controls. Microspheres (15 +/- 3 micron diameter, 0.5 X 10(6)/kg body weight) were injected via a catheter into the apex of the left ventricle while arterial blood was sampled at a constant rate for calculating cardiac output. Microspheres with different labels were injected at six intervals of 20 minutes to several hours. On sacrifice, the hearts were sectioned into 204 locatable pieces (left ventricle, 168; right ventricle, 27; and atria, 9). Average resting myocardial flow was 2.1 +/- 0.2 ml/g per min (mean +/- SD, n = 11). Left and right ventricles and atria comprised 70 +/- 2% (n = 13), 20 +/- 2%, and 10 +/- 2% respectively of the total heart mass while receiving 80 +/- 3%, 16 +/- 2%, and 4 +/- 2% of the total myocardial flow. Thus, mean left ventricular flow was 114 +/- 5% of the average for the whole heart, right ventricular flow was 81 +/- 13%, and atrial flow was 41 +/- 13%. Myocardial flow heterogeneity was marked; in left ventricle, regional flows ranged from one-third to two times the mean, the relative dispersion (= standard deviation/mean) of regional flows, corrected for methodological scatter and temporal variation, was 0.33 +/- 0.06 (n = 67) in the whole heart, 0.26 +/- 0.07 in left ventricle, 0.32 +/- 0.11 in right ventricle, and 0.22 +/- 0.19 in the atria. The pattern of regional flows in each heart tended to remain stable with time. In each piece averaged over time, the relative dispersion due to temporal heterogeneity was 0.11 +/- 0.03 (n = 2040) in the whole heart, 0.09 +/- 0.03 in the left ventricle, 0.15 +/- 0.05 in the right ventricle, and 0.23 +/- 0.06 in the atria. The conclusion is that the degree of spatial heterogeneity of local myocardial flows in conscious primates is similar to that of anesthetized animals and isolated hearts, and is much greater than that due to temporal fluctuations.

Animals↗
PubMed1984

Cardiovascular responses to heat stress and blood volume displacements during exercise in man.

Subjects exercised in the upright position at approximately 50% of maximal oxygen consumption in four situations: in 25 degrees C air, in 45 degrees C air [mean skin temperature (Tsk) 35 degrees C], in 35 degrees C water immersed to the level of the xiphoid process, and finally wearing a suit perfused with 35 degrees C water. The water immersion prevented gravitational shifts of blood volume to the legs. In this situation the forearm blood flow (FBF) rose continually with increasing core temperature (Tes) in contrast to the attenuation in rise above 38 degrees C Tes in 45 degrees C air. The differences were significant above 38.6 degrees C Tes in experiments in eight subjects. The effects of immersion on cardiac output (CO), stroke volume (SV), and heart rate (HR) were studied in five of the subjects in relation to Tes, since the rate of rise of Tes was different in the four situations. CO and SV tended to be higher during both rest and exercise in the water than in the other three conditions, while HR rose in the same manner with increasing core temperature, except that it was lower in 25 degrees C air, where Tsk was lower. Thus, the prevention of hydrostatic shifts of peripheral venous volume permitted the maintenance of a higher SV and peripheral blood flow, and enhanced the ability of the circulation to deal with the combined exercise and heat stress.

Adolescent↗
PubMed1984

Reflex control of regional circulations in humans.

This study of autonomic control of the peripheral vascular system deals with reflex control of regional circulations, vasoconstriction in the upright posture, disturbances in the normal regulation caused by dysautonomia and spinal cord transection, regional vasomotor responses to thermal stress, and the overall sympathetic nerve activity in humans under stress. Data presented describe local and overall reactions that occur in normal and abnormal states. In varieties of stresses, humans adjust by increasing sympathetic nerve outflow in a highly predictable fashion. However, powerful local or humoral influences, such as those generated by hypoxia, hemorrhage, etc., are pitted against neurogenic vasoconstriction so that prediction of responses is very difficult.

Autonomic Nervous System↗
PubMed1984

Splanchnic vasomotor and metabolic adjustments to hypoxia and exercise in humans.

