Cyanophages Infection of Microcystis Bloom in Lowland Dam Reservoir of Sulejów, Poland.

An increased incidence of cyanobacterial blooms, which are largely composed of toxigenic cyanobacteria from the Microcystis genus, leads to a disruption of aquatic ecosystems worldwide. Therefore, a better understanding of the impact of environmental parameters on the development and collapse of blooms is important. The objectives of the present study were as follows: (1) to investigate the presence and identity of Microcystis-specific cyanophages capable of cyanobacterial cell lysis in a lowland dam reservoir in Central Europe; (2) to investigate Microcystis sensitivity to phage infections with regard to toxic genotypes; and (3) to identify key abiotic parameters influencing phage infections during the summer seasons between 2009 and 2013. Sequencing analysis of selected g91 gene amplification products confirmed that the identified cyanophages belonged to the family Myoviridae (95 % homology). Cyanophages and Microcystis hosts, including toxic genotypes, were positively correlated in 4 of the 5 years analyzed (r = 0.67-0.82). The average percentage of infected Microcystis cells varied between 0.1 and 32 %, and no particular sensitivity of the phages to toxigenic genotypes was recorded. The highest number of cyanophages (>10(4) gene copy number per microliter) was observed in the period preceded by the following: an increase of the water retention time, growth of the water temperature, optimum nutrient concentrations, and the predomination of Microcystis bloom.

A giant primary thyroid fibrosarcoma in an octogenarian.

We present an 89-year-old patient who was suffering from severe dyspnoea and mild dysphagia due to tracheal and esophagus compression by a giant goitre. The patient was euthyreotic. A total thyroidectomy was successfully performed. The pathology examination revealed fibrosarcoma G1, which is an extremely rare tumor of the thyroid.

Sex differences in vasoconstrictor reserve during 70 deg head-up tilt.

Women are generally recognized to be less orthostatically tolerant than men. We hypothesized that during head-up tilt (HUT), women would demonstrate less splanchnic vasoconstriction, leading to splanchnic pooling, lower blood pressure and lower orthostatic tolerance. Mean arterial blood pressure (MAP), heart rate (HR), cardiac output ((.)Q(c), assessed by C2H2 rebreathing), stroke volume, splanchnic blood flow (SpBF, assessed by Indocyanine Green clearance) and vascular conductance (systemic, SVC = (.)Qc/MAP; splanchnic, SpVC = SpBF/MAP; non-splanchnic, non-SpVC = SVC - SpVC) were measured during supine baseline conditions, 70 deg HUT and recovery in 14 healthy women (23 +/- 6 years old; mean +/- S.D.) and 16 men (23 +/- 5 years old). The proportion of sexes surviving 45 min of HUT trended towards significance (chi(2) = 2.92, P = 0.09). The MAP was lower in women than in men (supine, 77 +/- 5 versus 86 +/- 9 mmHg, P < 0.01; tilt, 72 +/- 8 versus 83 +/- 10 mmHg, P < 0.01), while HR and cardiac index ( /body surface area) were not different between the sexes (heart rate supine, 66 +/- 6 versus 64 +/- 8 beats min(-1); heart rate tilt, 96 +/- 13 versus 94 +/- 10 beats min(-1); cardiac index supine, 3.8 +/- 0.9 versus 3.7 +/- 0.7 l min(-1) m(2); cardiac index tilt, 2.7 +/- 0.8 versus 2.3 +/- 0.5 l min(-1) m(2)). The SpBF and SpVC were lower in women at rest but not during tilt (SpBF supine, 1174 +/- 243 versus 1670 +/- 391 ml min(-1), P < 0.01; SpVC supine, 14.83 +/- 3.61 versus 19.59 +/- 4.95 ml min(-1) mmHg(1), P < 0.01; SpBF tilt, 884 +/- 300 versus 1094 +/- 271 ml min(-1); SpVC tilt, 13.14 +/- 4.28 versus 14.82 +/- 4.16 ml min(-1) mmHg(-1)). However, in the women the SpVC did not decrease from baseline to tilt (SpVC, in women, 1.70 +/- 3.19 ml min(-1) mmHg(-1), n.s.; in men, 4.81 +/- 3.44 ml min(-1) mmHg(-1), P < 0.01), suggesting a blunted vasoconstrictor response. In conclusion, women tended to have lower tilt-table tolerance associated with a smaller splanchnic vasoconstrictor reserve than men.

