From Peruvian mummies to living humans: first case of pulmonary tuberculosis caused by Mycobacterium pinnipedii.

The zoonotic potential of Mycobacterium tuberculosis complex species is well known. However, M. pinnipedii, the causative agent of tuberculosis (TB) predominantly in seals and sea lions, has never been isolated from a respiratory specimen in humans. Here we describe the first known human case of pulmonary TB caused by M. pinnipedii in a 79-year-old female patient with rheumatoid arthritis and chronic respiratory disease. The epidemiological data did not explain where the patient was exposed to M. pinnipedii, thus leaving the source of transmission unknown.

Cholinergic induced mesenteric vasorelaxation in response to head-up tilt.

Central hypovolaemia induced by head-up tilt evokes a reduction in superior mesenteric artery resistance resulting in maintenance of regional blood flow. Mechanisms of importance for this response are not known, but a parasympathetic contribution could be expected. To evaluate this hypothesis, superior mesenteric artery blood flow and resistance were evaluated by duplex ultrasound in eight healthy volunteers during postprandial head-up tilt with and without cholinergic blockade. During supine rest, cholinergic blockade did not influence the postprandial reduction in peripheral mesenteric artery resistance as expressed by analogous elevations in the diastolic blood velocity (to 62 +/- 9 vs. 56 +/- 7 cm s-1 with placebo). Throughout the normotensive and hypotensive phases of head-up tilt, cholinergic blockade reduced mesenteric artery mean blood velocity by 39 and 42%, respectively, corresponding to volume flow reductions by 35 and 41% (0.62 +/- 0.10 vs. 0.96 +/- 0.13 L min-1 and 0.52 +/- 0.07 vs. 0.88 +/- 0.16 L min-1; P < 0.05). Also, during both phases of head-up tilt, cholinergic blockade increased mesenteric artery resistance as reflected in a reduction in the diastolic blood velocity by 41 and 56%, respectively (44 +/- 4 vs. 74 +/- 13 cm s-1 and 24 +/- 6 vs. 54 +/- 8 cm s-1). These results support a cholinergic contribution to the mesenteric artery vasorelaxing response to central hypovolaemia induced by head-up tilt.

Cardiovascular and neuroendocrine responses to exercise in hypoxia during impaired neural feedback from muscle.

Reflex mechanisms from contracting skeletal muscle have been shown to be important for cardiovascular, neuroendocrine, and extramuscular fuel-mobilization responses in exercise. Furthermore, because hypoxia results in exaggerated metabolic changes in contracting muscle, the present study evaluated whether enhancement of cardiovascular and neuroendocrine responses by hypoxia during exercise is influenced by neural feedback from contracting muscle. Seven healthy males cycled at 46% maximal O(2) uptake for 20 min both during normoxia and at 11.5% O(2), and both without and with epidural anesthesia (EA; 20 ml 0.25% bupivacain, resulting in cutaneous hypesthesia below T10-T12 and 25% reduction in maximal leg strength). Exercise to exhaustion was also performed at 7.8% O(2). The exercise-induced increases in heart rate; cardiac output; leg blood flow; plasma concentrations of growth hormone, adrenocorticotropin, cortisol, and catecholamines; renin activity; glucose production and disappearance; norepinephrine spillover [2, 190 +/- 341 ng/min (exercise at 11.5% O(2)) vs. 988 +/- 95 ng/min (exercise during normoxia)]; lactate release from and glucose uptake in the leg; and the decreases in plasma insulin and free fatty acids were exaggerated in hypoxia (P < 0.05). In muscle, concentrations of lactate, creatine, and inosine 5'-monophosphate were higher, and those of phosphocreatine were lower after exercise in hypoxia compared with normoxia. The exercise-induced increase in mean arterial blood pressure was not affected by hypoxia, but it was reduced by EA [108 +/- 4 mmHg (control) vs. 97 +/- 4 mmHg (EA); P < 0.05], and the reduction was more pronounced during severe hypoxia compared with normoxia. Apart from this, time to exhaustion at extreme hypoxia, circulatory responses, concentrations of neuroendocrine hormones, and extramuscular substrate mobilization were not diminished by EA. In conclusion, in essence the hypoxia-induced enhancement of systemic adaptation to exercise is not mediated by neural feedback from working muscle in humans.

