Differential effects of sevoflurane and propofol anesthesia on left ventricular-arterial coupling in dogs.

BACKGROUND: General anesthetics interfere with arterial and ventricular mechanical properties, often altering left ventricular-arterial (LVA) coupling. We hypothesized that sevoflurane and propofol alter LVA coupling by different effects on arterial and ventricular properties. METHODS: Experiments were conducted in six anesthetized open-chest dogs for the measurement of left ventricular pressure and aortic pressure and flow. Measurements were performed during anesthesia with 0.5, 1.0 and 1.5 minimum alveolar concentration sevoflurane and 12, 24 and 36 mg/kg/h propofol. LVA coupling was assessed as the ratio of ventricular end-systolic elastance (E(es), measuring ventricular contractility) to effective arterial elastance (E(a), measuring ventricular afterload). The steady component of afterload, arterial tone, was assessed by systemic vascular resistance and arterial pressure-flow curves. The pulsatile component of afterload was assessed by aortic impedance and compliance. RESULTS: Sevoflurane decreased aortic pressure and cardiac output more than propofol. Sevoflurane reduced arterial tone, increased arterial stiffness and did not affect wave reflections. It increased E(a), decreased E(es) and reduced LVA coupling. Propofol reduced arterial tone, did not affect arterial stiffness and decreased wave reflections. It did not affect E(a), E(es) or LVA coupling. CONCLUSIONS: Sevoflurane increased ventricular afterload and decreased ventricular performance, thereby altering LVA coupling. Propofol did not affect ventricular afterload or ventricular performance, thereby preserving LVA coupling. Thus, propofol preserves LVA coupling in dogs better, and might be a better choice for patients with compromised left ventricular function.

Non-heart-beating donation: ethical aspects.

Non-heart-beating donation (NHBD) is under considerable ethical debate including concerns that the donor is not really dead when organs are procured and that withdrawing therapy may be expedited to harvest needed organs. We suggest a two-step process to NHBD based largely on the ethical principle of beneficence. First, once a decision has been made that there is no reasonable hope of survival for the patient and that active treatment is of no further benefit and should be withdrawn, NHBD can be suggested. Second, once the decision for NHBD has been made, there is no reason for further delay and withdrawal of treatment should be implemented as rapidly as possible to ensure that the quality of the donated organs remains optimal for the maximal benefit of the organ recipient.

Survival and quality of life after prolonged intensive care unit stay.

There are few data on long-term outcomes in mixed groups of intensive care unit (ICU) patients with prolonged stays. We evaluated the relationship between length of stay in the ICU and long-term outcome in all patients admitted to our 31-bed department of medico-surgical intensive care over a one-year period who stayed in the department for more than 10 days (n = 189, 7% of all ICU admissions). Mortality increased with length of stay from 1 to 10 days (1 day 5%, 5 days 15%, 9 days 24%, 10 days 33%) but remained stable at about 35% for longer ICU stays. In the long-stay patients, the most common reasons for ICU admission were intracranial bleeding (23%), polytrauma (14%), respiratory failure (13%) and septic shock (11%). The main reasons for prolonged ICU stay were ventilator dependency (40%), infectious complications (23%) and coma (16%). Long-stay patients had a 65% ICU survival, 55% hospital survival and 37% one-year survival. At one-year follow-up, 73% of surviving patients reported no or minor persistent physical complaints compared to before the acute illness; 27% had a major functional impairment, including 8% who required daily assistance. In conclusion, in ICU patients, mortality increases with length of stay up to 10 days. Patients staying in the ICU for more than 10 days have a relatively good long-term survival. Most survivors have an acceptable quality of life.

Expression of the serotonin 1b receptor in experimental pulmonary hypertension.