Simultaneous determination of the accuracy and precision of closed-circuit cardiac output rebreathing techniques.

Foreign and soluble gas rebreathing methods are attractive for determining cardiac output (Q(c)) because they incur less risk than traditional invasive methods such as direct Fick and thermodilution. We compared simultaneously obtained Q(c) measurements during rest and exercise to assess the accuracy and precision of several rebreathing methods. Q(c) measurements were obtained during rest (supine and standing) and stationary cycling (submaximal and maximal) in 13 men and 1 woman (age: 24 +/- 7 yr; height: 178 +/- 5 cm; weight: 78 +/- 13 kg; Vo(2max): 45.1 +/- 9.4 ml.kg(-1).min(-1); mean +/- SD) using one-N(2)O, four-C(2)H(2), one-CO(2) (single-step) rebreathing technique, and two criterion methods (direct Fick and thermodilution). CO(2) rebreathing overestimated Q(c) compared with the criterion methods (supine: 8.1 +/- 2.0 vs. 6.4 +/- 1.6 and 7.2 +/- 1.2 l/min, respectively; maximal exercise: 27.0 +/- 6.0 vs. 24.0 +/- 3.9 and 23.3 +/- 3.8 l/min). C(2)H(2) and N(2)O rebreathing techniques tended to underestimate Q(c) (range: 6.6-7.3 l/min for supine rest; range: 16.0-19.1 l/min for maximal exercise). Bartlett's test indicated variance heterogeneity among the methods (P < 0.05), where CO(2) rebreathing consistently demonstrated larger variance. At rest, most means from the noninvasive techniques were +/-10% of direct Fick and thermodilution. During exercise, all methods fell outside the +/-10% range, except for CO(2) rebreathing. Thus the CO(2) rebreathing method was accurate over a wider range (rest through maximal exercise), but was less precise. We conclude that foreign gas rebreathing can provide reasonable Q(c) estimates with fewer repeat trials during resting conditions. During exercise, these methods remain precise but tend to underestimate Q(c). Single-step CO(2) rebreathing may be successfully employed over a wider range but with more measurements needed to overcome the larger variability.

Naloxone does not affect the cardiovascular and sympathetic adjustments to static exercise in humans.

Previous studies suggested that endogenous opiates may attenuate the cardiovascular and sympathetic adjustments to static exercise. We tested whether this effect originates from exercising skeletal muscle. Eight men performed 2 min of static handgrip (30% maximum) followed by 2 min of posthandgrip muscle ischemia after three interventions: 1) control, 2) intra-arterial injection of naloxone HCl (60 micrograms) or vehicle (saline) in the exercising arm, and 3) systemic infusion of naloxone (4 mg) or vehicle. Naloxone and vehicle trials were performed double blind on separate days. Preexercise baseline muscle sympathetic nerve activity (burst frequency), heart rate, and blood pressure were similar across interventions on either day. During static handgrip, control, intra-arterial, and systemic administration of vehicle and naloxone elicited similar increases in total muscle sympathetic nerve activity (58 +/- 24 vs. 68 +/- 26, 146 +/- 49 vs. 132 +/- 42, 137 +/- 54 vs. 164 +/- 44%, respectively), heart rate (9 +/- 2 vs. 8 +/- 3, 16 +/- 3 vs. 16 +/- 2, 20 +/- 4 vs. 19 +/- 3 beats/min, respectively), and mean arterial pressure (22 +/- 4 vs. 21 +/- 4, 29 +/- 5 vs. 26 +/- 3, 28 +/- 4 vs. 27 +/- 4 mmHg, respectively). Additionally, there were no differences between vehicle and naloxone trials during posthandgrip muscle ischemia. Thus, contrary to previous reports, we conclude that the endogenous opiate peptide system does not modulate cardiovascular and sympathetic responses to brief periods of static exercise or muscle ischemia in humans.

Effects of head-down-tilt bed rest on cerebral hemodynamics during orthostatic stress.

