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The interaction of central command and the exercise pressor reflex in mediating baroreflex resetting during exercise in humans.

Central command and the exercise pressor reflex can independently reset the carotid baroreflex (CBR) during exercise. The present investigation assessed the interactive relationship between these two neural mechanisms in mediating baroreflex resetting during exercise. Six men performed static leg exercise at 20% maximal voluntary contraction under four conditions: control, no perturbation; neuromuscular blockade (NMB) induced by administration of the neuromuscular blocking agent Norcuron (central command activation); MAST, application of medical antishock trousers inflated to 100 mmHg (exercise pressor reflex activation); and Combo, NMB plus MAST (concomitant central command and exercise pressor reflex activation). With regard to CBR control of heart rate (HR), both NMB and Combo conditions resulted in a further resetting of the carotid-cardiac stimulus-response curve compared to control conditions, suggesting that CBR-HR resetting is predominately mediated by central command. In contrast, it appears that CBR control of blood pressure can be mediated by signals from either central command or the exercise pressor reflex, since both NMB and MAST conditions equally augmented the resetting of the carotid-vasomotor stimulus-response curve. With regard to the regulation of both HR and blood pressure, the extent of CBR resetting was greater during the Combo condition than during overactivation of either central command or the exercise pressor reflex alone. Therefore, we suggest that central command and the exercise pressor reflex interact such that signals from one input facilitate signals from the other, resulting in an enhanced resetting of the baroreflex during exercise.

Adult↗

Bioengineering studies of periodic external compression as prophylaxis against deep vein thrombosis-part I: numerical studies.

This paper presents the results of a numerical study of the technique of periodic external compression for the prevention of deep vein thrombosis. In the model the veins of the lower leg are portrayed as a continuous system rather than as discrete elements as in previous models. Consequently, we are able to explore the detailed effects of different modes of compression including (i) uniform compression, the simultaneous application of uniform pressure over the entire lower leg, (ii) graded compression, the application of nonuniform pressure, maximum at the ankle and minimum at the knee, and (iii) wavelike compression, a wave of compression proceeding from the ankle toward the knee. These numerical results indicate that the effectiveness of uniform compression is severely compromised by the formation of a flow-limiting throat at the proximal end of the compression cuff that reduces both the rate at which blood is discharged from the lower leg and the total blood volume removed. Both of these detrimental effects can be avoided by the use of either wavelike of graded compression. Both alternated methods are shown to produce more uniform augmentation of volume flow rate, flow velocity and shear stress, throughout the entire lower leg. In the companion paper, Part II [18] (see following article), these same compression modes are tested using a simple hydraulic model consisting of a single latex tube inside a foam cylinder as a highly simplified representation of a human leg.

Blood Flow Velocity↗

Bioengineering studies of periodic external compression as prophylaxis against deep vein thrombosis-part II: experimental studies on a stimulated leg.

In this companion paper to "Part I: Numerical Simulations, " we report in vitro experimental studies performed on a simple model leg consisting of a "vein" of thin-walled latex tubing surrounded by "tissue" of open-pore foam rubber. Three modes of periodic external compression, were investigated: i) uniform compression; (ii) graded compression, decreasing from ankle to knee; and (iii) sequential compression, progressing from ankle to knee. The modes are compared on the basis of three hemodynamic criteria: degree of vessel collapse, level of fluid velocity, and level of shear stress. In uniform compression these measures of merit are distributed very nonuniformly along the length of the leg: they are high near the proximal end of the cuff but low elsewhere, a result due to the formation proximally of a partially occlusive throat. The latter does not form in either graded or sequential compression, with the consequence that favorable values of the three measures of merit occur more uniformly along the length of the pressurized region. It is concluded that either the graded or sequential mode of compression, or perhaps a combination of the two, would be more effective than uniform compression as a prophylaxis against deep vein thrombosis.

Gravity Suits↗

Pneumatic anti-shock garment--does it have a future?