Cholinergic blockade and the mesenteric artery response to head-up tilt-induced central hypovolaemia.

The influence of muscarinic blockade on the superior mesenteric artery (SMA) response to head-up tilt (HUT) was assessed by Doppler ultrasound in eight healthy adults pretreated with i.v. glycopyrron. During supine rest, cholinergic blockade increased heart rate from 58 +/- 3 to 106 +/- 6 beats min-1 (mean +/- SE) and mean arterial pressure from 81 +/- 3 to 97 +/- 4 mmHg (P < 0.01) and it reduced the cardiac stroke volume from 89 +/- 6 to 59 +/- 7 ml (P < 0.01) with no significant effect on the SMA diameter and blood flow velocities. HUT provoked a further increase in heart rate to 134 +/- 5 beats min-1 (P < 0.01) and a reduction in stroke volume to 45 +/- 4 ml (P < 0.01). The early diastolic velocity increased from -51 +/- 4 to 6 +/- 8 cm s-1 during the normotensive stage of HUT and further to 21 +/- 9 cm s-1 during the hypotensive stage with a reduction in mean arterial pressure from 97 +/- 4 to 73 +/- 7 mmHg (P < 0.01) but, in contrast to control HUT (without cholinergic blockade), the end-diastolic velocity did not change significantly. Maintenance of blood velocity and diameter in spite of an increase in arterial pressure at rest indicates increased SMA impedance. Likewise, during hypovolaemia, a glycopyrron-induced inhibition in diastolic velocity supports an increase in SMA impedance. The results indicate cholinergic vasorelaxing influence on the superior mesenteric artery both at rest and during normotensive central hypovolaemia.

Mesenteric artery response to head-up tilt-induced central hypovolaemia and hypotension.

Superior mesenteric artery (SMA) blood flow and impedance were evaluated by duplex ultrasound during head-up tilt (HUT)-induced central hypovolaemia and hypotension in eight healthy volunteers. HUT induced a reduction in cardiac stroke volume from 88.8 +/- 6.3 to 64.7 +/- 6.3 ml (mean +/- SEM; P < 0.01) and an increase in thoracic electric impedance from 38.6 +/- 2.1 to 42.6 +/- 2.1 omega (P < 0.01) reflecting a reduced central blood volume. Maintained tilt provoked a 30% reduction in mean arterial pressure (from 87.1 +/- 3.3 to 63.4 +/- 3.6 mmHg: P < 0.01) and the appearance of presyncopal symptoms. During both the normotensive and the hypotensive phase of HUT, the SMA diameter (5.7 +/- 0.03 mm) and blood flow (514 +/- 75 ml min-1) did not change significantly, although the end-diastolic velocity increased from 9.7 +/- 4.8 to 39.7 +/- 4.0 cm s-1 (P < 0.01). The increase in diastolic velocity, despite a maintained or reduced arterial pressure, supports a reduction in the SMA impedance as it was reproduced during a meal test when a moderate reduction in mean arterial pressure (87 +/- 4 to 80 +/- 4 mm Hg; P = 0.04) was accompanied by a ninefold increase in the end-diastolic velocity (P < 0.01). The results indicate a reduction in the mesenteric vascular impedance to the extent that superior mesenteric artery blood flow is maintained during HUT-induced central hypovolaemia and hypotension.

Subcutaneous emphysema and pneumothorax during laparoscopy for ectopic pregnancy removal.

We report a case of subcutaneous emphysema and pneumothorax during laparoscopic removal of ectopic pregnancy. Increases in airway pressures and end-tidal carbon dioxide, simultaneously with decrease of lung compliance, led quickly to diagnosis of pneumothorax. We recommend a careful monitoring of these variables during laparoscopic procedures. Carbon dioxide pneumothorax can occur even without pulmonary or pleural trauma.

Hormonal and metabolic responses to electrically induced cycling during epidural anesthesia in humans.