Our aim was to determine whether the adaptation to simulated microgravity (microG) impairs regulation of cerebral blood flow (CBF) during orthostatic stress and contributes to orthostatic intolerance. Twelve healthy subjects (aged 24 +/- 5 yr) underwent 2 wk of -6 degrees head-down-tilt (HDT) bed rest to simulate hemodynamic changes that occur when humans are exposed to microG. CBF velocity in the middle cerebral artery (transcranial Doppler), blood pressure, cardiac output (acetylene rebreathing), and forearm blood flow were measured at each level of a ramped protocol of lower body negative pressure (LBNP; -15, -30, and -40 mmHg x 5 min, -50 mmHg x 3 min, then -10 mmHg every 3 min to presyncope) before and after bed rest. Orthostatic tolerance was assessed by using the cumulative stress index (CSI; mmHg x minutes) for the LBNP protocol. After bed rest, each individual's orthostatic tolerance was reduced, with the group CSI decreased by 24% associated with greater decreases in cardiac output and greater increases in systemic vascular resistance at each level of LBNP. Before bed rest, mean CBF velocity decreased by 14, 10, and 45% at -40 mmHg, -50 mmHg, and maximal LBNP, respectively. After bed rest, mean velocity decreased by 16% at -30 mmHg and by 21, 35, and 39% at -40 mmHg, -50 mmHg, and maximal LBNP, respectively. Compared with pre-bed rest, post-bed-rest mean velocity was less by 11, 10, and 21% at -30, -40, and -50 mmHg, respectively. However, there was no significant difference at maximal LBNP. We conclude that cerebral autoregulation during orthostatic stress is impaired by adaptation to simulated microG as evidenced by an earlier and greater fall in CBF velocity during LBNP. We speculate that impairment of cerebral autoregulation may contribute to the reduced orthostatic tolerance after bed rest.

Cardiovascular and renal nerve responses to static muscle contraction of decerebrate rabbits.

The purpose of this study was to determine whether the biphasic arterial blood pressure responses elicited by static muscle contraction of decerebrate rabbits are mediated, at least in part, by an initial decrease and a subsequent increase in sympathetic outflow. Renal sympathetic nerve activity (RSNA) was used as an index of sympathetic outflow. Static contraction of the triceps surae muscle (n = 14) initially decreased mean arterial blood pressure (MAP) -20 +/- 3 mmHg and heart rate (HR) -15 +/- 5 beats/min (nadir values). After this initial decrease, MAP increased 12 +/- 2 mmHg (peak increase) above baseline and there was a tendency for HR to be elevated (6 +/- 3 beats/min). The changes in RSNA during muscle contraction (n = 6) mirrored the nadir and peak responses of MAP (-50 +/- 9 and 32 +/- 11%). Muscle stretch (n = 11) also evoked similar nadir and peak responses of MAP (-20 +/- 5 and 9 +/- 1 mmHg), HR (-17 +/- 7 and 3 +/- 3 beats/min), and RSNA (-43 +/- 9 and 46 +/- 15%). These data suggest that the initial depressor and subsequent pressor responses elicited by skeletal muscle contraction and stretch are mediated, at least in part, by biphasic changes in sympathetic outflow.

Leg vasoconstriction during dynamic exercise with reduced cardiac output.

We evaluated whether a reduction in cardiac output during dynamic exercise results in vasoconstriction of active skeletal muscle vasculature. Nine subjects performed four 8-min bouts of cycling exercise at 71 +/- 12 to 145 +/- 13 W (40-84% maximal oxygen uptake). Exercise was repeated after cardioselective (beta 1) adrenergic blockade (0.2 mg/kg metoprolol iv). Leg blood flow and cardiac output were determined with bolus injections of indocyanine green. Femoral arterial and venous pressures were monitored for measurement of heart rate, mean arterial pressure, and calculation of systemic and leg vascular conductance. Leg norepinephrine spillover was used as an index of regional sympathetic activity. During control, the highest heart rate and cardiac output were 171 +/- 3 beats/min and 18.9 +/- 0.9 l/min, respectively. beta 1-Blockade reduced these values to 147 +/- 6 beats/min and 15.3 +/- 0.9 l/min, respectively (P < 0.001). Mean arterial pressure was lower than control during light exercise with beta 1-blockade but did not differ from control with greater exercise intensities. At the highest work rate in the control condition, leg blood flow and vascular conductance were 5.4 +/- 0.3 l/min and 5.2 +/- 0.3 cl.min-1.mmHg-1, respectively, and were reduced during beta 1-blockade to 4.8 +/- 0.4 l/min (P < 0.01) and 4.6 +/- 0.4 cl.min-1.mmHg-1 (P < 0.05). During the same exercise condition leg norepinephrine spillover increased from a control value of 2.64 +/- 1.16 to 5.62 +/- 2.13 nM/min with beta 1-blockade (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Age alters the cardiovascular response to direct passive heating.