A total of 100 accident and emergency (A&E) departments in the UK responded to a questionnaire about their use of the pneumatic anti-shock garment (PASG). Less than one in 10 departments used PASG in their prehospital care system, less than one in five departments used PASG during in-patient care, and there was wide variation in PASG usage in those situations for which their use is recommended by the Advanced Trauma Life Support (ATLS) course.

Emergency Service, Hospital↗

Endothelial nitric oxide production during in vitro simulation of external limb compression.

External pneumatic compression (EPC) is effective in preventing deep vein thrombosis (DVT) and is thought to alter endothelial thromboresistant properties. We investigated the effect of EPC on changes in nitric oxide (NO), a critical mediator in the regulation of vasomotor and platelet function. An in vitro cell culture system was developed to simulate flow and vessel collapse conditions under EPC. Human umbilical vein endothelial cells were cultured and subjected to tube compression (C), pulsatile flow (F), or a combination of the two (FC). NO production and endothelial nitric oxide synthase (eNOS) mRNA expression were measured. The data demonstrate that in the F and FC groups, there is a rapid release of NO followed by a sustained increase. NO production levels in the F and FC groups were almost identical, whereas the C group produced the same low amount of NO as the control group. Conditions F and FC also upregulate eNOS mRNA expression by a factor of 2.08 +/- 0.25 and 2.11 +/- 0.21, respectively, at 6 h. Experiments with different modes of EPC show that NO production and eNOS mRNA expression respond to different time cycles of compression. These results implicate enhanced NO release as a potentially important factor in the prevention of DVT.

Blotting, Northern↗

ANP-mediated volume depletion attenuates renal responses in humans.

Brief low-dose infusions of atrial natriuretic peptide (ANP) that emulate physiological plasma concentrations in humans have little if any effect on renal excretory function. This study explored the possibility that ANP-mediated reductions in cardiac filling pressures (through ANP's rapid effect on capillary dynamics) could attenuate its purported renal effects. Protocol A consisted of 16 healthy subjects (ages 19-27 yr old) who underwent three consecutive 45-min experimental sequences: 1) placebo, 2) ANP (10 ng.kg-1 x min-1), and 3) ANP alone (n = 8) or ANP with simultaneous lower body positive pressure (LBPP, n = 8). Electrocardiogram and direct measures of arterial and central venous pressures were continuously monitored. Blood was sampled at the end of each 45-min sequence before subjects stood to void. Compared with control (placebo), ANP produced a hemoconcentration and increased plasma norepinephrine, but did not change heart rate, blood pressure, plasma levels of renin, aldosterone, or vasopressin, or renal excretion of volume or sodium. In subjects receiving LBPP to maintain central venous pressure during the last 45 min of ANP infusion, norepinephrine did not increase and urine volume and sodium excretion increased (P < 0.05). In a second study (protocol B), five healthy subjects received a placebo infusion for 45 min followed by two consecutive 45-min infusions of ANP (10 ng.kg-1 x min-1). Central venous pressure was maintained (LBPP) at placebo baseline throughout the two ANP infusion periods. Urine volume and sodium excretion rates increased progressively and significantly during both ANP infusion periods (P < 0.05) without significant changes in creatinine clearance, blood pressure, or heart rate.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

A respiratory function jacket for measuring tidal volume and changes in FRC.

We describe a simple application of a mercury-in-rubber strain gauge in a jacket used to measure tidal volume in paralyzed, mechanically ventilated rabbits. The jacket produces a record with a straight base line. Shifts of this base line can be used to assess changes in functional residual capacity (FRC).

Animals↗

Hemodynamic, gas exchange, and hormonal consequences of LBPP during PEEP ventilation.