Hormonal and metabolic responses to electrically induced dynamic exercise were investigated in eight healthy young men with afferent neural influence from the legs blocked by epidural anesthesia (25 ml of 2% lidocaine) at L3-L4. This caused cutaneous sensory anesthesia below T8-T9 and complete paralysis of the legs. Cycling increased oxygen uptake to 1.90 +/- 0.13 (SE) l/min, and fatigue developed after 22.7 +/- 2.7 min. Compared with voluntary exercise at the same oxygen uptake and heart rate, concentrations of blood and muscle lactate (musculus vastus lateralis) as well as plasma potassium increased more while muscle glycogen decreased more during electrically induced exercise. Hepatic glucose production always rose during exercise. However, during involuntary exercise with sensory blockade, it did not match the rise in peripheral glucose uptake and plasma glucose decreased (P < 0.05). Plasma glycerol increased less in electrically induced vs. voluntary exercise, and free fatty acids and beta-hydroxybutyrate decreased only during electrically induced exercise. Epinephrine, growth hormone, adrenocorticotropic hormone, and cortisol levels were higher during involuntary vs. voluntary exercise (P < 0.05). In conclusion, neural and humoral mechanisms exert redundant control with regard to responses of catecholamines and pituitary hormones (growth hormone and adrenocorticotropic hormone). In contrast, neural input from motor centers and feedback from working muscle are important for glucose production and lipolysis during exercise in humans. Humoral feedback is apparently not sufficient to trigger normal mobilization of extramuscular fuel stores.

Changes in superior mesenteric artery Doppler waveform during reduction of cardiac stroke volume and hypotension.

Influence of stroke volume reduction and hypotension on the superior mesenteric artery (SMA) Doppler waveform was evaluated during head-up tilt-induced central hypovolemia in 11 healthy volunteers. During normotensive reduction in stroke volume, peak systolic velocity (pV), mean velocity, pulsatility and resistivity indices decreased, while diastolic velocities increased. During hypotension, a further decrease in pV was accompanied by maintained elevation of diastolic velocities and reduction in pulsatility and resistivity indices. Power of backscattered Doppler wave was elevated throughout the hypovolemia. Alterations in pV and pulsatility indices were closely related to changes in stroke volume, and a negative correlation was found between diastolic velocities and stroke volume. regression analysis showed no significant relation between variations in velocity parameters and blood pressure. Results of the study indicate that alterations in stroke volume induce consequential changes in the SMA Doppler waveform. These changes originate from both direct influence of stroke volume and/or pressure on blood flow velocity, and alterations in SMA peripheral resistance that follow variations in stroke volume. Presented interdependencies should be taken into consideration while studying mesenteric physiology with the use of Doppler technique and while interpreting the duplex results in patients suffering from diseases that may influence flow velocity and mimic or obscure Doppler effects of the SMA stenosis.

Pharmacological manipulation of cardiovascular responses to lower body negative pressure.

To evaluate influences on blood volume distribution, atrial natriuretic peptide concentrations (ANP) and thoracic and leg electrical impedance at 2.5 (TI2.5 and LI2.5, respectively) and 100 kHz (TI100 and LI100, respectively) were monitored during administration of ketanserin, noradrenaline and trimetaphan combined with lower body negative pressure (LBNP) in 12 subjects. Administration of clinically relevant doses of ketanserin alone did not induce changes in mean arterial pressure (MAP) or in the central blood volume, as electrical impedance and ANP concentrations did not change. During continued infusion of ketanserin an increase in MAP from a mean of 90 (range 83-108) to 113 (range 98-138) mmHg was induced by noradrenaline, but TI2.5 [mean 45.6 (range 39.3-54.2)] and TI100 [mean 33.8 (range 27.5-38.5) omega] remainded stable until ganglionic blockade and LBNP were applied, when they increased by a mean of 3.1 (range 2.0-6.1) and 2.7 (range 1.1-4.2) omega, respectively (P < 0.05). Conversely, LI2.5 [mean 79.6 (range 74.1-89.4)] and LI100 [mean 56.7 (range 52.4-63.3) omega] decreased by a mean of 3.2 (range 1.2-8.0) and 2.3 (range 0.9-3.9) omega, ANP from a mean of 27.7 (range 10.2-62.7) to 12.7 (range 7.1-27.5) pmol.l-1 and MAP fell to a mean of 62 (range 42-70) mmHg (P < 0.05). The heart rate was a mean of 75 (range 69-77) beats.min-1 and did not change until LBNP, when it increased to a mean of 102 (range 78-104) beats.min-1, as presyncopal symptoms appeared. The data indicated that serotonergic blockade by ketanserin and alpha-sympathetic stimulation by noradrenaline did not affect blood volume distribution in normal humans, but that ganglionic blockade combined with LBNP reduced the central blood volume as leg volume increased; during central hypovolaemia tachycardia induced by ganglionic blockade did not prevent the fall in MAP, and thereby the appearance of presyncopal symptoms.