During direct passive heating in young men, a dramatic increase in skin blood flow is achieved by a rise in cardiac output (Qc) and redistribution of flow from the splanchnic and renal vascular beds. To examine the effect of age on these responses, seven young (Y; 23 +/- 1 yr) and seven older (O; 70 +/- 3 yr) men were passively heated with water-perfused suits to their individual limit of thermal tolerance. Measurements included heart rate (HR), Qc (by acetylene rebreathing), central venous pressure (via peripherally inserted central catheter), blood pressures (by brachial auscultation), skin blood flow (from increases in forearm blood flow by venous occlusion plethysmography), splanchnic blood flow (by indocyanine green clearance), renal blood flow (by p-aminohippurate clearance), and esophageal and mean skin temperatures. Qc was significantly lower in the older than in the young men (11.1 +/- 0.7 and 7.4 +/- 0.2 l/min in Y and O, respectively, at the limit of thermal tolerance; P < 0. 05), despite similar increases in esophageal and mean skin temperatures and time to reach the limit of thermal tolerance. A lower stroke volume (99 +/- 7 and 68 +/- 4 ml/beat in Y and O, respectively, P < 0.05), most likely due to an attenuated increase in inotropic function during heating, was the primary factor for the lower Qc observed in the older men. Increases in HR were similar in the young and older men; however, when expressed as a percentage of maximal HR, the older men relied on a greater proportion of their chronotropic reserve to obtain the same HR response (62 +/- 3 and 75 +/- 4% maximal HR in Y and O, respectively, P < 0.05). Furthermore, the older men redistributed less blood flow from the combined splanchnic and renal circulations at the limit of thermal tolerance (960 +/- 80 and 720 +/- 100 ml/min in Y and O, respectively, P < 0. 05). As a result of these combined attenuated responses, the older men had a significantly lower increase in total blood flow directed to the skin.

Effect of skeletal muscle fiber type on the pressor response evoked by static contraction in rabbits.

The purpose of this study was to determine whether the reflex hemodynamic responses to static contraction of predominately glycolytic muscle are greater than the changes elicited by primarily oxidative muscle. Low-frequency electrical stimulation (continuous 21 days) of the tibial nerve of one hindlimb of adult rabbits converted the metabolic characteristics of the predominately glycolytic gastrocnemius to a muscle that was primarily oxidative. After 21 days of stimulation, the rabbits were decerebrated, and static contraction of the glycolytic muscle (unstimulated gastrocnemius) initially decreased heart rate (HR; -16 +/- 3 beats/min) and mean arterial pressure (MAP; -17 +/- 3 mmHg). Thereafter, MAP increased 13 +/- 3 mmHg above baseline. Static contraction of the oxidative muscle (stimulated gastrocnemius) produced similar decreases in HR and MAP (-12 +/- 4 beats/min and -12 +/- 3 mmHg, respectively). However, the subsequent increase in MAP (8 +/- 3 mmHg; above baseline) was less than that evoked by contraction of the glycolytic muscle. The responses evoked by stretch of each muscle and high-intensity electrical stimulation were the same, indicating that the afferents from the muscle were not destroyed by the chronic-stimulation technique. These results support the hypothesis that metabolic by-products play a role in the pressor response to static contraction of skeletal muscle. In addition, these data confirm that contraction of predominately oxidative muscle can evoke a reflex pressor response, albeit smaller than the change elicited from primarily glycolytic muscle.

Effects of 18 days of bed rest on leg and arm venous properties.