Hemodynamic, gas exchange, and hormonal response induced by application of a 25- to 40-mmHg lower body positive pressure (LBPP), during positive end-expiratory pressure (PEEP; 14 +/- 2.5 cmH2O) were studied in nine patients with acute respiratory failure. Compared with PEEP alone, LBPP increased cardiac index (CI) from 3.57 to 4.76 l X min-1 X m-2 (P less than 0.001) in relation to changes in right atrial pressure (RAP) (11 to 16 mmHg; P less than 0.01). Cardiopulmonary blood volume (CPBV) measured in five patients increased during LBPP from 546 +/- 126 to 664 +/- 150 ml (P less than 0.01), with a positive linear relationship between changes in RAP and CPBV (r = 0.88; P less than 0.001). Venous admixture (Qva/QT) decreased with PEEP from 24 to 16% (P less than 0.001) but did not change with LBPP despite the large increase in CI, leading to a marked O2 availability increase (P less than 0.001). Although PEEP induced a significant rise in plasma norepinephrine level (NE) (from 838 +/- 97 to 1008 +/- 139 pg/ml; P less than 0.05), NE was significantly decreased by LBPP to control level (from 1,008 +/- 139 to 794 +/- 124 pg/ml; P less than 0.003). Plasma epinephrine levels were not influenced by PEEP or LBPP. Changes of plasma renin activity (PRA) paralleled those of NE. No change in plasma arginine vasopressin (AVP) was recorded. We concluded that LBPP increases venous return and CPBV and counteracts hemodynamic effects of PEEP ventilation, without significant change in Qva/QT. Mechanical ventilation with PEEP stimulates sympathetic activity and PRA apparently by a reflex neuronal mechanism, at least partially inhibited by the loading of cardiopulmonary low-pressure reflex and high-pressure baroreflex. Finally, AVP does not appear to be involved in the acute cardiovascular adaptation to PEEP.

Adult↗

Effects of pneumatic antishock garment inflation in normovolemic subjects.

This study examines the effects of inflation of pneumatic antishock garments (PASG) in 10 normovolemic men (mean age 44 +/- 6 yr) undergoing diagnostic catheterization. Seven subjects had normal heart function and no evidence of coronary artery disease (CAD); three patients had CAD. High-fidelity multisensor catheters were employed to simultaneously record right and left heart pressures before PASG inflation and after inflation to 40, 70, and 100 mmHg. A thermal dilution catheter was used to obtain pulmonary capillary wedge pressure and cardiac output. Counterpressure increases greater than or equal to 40 mmHg were associated with significant changes in left and right heart pressures. Right and left ventricular end-diastolic pressures increased 100% (P less than 0.01); mean pulmonary arterial and aortic pressures increased 77 and 25%, respectively (P less than 0.01); systemic vascular resistance increased 22% (P less than 0.05) and pulmonary vascular resistance did not change in normal subjects at maximum PASG inflation. Heart rate, cardiac output, and aortic and pulmonary arterial pulse pressures did not change during inflation in either group. Right and left ventricular end-diastolic pressures and pulmonary capillary wedge pressure were greater (P less than 0.05) in the CAD group compared with the normal subjects during PASG inflation. The data suggest that the primary mechanism whereby PASG inflation induces changes in central hemodynamics in normovolemic subjects is through an acute increase in left ventricular afterload. PASG changes in afterload and pulmonary capillary wedge pressure imply that these devices should be used with caution in patients with compromised cardiac function.

Adult↗

Inflation of antishock trousers increases bronchial response to methacholine in healthy subjects.

We studied changes in lung volumes and in bronchial response to methacholine chloride (MC) challenge when antishock trousers (AST) were inflated at venous occlusion pressure in healthy subjects in the standing posture, a maneuver known to shift blood toward lung vessels. On inflation of bladders isolated to lower limbs, lung volumes did not change but bronchial response to MC increased, as evidenced by a greater fall in the forced expiratory volume in 1 s (FEV1) at the highest dose of MC used compared with control without AST inflation (delta FEV1 = 0.94 +/- 0.40 vs. 0.66 +/- 0.46 liter, P less than 0.001). Full inflation of AST, i.e., lower limb and abdominal bladder inflated, significantly reduced vital capacity (P less than 0.001), functional residual capacity (P less than 0.01), and FEV1 (P less than 0.01) and enhanced the bronchial response to MC challenge compared with partial AST inflation (delta FEV1 = 1.28 +/- 0.47 liter, P less than 0.05). Because there was no significant reduction of lung volumes on partial AST inflation, the enhanced bronchial response to MC cannot be explained solely by changes in base-line lung volumes. An alternative explanation might be a congestion and/or edema of the airway wall on AST inflation. Therefore, to investigate further the mechanism of the increased bronchial response to MC, we pretreated the subjects with the inhaled alpha 1-adrenergic agonist methoxamine, which has both direct bronchoconstrictor and bronchial vasoconstrictor effects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Mechanisms of blood flow during pneumatic vest cardiopulmonary resuscitation.