The pathogenesis of pulmonary arterial hypertension (PAH) remains uncertain. Both the serotonin and endothelin (ET) systems are believed to be involved. Recent studies pointed to the importance of the serotonin 2B receptor as a limiting step. The current authors investigated the lung tissue expression of serotonin receptors and of the serotonin transporter (5-HTT) by real-time-quantitative polymerase chain reaction in chronic overcirculation-induced PAH in growing piglets, with and without treatment with the dual ET receptor blocker bosentan. Pulmonary haemodynamic changes were described by pulmonary arterial impedance spectra. Three months after the surgical anastomosis of the left subclavian artery to the pulmonary arterial trunk, there was a shift of the impedance spectra to higher ratios of pressure and flow moduli, with increases in both 0 Hz impedance and characteristic impedance, and these changes were completely prevented by bosentan therapy. There was an increase in the expression of the serotonin 1B receptor. There was no change in the expression of the 5-HTT, and of the serotonin 2B, 1D, and 4 receptors. The overexpression of the serotonin 1B receptor was partially prevented by bosentan therapy. The present authors conclude that this early pulmonary arterial hypertension model is characterised by an endothelin receptor-dependent increased expression of the serotonin 1B receptor.

Single arterial occlusion to locate resistance in patients with pulmonary hypertension.

The purpose of this study was to determine the site of increased resistance using the arterial occlusion technique in patients with severe pulmonary hypertension. Pulmonary vascular resistance was partitioned in arterial and venous components based on double exponential fitting analysis of the pulmonary artery pressure decay curve: after balloon occlusion in 36 patients with pulmonary arterial hypertension (PAH); at baseline and during the inhalation of 20 parts per million of nitric oxide (NO); in four patients with chronic thromboembolic pulmonary hypertension; and in two patients with pulmonary veno-occlusive disease. In the patients with PAH, at baseline, mean pulmonary artery pressure was 56+/-2 mmHg (mean+/-SE), with an arterial component of resistance of 63+/-1%. Inhaled NO did not change the partition of resistance. The arterial component of resistance amounted on average to 42% and 77% in the patients with veno-occlusive disease and the patients with thromboembolic pulmonary hypertension, respectively. However, the partitioning of resistance did not discriminate between these three diagnostic categories. The occlusion technique may help to locate the predominant site of increased resistance in patients with severe pulmonary hypertension, but does not allow for a satisfactory differential diagnosis on an individual basis.

Haemodynamic evaluation of pulmonary hypertension.

Pulmonary hypertension is characterised by the chronic elevation of pulmonary artery pressure (PAP) and pulmonary vascular resistance (PVR) leading to right ventricular enlargement and hypertrophy. Pulmonary hypertension may result from respiratory and cardiac diseases, the most severe forms occurring in thromboembolic and primary pulmonary hypertension. Pulmonary hypertension is most often defined as a mean PAP >25 mmHg at rest or >30 mmHg during exercise, the pressure being measured invasively with a pulmonary artery catheter. Doppler echocardiography allows serial, noninvasive follow-up of PAPs and right heart function. When the adaptive mechanisms of right ventricular dilatation and hypertrophy cannot compensate for the haemodynamic burden, right heart failure occurs and is associated with poor prognosis. The haemodynamic profile is the major determinant of prognosis. In both primary and secondary pulmonary hypertension, special attention must be paid to the assessment of pulmonary vascular resistance index (PVRI), right heart function and pulmonary vasodilatory reserve. Recent studies have stressed the prognostic values of exercise capacity (6-min walk test), right atrial pressure, stroke index and vasodilator challenge responses, as well as an interest in new imaging techniques and natriuretic peptide determinations. Overall, careful haemodynamic evaluation may optimise new diagnostic and therapeutic strategies in pulmonary hypertension.

[The intensive care department]. / Le Service des Soins Intensifs.

Intensive Care Departments are designed for the care of the critically ill, and are equipped with all the material necessary for monitoring and treatment, as well as specially trained medical, nursing, and paramedical staff. With a team of more than 170 highly qualified staff, the Department of Intensive Care at Erasme Hospital, has acquired a national and international reputation in the fields of clinical and experimental research and education, as well as for its standards of clinical practice. Clinical and experimental studies have been high in quantity and quality, and have covered all the key areas in the field of intensive care medicine: severe sepsis, multiple organ failure, transport and metabolism of oxygen, systemic and regional hemodynamic alterations (pulmonary, cerebral, hepato-splanchnic,...), metabolic disorders,... not forgetting issues associated with the complexities of medical ethics. The quality of care, clinical, scientific and personal, offered by the Department of Intensive Care at Erasme Hospital has earned it the high level reputation for which it is renowned in Belgium, and indeed worldwide.