Venous function may be altered by bed rest deconditioning. Yet the contribution of altered venous compliance to the orthostatic intolerance observed after bed rest is uncertain. The purpose of this study was to assess the effect of 18 days of bed rest on leg and arm (respectively large and small change in gravitational gradients and use patterns) venous properties. We hypothesized that the magnitude of these venous changes would be related to orthostatic intolerance. Eleven healthy subjects (10 men, 1 woman) participated in the study. Before (pre) and after (post) 18 days of 6 degrees head-down tilt bed rest, strain gauge venous occlusion plethysmography was used to assess limb venous vascular characteristics. Leg venous compliance was significantly decreased after bed rest (pre: 0.048 +/- 0.007 ml x 100 ml(-1) x mmHg(-1), post: 0.033 +/- 0.007 ml x 100 ml(-1) x mmHg(-1); P < 0.01), whereas arm compliance did not change. Leg venous flow resistance increased significantly after bed rest (pre: 1.73 +/- 1.08 mmHg x ml(-1) x 100 ml x min, post: 3.10 +/- 1.00 mmHg x ml(-1) x 100 ml x min; P < 0.05). Maximal lower body negative pressure tolerance, which was expressed as cumulative stress index (pressure x time), decreased in all subjects after bed rest (pre: 932 mmHg x min, post: 747 mmHg x min). The decrease in orthostatic tolerance was not related to changes in leg venous compliance. In conclusion, this study demonstrates that after bed rest, leg venous compliance is reduced and leg venous outflow resistance is enhanced. However, these changes are not related to measures of orthostatic tolerance; therefore, alterations in venous compliance do not to play a major role in orthostatic intolerance after 18 days of head-down tilt bed rest.

Chronic endurance exercise training: a condition of inadequate blood pressure regulation and reduced tolerance to LBNP.

We review the hypotheses presented to account for the anecdotal and literature-based reports that chronic endurance exercise training reduces orthostatic tolerance. The findings from cross-sectional investigations of unfit subjects and endurance athletes are examined, as well as limited data from recent investigations of the changes in orthostatic tolerance and blood pressure regulation that occur after 8 d to 8 months of endurance exercise training. Statistical models have not found wide variations in maximal aerobic power (VO2max) to contribute to the prediction of orthostatic responses. However, research data are generally consistent that the orthostatic tolerance of athletes whose VO2max exceeds 65 ml.kg-1.min-1 is lower than that of sedentary control subjects. These two findings suggest that it is exercise training, rather than VO2max, that reduces orthostatic tolerance. Findings from a recent longitudinal investigation corroborate this theory. We conclude that at least four factors associated with exercise training contribute to the development of orthostatic intolerance. These include: a) increased limb compliance (although its effect is likely to be trivial), b) eccentric ventricular hypertrophy, and c) increases in total blood volume, which may attenuate cardiopulmonary baroreflex responsiveness, shift ventricular function to a steeper portion of the ventricular compliance curve, and increase the inhibitory effect of cardiopulmonary baroreceptors on carotid baroreflex responsiveness; and d) an independent effect that reduces carotid and aortic baroreflex responsiveness. These mechanisms mimic changes observed in pathological states such as heart failure and hypertension. Our conclusions are best summarized by Greenleaf et al. (J. Appl. Physiol. 51:298-305, 1981): ""Trained men can run, but they cannot stand.''

Velocity, stroke rate, and distance per stroke during elite swimming competition.

The mean velocity of 9 out of 10 women's events during the U.S. Olympic Swimming Trials was greater in 1984 as compared to 1976. Three of the 10 men's events showed improvement. In 9 out of these 12 events, the increased velocity was accounted for by increased distance per stroke (range, -3 to -13%). In the women's 100-m butterfly and 100-m backstroke, increased velocity was due solely to faster stroke rates. The finalists in each event were compared to those whose velocities were 3-7% slower. In almost all events and stroke styles, the finalists achieved greater distances per stroke than did the slower group. In the men's events increased distance per stroke was associated with decreased stroke rate, except in the backstroke, in which both were increased for the finalists. Although the faster women swimmers generally had greater distances per stroke, they were more dependent than men on faster stroke rates to achieve superiority. The profile of velocity for races of 200 m and longer indicated that as fatigue developed the distance per stroke decreased. The faster swimmers compensated for this change by maintaining or increasing stroke rate more than did their slower competitors. This study indicates that improvements and superiority in stroke mechanics are reflected in the stroke rate and distance per stroke used to swim a race.