The venous pump does not affect the indifference point for electrical impedance in humans.

We have used regional electrical impedance at 2.5 and 100 kHz over nine body sections (two thoracic, one abdominal, two thigh, two around the knee, and two lower leg) in eight subjects to determine the volume indifference point defined as the level at which fluid volume remained constant independent of body position changes in space. Passive head-up tilt and tilt with activation of the venous muscle pump of the legs were performed in 10 degrees increments from 0 to 60 degrees over 6 min. The impedance changes in relation to 0 degree were similar for the two frequencies. Over the thorax it increased in proportion to the head-up tilt angle by a mean of 3.8 (range 1.9 to 9.3) omega (100 kHz) at 60 degrees (P < 0.05), while the abdominal impedance did not change significantly. Over the thigh it decreased with increasing head-up tilt angle by a mean maximum of -2.3 (range -9.4 to -0.4) omega and over the lower leg by a mean of -2.7 (range -6.0 to -0.8) omega. There were only marginal changes around the knee, mean -1.5 (range -2.3 to -0.2) omega (P < 0.05), and no change around the ankle indicating that little or no fluid was accumulated in these regions. Changes in impedance during passive and active head-up tilt did not differ significantly in any but one position: between the greater trochanter and the mid thigh, where during passive tilt it decreased by a mean of -4.8 (range -9.4 to -1.9) omega, and with activation of the venous pump by a mean of only -1.2 (range -1.9 to -0.4) omega (P < 0.05). These results indicated that the vascular volume indifference point was positioned between the navel and iliac crest both during the passive and active head-up tilts although during the passive tilt, apparently more fluid was accumulated in the vessels of the thigh.

Cardiovascular and ventilatory responses to electrically induced cycling with complete epidural anaesthesia in humans.

Cardiovascular and ventilatory responses to electrically induced dynamic exercise were investigated in eight healthy young males with afferent neural influence from the legs blocked by epidural anaesthesia (25 ml 2% lidocaine) at L3-L4. This caused cutaneous sensory anaesthesia below T8-T9 and complete paralysis of the legs. Cycling was performed for 22.7 +/- 2.7 min (mean, SE) (fatigue) and oxygen uptake (VO2) increased to 1.90 +/- 0.13 1 min-1. Compared with voluntary exercise at the same VO2, increases in heart rate (HR) (135 +/- 7 vs. 130 +/- 9 beats min-1) and cardiac output (16.9 +/- 1.1 vs. 17.3 +/- 0.91 min-1) were similar, and ventilation (54 +/- 5 vs. 45 +/- 41 min-1) was higher (P < 0.05). In contrast, the rise in mean arterial blood pressure during voluntary exercise (93 +/- 4 (rest) to 119 +/- 4 mmHg (exercise)) was not manifest during electrically induced exercise with epidural anaesthesia [93 +/- 3 (rest) to 95 +/- 5 mmHg (exercise)]. As there is ample evidence for similar cardiovascular and ventilatory responses to electrically induced and voluntary exercise (Strange et al. 1993), the present results support the fact that the neural input from working muscle is crucial for the normal blood pressure response to exercise. Other haemodynamic and/or humoral mechanisms must operate in a decisive manner in the control of HR, CO and VE during dynamic exercise with large muscle groups.

Thoracic impedance and pulmonary atrial natriuretic peptide during head-up tilt induced hypovolaemic shock in humans.