Physiology in medicine: importance of hypoxic pulmonary vasoconstriction in maintaining arterial oxygenation during acute respiratory failure.

Hypoxic pulmonary vasoconstriction continues to attract interest more than half a century after its original report because of persistent mystery about its biochemical mechanism and its exact physiological function. Recent work suggests an important role for pulmonary arteriolar smooth muscle cell oxygen-sensitive voltage-dependent potassium channels. Inhibition of these channels by decreased PO2 inhibits outward potassium current, causing membrane depolarization, and calcium entry through voltage-dependent calcium channels. Endothelium-derived vasoconstricting and vasodilating mediators modulate this intrinsic smooth muscle cell reactivity to hypoxia. However, refined modeling of hypoxic pulmonary vasoconstriction operating as a feedback mechanism in inhomogeneous lungs, using more realistic stimulus-response curves and confronted with direct measurements of regional blood flow distribution, shows a more effective than previously assessed ability of this remarkable intrapulmonary reflex to improve gas exchange and arterial oxygenation. Further studies could show clinical benefit of pharmacological manipulation of hypoxic pulmonary vasoconstriction, in circumstances of life-threatening hypoxemia.

Inhibition of hypoxic pulmonary vasoconstriction by carbon monoxide in dogs.

OBJECTIVE: We tested the hypothesis that carbon monoxide might participate in the modulation of hypoxic pulmonary vasoconstriction (HPV) by prostacyclin (PGI2) and nitric oxide. DESIGN: Prospective, interventional study. SETTING: University laboratory. SUBJECTS: Nineteen intact anesthetized mongrel dogs. INTERVENTIONS: Right heart catheterization for the measurements of mean pulmonary artery pressure (Ppa), left atrial pressure estimated from occluded Ppa (Ppao), pulmonary capillary pressure (Pcp) calculated from the Ppa decay curve after balloon occlusion, and cardiac output (Q); inferior vena cava balloon for the control of Q by manipulation of venous return; ventilation in hyperoxia (fraction of inspired O2, 0.4) or in hypoxia (Fio2, 0.1); inhibition of cyclooxygenase by indomethacin (Indo); inhibition of nitric oxide synthase by NG-nitro-l-arginine (L-NA); inhibition of heme oxygenase by mesoporphyrin IX (SnMP); inhalation of nitric oxide (20 ppm); and inhalation of carbon monoxide (100 ppm). MEASUREMENTS AND MAIN RESULTS: The first seven dogs were weak responders to hypoxia as assessed by a hypoxia-induced increase in the gradient between Ppa and Ppao, measured at one level of Q kept constant, by an average of only 2 mm Hg (p = NS). This HPV was markedly increased by the combined administration of Indo and L-NA. A further enhancement of HPV was observed after the addition of SnMP, leading to severe pulmonary hypertension with an average increase in Ppa to 39 mm Hg. Inhaled nitric oxide inhibited HPV only after the combined administration of Indo, L-NA, and SnMP. Inhaled carbon monoxide had no effect. The next 12 dogs were stronger responders to hypoxia, as assessed by a hypoxia-induced increase in the gradient between Ppa and Ppao, measured at several levels of Q, by an average of 3 mm Hg (p <.05). This HPV was of the same magnitude after administration of placebo (n = 6) or SnMP (n = 6). Addition of Indo enhanced HPV to the same extent in the placebo and in the SnMP groups. Addition of L-NA induced a further enhancement of HPV, which was, however, greater in the SnMP group. There was a slight increase in the capillary-venous segment relative to the arterial segment in hypoxic conditions, but the partitioning of pulmonary vascular resistance was otherwise unaffected by nitric oxide, carbon monoxide, or PGI2. CONCLUSIONS: Endogenous carbon monoxide modulates canine HPV only in the absence of nitric oxide. The vasodilation mediated by nitric oxide, PGI2, or carbon monoxide is essentially distributed between proximal and distal sites proportionally to the degree of constriction produced during hypoxia.