Cardiovascular responses to head-up tilt after an endurance exercise program.

The cardiovascular responses to 10 min of orthostasis were assessed before and after an aerobic exercise program. Five men and five women (18-25 years old) exercised for 7 weeks, four times per week, for 50 min per session at 70% of maximal heart rate (HR). Before and after the exercise program, maximal aerobic power (VO2max) was determined, and HR, systolic (SBP), diastolic (DBP), and pulse (PP) blood pressures were measured each minute during 5 min of supine rest, 10 min of foot-supported 70 degree head-up tilt (HUT), and 5 min of supine rest. Orthostatic tolerance was not determined. Calf compliance was measured in five of the subjects before and after the program as the change in leg volume at occluding pressures of 20, 40, 60, 80, and 100 mm Hg. Following the program, VO2max increased by 8.7% (p = 0.012), while decreases were noted in resting HR (9.4%, p = 0.041), SBP (5.0%, p less than 0.0005), and DBP (14.2%, p less than 0.0005). Despite a greater HR increase during HUT (7.1 beat.min-1, p = 0.034), SBP decreased by 3.4 mm Hg during HUT after the exercise program (p = 0.008). No differences were noted in the changes in DBP, MAP, or PP upon tilting (p greater than 0.05). After the program, the amount of fluid pooled in the calf at high occluding pressures (80 and 100 mm Hg) increased by 0.96 +/- 0.24 and 1.10 +/- 0.33 ml.100 ml tissue-1 (X +/- S.E.M., p = 0.017 and p = 0.028, respectively). We suggest that control of blood pressure during 10 min of orthostasis may be altered by endurance exercise training.

Power spectral and time based analysis of heart rate variability following 15 days head-down bed rest.

Power spectral and time based analyses were applied to the cardiac inter-beat interval (RRI) of 8 healthy men before and after 15 d of bed rest in the 6 degrees head-down tilt position (HDT) to determine changes in indices of cardiac parasympathetic and sympathetic activity after this exposure. At 24 h prior to HDT and on HDT day 15, a minimum of 256 RRI's were obtained from an electrocardiogram (ECG) while the subjects were in the supine position. RRI was subjected to power spectral and two methods of time-based analyses. Power spectral analysis demonstrated that the index of cardiac vagal activity was reduced (95.2 +/- 28.5 to 48.2 +/- 17.4 ms2) without affecting the index of cardiac sympathetic activity (1.18 +/- 0.7 to 0.69 +/- 0.4). The two methods of time-based analyses, time series and standard deviation analyses, further demonstrated a reduction of cardiac vagal activity post-HDT (5.5 +/- 4 to 4.8 +/- 0.6 ms2; and 42.8 +/- 4.8 to 33.9 +/- 3.3 ms, respectively). These data suggest that exposure to 15 d of HDT reduces cardiac vagal activity, while changes in cardiac sympathetic activity were indistinguishable.

Human baroreflex rhythms persist during handgrip and muscle ischaemia.

AIM: To determine whether physiological, rhythmic fluctuations of vagal baroreflex gain persist during exercise, post-exercise ischaemia and recovery. METHODS: We studied responses of six supine healthy men and one woman to a stereotyped protocol comprising rest, handgrip exercise at 40% maximum capacity to exhaustion, post-exercise forearm ischaemia and recovery. We measured electrocardiographic R-R intervals, photoplethysmographic finger arterial pressures and peroneal nerve muscle sympathetic activity. We derived vagal baroreflex gains from a sliding (25-s window moved by 2-s steps) systolic pressure-R-R interval transfer function at 0.04-0.15 Hz. RESULTS: Vagal baroreflex gain oscillated at low, nearly constant frequencies throughout the protocol (at approx. 0.06 Hz - a period of about 18 s); however, during exercise, most oscillations were at low-gain levels, and during ischaemia and recovery, most oscillations were at high-gain levels. CONCLUSIONS: Vagal baroreflex rhythms are not abolished by exercise, and they are not overwhelmed after exercise during ischaemia and recovery.

A somatostatin analog improves tilt table tolerance by decreasing splanchnic vascular conductance.