Head up and down tilts were used for manipulating the central blood volume in eight volunteers. During head-up tilt thoracic electrical impedance (TI) increased from 36.7 (33.9-52.1) ohm (mean and range) to 41.9 (36.9-59.2) ohm, heart rate from 60 (49-72) to 80 (65-90) beats min-1 (P < 0.05) and decreased again to 57 (48-67) beats min-1 accompanying a fall in mean arterial pressure from 86 (76-97) to 54 (41-79) mmHg and in cardiac output from 9.2 (5.9-12.1) to 6.9 (3.4-8.8) 1 min-1 (n = 7, P < 0.07). Central venous pressure did not change significantly. Pulmonary arterial mean, 6 (3-12) mmHg, and wedge pressures, 4 (1-9) mmHg, decreased to 4 (1-11) and 1 (0-7) mmHg, respectively, and mixed, 78 (77-79%), and central venous oxygen saturations, 72 (71-73)%, fell to 62 (46-75) and 54 (44-58)%, respectively (P < 0.05). Atrial natriuretic peptide (ANP) was determined from blood of the superior vena cava and pulmonary and brachial arteries. Pulmonary artery ANP, 18.4 (7.5-30.7) pmol l-1, was higher than in vena cava, 13.3 (5.2-20.9) pmol l-1 (P < 0.05). At the time of presyncope, pulmonary artery ANP decreased from 20.8 (37.4-10.1) to 13.7 (19.7-5.7) pmol l-1, in vena cava from 13.8 (23.1-7.1) to 10.2 (17.9-6.7) pmol l-1 and in the brachial artery from 16.9 (34.1-5.2) to 11.3 (18.5-5.1) pmol l-1 (P < 0.05). Head-down tilt did not affect the recorded variables significantly. Thoracic electrical impedance, pulmonary artery pressure and venous oxygen saturations were sensitive indices of the central blood volume as reflected in the release of atrial natriuretic peptide from the right side of the heart.

Flumazenil facilitates intraoperative arousal during scoliosis surgery: a randomized, double-blind, placebo-controlled study.

Intraoperative arousal was evaluated in 24 patients (median age 16.5 years), undergoing spondylodesis with Cotrel-Dubousset or Harrington-Luque instrumentation. Flumazenil and placebo groups of 12 patients each were similar with respect to age, body weight, dosage of anaesthetic drugs and surgery times. Premedication consisted of diazepam 0.2-0.3 mg kg-1 orally. Anaesthesia was induced with thiopentone 5-7 mg kg-1, and maintained with 66% nitrous oxide in oxygen, and repeated doses of fentanyl, midazolam and atracurium. After placement and fixation of the metal rods, N2O was switched off, and either flumazenil or placebo was given in refracted doses until the patient responded to command. Intraoperative motor response times (medians with ranges), defined as the time from the injection of the first dose until the patient responded to command, were 2.5 min (1.0-5.2 min) after flumazenil, and 8.0 min (1.7-28.5 min) after placebo (P = 0.02). Five patients in the placebo group did not wake up within 10 min and received naloxone. The quality of awakening was similar in both groups. Two patients (one in each group) woke up violently and needed physical restraint. Postoperatively, motor responses were assessed after 12.0 min (5-42 min) in the flumazenil group, and after 15.2 min (4-40 min) in the placebo group (NS). Recovery from anaesthesia took 27.5 min (7-415 min) in the flumazenil group, and 25.0 min (8-160 min) in the placebo group (NS). One patient given flumazenil and one patient given placebo remembered moving their feet, but neither of them could recall anything unpleasant.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of serotonin receptor blockade on endocrine and cardiovascular responses to head-up tilt in humans.

Effects of blockade of serotonin (5-HT) receptors on the integrated cardiovascular and endocrine adaptations during head-up tilt were investigated in normal men. In control experiments 50 degrees head-up tilt increased heart rate (HR), total peripheral resistance (TPR), plasma renin activity (PRA) and sympathetic activity (plasma noradrenaline; NA). A moderate increase in pituitary-adrenal hormones (plasma ACTH, beta-END and cortisol) was observed. After a mean tilt time of 30 +/- 5 min (n = 20) presyncopal symptoms associated with decreases in HR, TPR and arterial pressure occurred. At this time pituitary hormones, cortisol, adrenomedullary (plasma adrenaline; A) as well as vagal activity (plasma pancreatic polypeptide) were markedly increased, whereas sympathetic activity (plasma NA) decreased. The 5-HT1+2 receptor antagonist methysergide did not significantly interfere with cardiovascular variables but attenuated the response of NA, prolactin (PRL), beta-endorphin (beta-END) and PRA (P < 0.02). The 5-HT2-receptor antagonist ketanserin reduced the tolerated tilt time (10 +/- 4 vs. 32 +/- 2 min; P < 0.0003, n = 7) but had no significant effects on hormonal variables. The 5-HT3-receptor antagonist ondansetron abolished the adrenomedullary response to hypotension without affecting cardiovascular tolerance or the activity of the pituitary-adrenal axis. The results suggest that serotonergic mechanisms may be involved in the integrated cardiovascular and endocrine responses to central blood volume depletion in humans.