Continuous versus pulsatile pulmonary hemodynamics in canine oleic acid lung injury.

Pulmonary hypertension occurs commonly in the acute respiratory distress syndrome (ARDS), but associated right ventricular failure is relatively rare. We tested the hypothesis that this apparent contradiction is explained by a peripheral location of the increased pulmonary vascular resistance (Rpva). Experimental ARDS was induced in eight dogs by injection of oleic acid (0.07 ml/kg). Changes in Rpva were evaluated by measurements of pulmonary artery pressure (Ppa) at several levels of flow (Q), which was altered by manipulation of venous return. The analysis of Ppa decay curves after arterial balloon occlusion was used to partition Rpva into arterial and venous segments. Right ventricular afterload was evaluated by determination of pulmonary vascular impedance (Zpva), which was calculated from spectral analysis of Ppa and Q waves. Oleic acid lung injury was associated with an increase in both the slope and the extrapolated pressure intercept of Ppa/Q plots, no change in the partitioning of Rpva, no change in time-domain indices in wave reflection or in pulmonary arterial compliance, and a decrease in both the characteristic impedance and pulsatile component of total right ventricular hydraulic load. We conclude that the site of increased Rpva in oleic acid lung injury is the smallest pulmonary arterioles, which, together with a decreased characteristic impedance, contributes to minimize right ventricular afterload.

Permissive hypercapnia impairs pulmonary gas exchange in the acute respiratory distress syndrome.

Current recommendations for mechanical ventilation in the acute respiratory distress syndrome (ARDS) include the use of small tidal volumes (VT), even at the cost of respiratory acidosis. We evaluated the effects of this permissive hypercapnia on pulmonary gas exchange with the multiple inert gas elimination technique (MIGET) in eight patients with ARDS. After making baseline measurements, we induced permissive hypercapnia by reducing VT from 10 +/- 2 ml/kg to 6 +/- 1 ml/kg (mean +/- SEM) at constant positive end-expiratory pressure. After restoration of initial VT, we infused dobutamine to increase cardiac output (Q) by the same amount as with hypercapnia. Permissive hypercapnia increased Q by an average of 1.4 L. min(-)(1). m(2), decreased arterial oxygen tension from 109 +/- 10 mm Hg to 92 +/- 11 mm Hg (p < 0.05), markedly increased true shunt (Q S/Q T), from 32 +/- 6% to 48 +/- 5% (p < 0.0001), and had no effect on the dispersion of VA/Q.VA/Q. On reinstatement of baseline V T with maintenance of a high Q, Q S/Q T remained increased, to 38 +/- 6% (p < 0.05), and Pa(O(2 ))remained decreased, to 93 +/- 4 mm Hg (p < 0. 05). These results agreed with effects of changes in VT and Q predicted by the mathematical lung model of the MIGET. We conclude that permissive hypercapnia increases pulmonary shunt, and that deterioration in gas exchange is explained by the combined effects of increased Q and decreased alveolar ventilation.

Pulse pressure method and the area method for the estimation of total arterial compliance in dogs: sensitivity to wave reflection intensity.

We estimated total arterial compliance (C) in eight anesthetized mongrel dogs with (i) the area method (AM), (ii) the pulse pressure method (PPM), and (iii) the stroke volume-to-pulse pressure ratio (SV/PP). Average compliance was C(AM)=1.1+/-0.73 ml mm Hg(-1) using AM; C(PPM)=0.60+/-0.31 ml mm Hg(-1) using PPM and C(SV/PP)=0.87+/-0.49 ml mm Hg(-1) using SV/PP. Mean aortic pressure was 64+/-23 mm Hg. The overall agreement between C(AM) and C(PPM) was relatively poor (C(AM)=0.15+/-1.61 C(PPM); r2=0.48), with a consistent overestimation of the area method with respect to the pulse pressure method. There was a significant correlation (r=-0.78) between the relative difference between PPM and AM, and the modulus of the first harmonic of the wave reflection coefficient [gamma] which was low in our dog population (0.37+/-0.18). SV/PP overestimated PPM, but both methods were highly correlated (C(SV/PP)=0.06+/-1.60C(PPM); r2=0.97). C(SV/PP) and C(AM) were similar only for [gamma]>0.4. The effect of isolated changes of [gamma] on PPM, AM, and SV/PP was studied using the linear wave separation technique. The area method appeared very sensitive to the wave reflection intensity. For low reflection coefficients, the diastolic wave profile was flattened and compliance was overestimated. PPM and SV/PP were relatively independent of [gamma] and remained even applicable for [gamma]=0. We believe that the pulse pressure method is the most consistent method for the estimation of total arterial compliance in hemodynamic conditions characterized by a low wave reflection intensity.