Splanchnic hemodynamics and tilt table tolerance were assessed after an infusion of placebo or octreotide acetate, a somatostatin analog whose vascular effects are largely confined to the splanchnic circulation. We hypothesized that reductions in splanchnic blood flow (SpBF) and splanchnic vascular conductance (SpVC) would be related to improvements in tilt table tolerance. In randomized, double-blind, crossover trials, hemodynamic variables were collected in 14 women and 16 men during baseline, 70° head-up tilt (HUT), and recovery. A repeated-measures analysis of variance was used to compare changes from baseline with respect to sex and condition. HUT elicited an increase in heart rate and decreases in mean arterial pressure, cardiac index, stroke index, and systemic vascular conductance. Additionally, SpVC and non-SpVC were lower during HUT. Octreotide reduced SpBF and SpVC and increased systemic vascular conductance and non-SpVC. Changes in SpBF and SpVC between supine and HUT were smaller in women (P < 0.05). Tilt table tolerance was increased after administration of octreotide [median tilt time: 15.7 vs. 37.0 min (P < 0.05) and 21.8 vs. 45.0 min (P < 0.05) for women and men, respectively]. A significant relationship existed between change (Δ) in SpBF (placebo-octreotide) and Δtilt time in women (Δtilt time = 2.5-0.0083 ΔSpBF, P < 0.01), but not men (Δtilt time = 3.41-0.0008 ΔSpBF, P = 0.59). In conclusion, administration of octreotide acetate improved tilt table tolerance, which was associated with a decrease in SpVC. In women, but not men, the magnitude of reduction in SpBF was positively associated with improvements in tilt tolerance.

Reductions in central venous pressure improve carotid baroreflex responses in conscious men.

To test the hypothesis that unloading cardiopulmonary receptors improves human carotid baroreceptor responsiveness we measured heart rate (HR) and mean radial artery blood pressure (BP) responses elicited by trains of neck pressure and neck suction from +40 to -65 Torr during graded lower body negative pressure (LBNP) at -5, -10, -15, -20, -35, and -50 Torr in eight healthy men. Gain of the carotid baroreflexes was determined from logistic modeling of the HR [expressed as R-R interval (RRI)] and BP responses to neck pressure and neck suction. Central venous pressure (CVP) decreased progressively from control values of 6.2 +/- 0.6 (SE) Torr to -0.8 +/- 0.1 Torr at -50 Torr LBNP (P less than 0.001). HR changed little from control values of 62.7 +/- 2.1 beat/min to 65.9 +/- 2.8 beat/min at -15 Torr (P = NS), but increased significantly to 80.6 +/- 2.6 beats/min at -50 Torr (P less than 0.001). Maximum gain of the HR and BP stimulus-response curves was linearly and inversely related to decreases in CVP and could be described by the relationships Max RRI gain = -0.694 (CVP) + 11.6 [r2 = 0.94, standard error of estimate (SEE) = 0.45, P less than 0.001] and Max BP gain = -0.0292 (CVP) + 0.391 (r2 = 0.81, SEE = 0.038, P less than 0.001). We suggest that reductions in central venous pressure and/or central blood volume augment both HR and BP carotid baroreflex responses in man by reducing an inhibitory influence from cardiopulmonary receptors.

Physical performance during combinations of hypercapnic, resistive, and hot air breathing.

Performance time for a 3.2-km (2-mi) run at maximal voluntary speed was determined for 12 subjects under seven experimental conditions: resistance breathing (R), hypercapnia (C), hot air breathing (H), and combinations R + C, R + H, H + C, and R + H + C. The tests were performed on a treadmill at 5% grade. Performance time was increased significantly when the subjects were exposed to resistance breathing alone (9%) or to any combination condition containing resistance (16%-31%). The effect of breathing resistance was not specific to the presence or absence of C, H, or their combination. Nevertheless, the physiological effects were not additive and could not be predicted by knowing the effects of the individual stresses. Performance time also was increased in Condition H + C (9%). Pulmonary ventilation was the most affected physiological variable, significantly reduced in Conditions R, H, C + R, H + R, and H + C + R. In conclusion, a multistress approach should be used when determining physiological responses or performance limitations brought about by real or simulated industrial respirator-wear conditions.