Middle cerebral artery velocity during head-up tilt induced hypovolaemic shock in humans.

Middle cerebral artery mean velocity (Vmean) and pulsatility index (PI) were followed during head-up tilt induced hypovolaemic shock in nine subjects. Mean arterial pressure (MAP), heart rate (HR), central venous pressure (CVP) and thoracic (TI) electrical impedance were also recorded. Vmean, PI, and CVP did not change during head-up tilt to 50 degrees, while MAP increased from 92 (81-106) (median and range) to 100 (97-112) mmHg, HR from 63 (53-74) to 84 (68-89) beats min-1 and TI100kHz from 30 (27-36) to 32 (30-39) Ohm (P < 0.01) (n = 8). During maintained tilt, Vmean decreased from 52 (32-72) to 34 (16-59) cm s-1, whereas HR increased to 87 (52-108) beats min-1 and TI100 kHz to 33 (31-39) Ohm (P < 0.01). Presyncopal symptoms appeared after 33 (3-46) min and were associated with a MAP of 65 (32-84) mmHg (P < 0.01) and a HR of 58 (52-71) beats min-1 (P < 0.05). Vmean decreased to 25 (16-36) cm s-1, and cerebral conductance index (Vmean/MAPbrain) and PI increased (P < 0.01). Arterial collapse was observed (diastolic velocity of zero) in one subject at a brain (diastolic) blood pressure of 21 mmHg and he developed tachycardia (131 beats min-1) during presyncope. PaCO2 did not change. Maintained tilt resulted in central volume depletion reflected by changes in MAP, HR, and thoracic electrical impedance but not in CVP. Transcranial Doppler derived indices of cerebral perfusion demonstrated critically low values despite marked increase in conductance index.

An indifference point for electrical impedance in humans.

Regional electrical impedance was used over eight sections of the human body (two thoracic; one abdominal; two thigh; two around the knee; and one lower leg) to determine the volume indifference point during passive head-up tilt in eight subjects. Head-up tilt was performed in 10 degrees increments from 0 degree to 60 degrees over 6 min. Electrical impedance increased over the thorax in proportion to the head-up tilt angle, while abdominal impedance did not change significantly, and over the thigh and the lower leg it decreased with increasing head-up tilt angle. No change in electrical impedance was noted just above the knee, and electrical impedance just below the knee decreased only marginally. Results demonstrate minimal fluid accumulation around the knee during head-up tilt. Furthermore, in humans the electrical impedance and therefore probably the volume indifference point is positioned between the umbilicus and crista iliaca.

Effect of limb anesthesia on middle cerebral response to handgrip.

Transcranial Doppler ultrasound was used to measure middle cerebral arterial mean flow velocity (Vmean) on both sides of the brain in 12 subjects during hand contractions before and during regional anesthesia of the left arm. At rest Vmean was 49 (36-104) cm/s (median and range) and was unaffected by regional anesthesia. During right-hand contractions Vmean remained unchanged on the right side of the brain, whereas it increased 20 (4-37)% (P < 0.01) on the left side of the brain. Similarly, during left-hand contractions Vmean increased 24 (2-42)% (P < 0.01) on the right side of the brain, while it remained unchanged on the left side of the brain. Regional anesthesia did not quantitatively affect Vmean during right-hand contractions. In contrast, during left-hand contractions, both right and left Vmean tended to decrease. Increases in Vmean appeared despite a decrease in arterial carbon dioxide tension (P < 0.01). Heart rate and blood pressure responses to hand contractions were enhanced during regional anesthesia (P < 0.01), but left-hand contractions resulted in a less pronounced increase in blood pressure (P < 0.01). These data demonstrate a contralateral increase in cerebral perfusion during hand contractions that is dependent on intact afferent input from the working limb.

Regional cerebral artery mean flow velocity and blood flow during dynamic exercise in humans.