To determine whether hypoxia increases splanchnic vasoconstriction and impedes splanchnic metabolism during exercise, 11 subjects were exercised for 72 min at O2 uptake (VO2) of 1.8 1/min; 11% O2 was breathed during 30-50 min. Splanchnic blood flow (SBF), arterial and hepatic venous concentrations of indocyanine green (ICG), O2, CO2, metabolites, and catecholamines were determined in seven subjects; complete sets of all measurements were obtained from four. Arterial O2 content and tension fell from normal values to 12.3 ml/100 and to 32.2 Torr, respectively, during hypoxia; heart rate rose to 159 from 117 beats/min, arterial blood pressure was unchanged, and plasma norepinephrine (NE) and epinephrine (E) concentrations rose from 0.79 (NE) and 0.2 (E) ng/ml (normoxia) to 2.7 and 0.72, respectively, during hypoxia. SBF rose insignificantly from 1.14 (normoxia) to 1.35 l/min during hypoxia and fell significantly to 1.01 1/min after return to normoxia. Splanchnic VO2 was maintained at normal levels by increased extraction as hepatic venous O2 fell to 1.7 ml/100 ml and hepatic venous O2 tension to 7.5 Torr. Hepatic glucose release rose from 642 (normoxia) to 1,164 mg/min (hypoxia); lactate uptake increased from 0.26 to 2.1 mM/min; NE uptake rose from 417 to 1,508 ng/min, but hypoxia reduced ICG extraction by 28%. Thus hypoxia did not cause splanchnic vasoconstriction normally accompanying increases in HR and NE concentration or reductions in maximum VO2. SBF was maintained at a level sufficient to maintain all metabolic functions except ICG extraction.

Adult↗
PubMed1984

Attenuated skin blood flow response to hyperthermia in paraplegic men.

To clarify how skin and internal temperatures interact in control of skin blood flow, five male paraplegic subjects (lesions at the level of thoracic vertebrae 1-11) (29-47 yr old) were heated in water-perfused suits to elevate oral temperature (To) 1-1.5 degrees C. In part I only the insensate skin was heated; sensate skin was kept at 32-34 degrees C. No appreciable elevation of forearm blood flow (FBF) or sweating occurred, even with To at 38 degrees C. In part II the suit was applied to the whole body so that skin temperature was 40 degrees C, except for one arm that remained at 32-34 degrees C for FBF measurement. Sweating was noted above the lesion in all but one subject. FBF increased in all subjects but was far below levels previously reported for hyperthermic normal men; also, thresholds appeared elevated. To the extent that effector connections are intact, attenuated FBF response implies that either 1) some vasoconstrictor bias associated with cardiovascular regulation is active or 2) thermoregulatory effector outflow is diminished. If the latter is true, it follows that the effector outflow reduction relates to diminished afferent input. But the component of the effector outflow contributed by peripheral thermoreception is small; thus these findings may indicate that what is lacking in the afferent input is central thermoreception from below the lesion, possibly from the spinal cord itself.

Adult↗
PubMed1984

Hypoxemia increases plasma catecholamine concentrations in exercising humans.

To determine whether plasma catecholamine concentrations (a measure of sympathetic nervous activity [SNA]) rise above normoxic levels during exercise with hypoxemia, we exercised seven men for 15 min at three loads that required from 40 to 88% of maximal O2 uptake (VO2max). Subjects breathed room air on one day and 11-12% O2 on another with relative work loads corrected for the 24% fall in VO2max during hypoxemia. Hypoxemia caused large increments in norepinephrine (NE) concentration (radioenzyme technique) to 1.21 +/- 0.20 ng/ml (mean +/- SE), 2.79 +/- 0.38, and up to 5.90 +/- 0.75 (hypoxemia) compared with 0.89 +/- 0.06, 1.66 +/- 0.16, and 3.95 +/- 0.39 in normoxia at the three loads, respectively (P less than 0.001). Epinephrine (E) concentration approximately doubled (P less than 0.001) in hypoxemia at each load when compared with normoxic levels (i.e., 0.10 +/- 0.01 ng/ml, 0.23 +/- 0.03, and 0.46 +/- 0.06 in normoxia). However, hypoxemia did not significantly alter linear relationships between log plasma NE concentration and either heart rate (HR) or percent VO2max utilized, or between HR and percent VO2max. Thus NE concentration, like HR, appeared to reflect relative severity of exercise and overall SNA in both hypoxemia and normoxia. Above 40% VO2max during hypoxemia, circulating NE and E far exceeded levels known to have direct vasoconstrictor and metabolic effects in normoxic humans, but hypoxemia may blunt vasoconstriction in some regions.

Adult↗