Mechanisms of blood flow during cardiopulmonary resuscitation (CPR) were studied in a canine model with implanted mitral and aortic flow probes and by use of cineangiography. Intrathoracic pressure (ITP) fluctuations were induced by a circumferential pneumatic vest, with and without simultaneous ventilation, and by use of positive-pressure ventilation alone. Vascular volume and compression rate were altered with each CPR mode. Antegrade mitral flow was interpreted as left ventricular (LV) inflow, and antegrade aortic flow was interpreted as LV outflow. The pneumatic vest was expected to elevate ITP uniformly and thus produce simultaneous LV inflow and LV outflow throughout compression. This pattern, the passive conduit of "thoracic pump" physiology, was unequivocally demonstrated only during ITP elevation with positive-pressure ventilation alone at slow rates. During vest CPR, LV outflow started promptly with the onset of compression, whereas LV inflow was delayed. At compression rates of 50 times/min and normal vascular filling pressures, the delay was sufficiently long that all LV filling occurred with release of compression. This is the pattern that would be expected with direct LV compression or "cardiac pump" physiology. During the early part of the compression phase, catheter tip transducer LV and left atrial pressure measurements demonstrated gradients necessitating mitral valve closure, while cineangiography showed dye droplets moving from the large pulmonary veins retrograde to the small pulmonary veins. When the compression rate was reduced and/or when intravascular pressures were raised with volume infusion, LV inflow was observed at some point during the compressive phase. Thus, under these conditions, features of both thoracic pump and cardiac pump physiology occurred within the same compression. Our findings are not explained by the conventional conceptions of either thoracic pump or cardiac compression CPR mechanisms alone.

Animals↗

Response of genioglossus EMG activity to passive tilt in men.

Increased blood pressure (BP) leads to inhibition of respiratory activity of hypoglossal nerve in anesthetized cats, implying that arterial baroreceptor activity may inhibit upper airway motor outputs. We examined the effect of passive tilt on upper airway muscle activity in men under the assumption that changes in degree of tilt would change local pressure at the carotid baroreceptors. We also examined the possibility that inhibition of upper airway muscle activity occurred secondary to a decrease in level of arousal. In seven normal awake adult males, we measured electromyogram activity of the genioglossus (EMGge), electroencephalogram (EEG), electrocardiogram, ventilation, end-tidal fractional concentration of CO2, and BP while the subject was on a tilt table wearing inflatable antishock pants. Three tilt table positions were used: 60 degrees head-up (60 degrees increases), supine (S), and 30 degrees head-down (30 degrees decreases), with pants either deflated (P-) or inflated (P+) to 40 mmHg. During P-, moving the subject from 60 degrees increases to S to 30 degrees decreases positions resulted in steady-state heart rates of 94.8 +/- 1.7, 66.9 +/- 0.7, and 68.9 +/- 0.8 beats/min and EMGge activities of 54.4 +/- 4.4, 37.7 +/- 2.0, and 31.5 +/- 2.4% of maximum, respectively. During P+, changes in heart rate were similar but significantly reduced from P-, and positional changes in EMGge were eliminated. The level of arousal was unchanged. The transient response of EMGge to tilt was biphasic: when moving from upright to supine position, there was a rapid increase in activity during the tilt maneuver followed by a progressive decline.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