Transcranial Doppler ultrasound-determined middle (MCA) and anterior (ACA) cerebral artery mean flow velocities (Vmean) and pulsatility indexes (PI) were measured during "no-load" [21, 60, and 102 revolutions/min (rpm)] and loaded cycling (30, 60, and 149 W) at approximately 60 rpm. At rest Vmean MCA was 51 (36-55) cm/s (median and range; n = 10) and Vmean ACA was 41 (36-49) cm/s (n = 7; P < 0.05). With no load on the cycle Vmean MCA increased 4 (2-36), 10 (0-47), and 27% (4-58) (P < 0.05) at the three pedaling frequencies, respectively; arterial PCO2 (PaCO2) remained constant. During loaded cycling the increases were 19 (6-42), 25 (2-45), and 32% (12-67) (P < 0.01), respectively, with only a minimal change in PaCO2. No significant changes were observed in Vmean ACA. Changes in Vmean MCA were similar to those recorded by the initial slope index (ISI) of the 133Xe clearance method (n = 11), which in turn were smaller than increases recorded by the fast-compartment flow. PI ACA followed PI MCA during no-load as well as loaded exercise and increased with work rate, perhaps reflecting an increase in pulse pressure from 56 (48-63) mmHg at rest to 109 (88-123) mmHg at 149 W (P < 0.01). Data demonstrate a graded increase in regional cerebral perfusion during dynamic exercise corresponding to the MCA territory.

Thoracic impedance as an index of body fluid balance during cardiac surgery.

Thoracic impedance at 2.5 (TI2.5) and 100 kHz (TI100), central venous pressure (CVP), and body fluid balance were recorded together with rectal temperature and arterial haematocrit in 15 consecutive patients subjected to coronary artery bypass grafting. I.v. fluid and blood were administered in an excess of 3.18 (1.38-9.35) 1 during the operation. TI2.5 decreased from 51.7 (39.2-66.4) to 34.9 (21.1-45.7) ohm (P = 0.001), while TI100 decreased from 41.9 (31.4-55.0) to 30.3 (18.3-40.8) ohm (P = 0.002). CVP, 6 (3-11) mmHg [0.8 (0.4-1.5) kPa], was the same before and after surgery. Temperature decreased during cardiopulmonary bypass from 35.4 (34.1-36.6) to 26.7 (22.9-31.0) degrees C and haematocrit from 39 (34-46)% to a lowest value of 27 (23-32)% (P = 0.0001). A close linear correlation between TI and body fluid balance was observed (TI2.5: r = -0.96, TI100: r = -0.95, P = 0.0001). Corrections of TI for temperature and/or haematocrit improved the correlation between TI and fluid balance to 0.99 (TI2.5) and 0.98 (TI100). The data indicate that changes in thoracic impedance can be used to monitor body fluid balance during cardiac surgery.

Blood volume distribution during head-up tilt induced central hypovolaemia in man.

We evaluated regional electrical impedance (Z degree) at 2.5 and 100 kHz to separate intra- and extracellular fluid changes and correlated Z degree over the thorax (TI) to relative changes in the central blood volume (CBV) induced by head-up tilt. In nine experiments head-up tilt resulted in normotensive central hypovolaemia associated with a 3.7 +/- 0.4 Ohm (mean +/- SE) increase in TI100 kHz after 60 min. In 24 experiments pre-syncopal symptoms were induced after 43 +/- 2 min, when TI100 kHz had increased 4.2 +/- 0.2 Ohm. Head-up tilt instantly decreased the activity of technetium labelled erythrocytes (99Tcm) over the thorax by 24 +/- 2%, and increased 99Tcm over the thigh by 68 +/- 10% (P less than 0.01, n = 8) with no further changes during the sustained tilt. Haematocrite increased during head-up tilt from 43.1 +/- 0.3 to 47.9 +/- 0.6% (P less than 0.01, n = 8). Accordingly, the increase in TI (6.3 +/- 0.6 vs. 4.5 +/- 0.4 Ohm, n = 6) and the decrease in Z degree through one leg (7.2 +/- 1.2 vs. 2.8 +/- 0.5 Ohm, n = 6) at 2.5 kHz was more pronounced than at 100 kHz. Also the changes in TI were correlated to CBV as calculated from 99Tcm and haematocrite (r = 0.90, P less than 0.01). The results suggest that: (1) Hypovolaemic shock is associated with a faster increase of TI than normotensive head-up tilt. (2) Head-up tilt is characterized by an initial decrease in CBV followed by a further decrease in plasma volume, which eventually leads to hypovolaemic shock. (3) Blood volume changes during head-up tilt are reflected in regional Z degree.