Effects of low flow on pulmonary vascular flow-pressure curves and pulmonary vascular impedance.

OBJECTIVE: Flow-pressure curves and vascular impedance are commonly used to investigate pulmonary circulation, but they may be affected at low flow by reflex neurohumoral activation. We therefore investigated the mechanical effects and the reflex effects of decreased flow on pulmonary vascular resistance and impedance. METHODS: In ten anaesthetized dogs, we compared flow-pressure curves generated in less than 10 s to prevent sympathetic activation (fast curves), or generated over 20-30 min to allow neurohumoral equilibration (slow curves), in hyperoxia (inspired oxygen, 40%) and in hypoxia (inspired oxygen, 10%), before and after adrenergic blockade by phentolamine and propranolol. Resistance was assessed from the flow-pressure relationship. Impedance was computed from instantaneous flow and pressure obtained with an ultrasonic flowmeter and a micromanometer-tipped catheter. RESULTS: At baseline, fast flow-pressure curves were steeper and had a lower pressure intercept. Transient low flow did not affect heart rate or pulmonary arterial elastance. Sustained low flow increased heart rate, resistance and elastance, suggesting baroreceptor-induced sympathetic stimulation. After adrenergic blockade, no difference persisted between effects of transient and sustained low flow. In hypoxia, slow and fast flow-pressure curves were similar. Hypoxia increased heart rate and resistance but did not decrease elastance, suggesting chemoreceptor-induced sympathetic stimulation. In hypoxia, differences between transient and sustained low flow were no longer significant, and were completely suppressed by adrenergic blockade. In two additional dogs, epinephrine infusion increased pulmonary vascular resistance and elastance. CONCLUSIONS: We conclude that (1) compared to transient low flow, sustained low flow is associated with increases in distal resistance and proximal elastance due to sympathetic stimulation and (2) these differences between the effects of transient and sustained low flow do not persist in hypoxia, because of an already present chemoreceptor-induced sympathetic stimulation.

Pulmonary arterial compliance in dogs and pigs: the three-element windkessel model revisited.

In six dogs and six weight-matched miniature pigs at baseline and after pulmonary embolization, pulmonary arterial compliance was determined using the pulse pressure method (C(PPM)), the three-element windkessel model (C(WK-3)), and the ratio of stroke volume to pulse pressure (SV/PP). C(PPM) was lower in pigs than in dogs at baseline (0.72 +/- 0.23 vs. 1.14 +/- 0.29 ml/mmHg, P < 0.05) and after embolism (0.37 +/- 0.14 vs. 0.54 +/- 0.16 ml/mmHg, P = 0. 07) at matched flow, but not at matched flow and pressure. C(PPM) showed the expected inverse relation with pressure and a direct relation with flow. C(WK-3) was closely correlated with C(PPM), except for all dogs at baseline where C(WK-3) was up to 100% higher than C(PPM). Excluding these data, regression analysis yielded C(WK-3) = -0.01 + 1.30. C(PPM) (r(2) = 0.97). C(WK-3) was found to be unreliable when input impedance first harmonic modulus was close to characteristic impedance, i.e., when reflections were small. SV/PP correlated well with C(PPM) (SV/PP = -0.10 + 1.76. C(PPM), r(2) = 0.89). We conclude that 1) C(PPM) is a consistent estimate of pulmonary arterial compliance in pigs and dogs, 2) C(WK-3) and SV/PP overestimate compliance, and 3) C(WK-3) is unreliable when wave reflections are small.

Septic shock without documented infection: an uncommon entity with a high mortality.

OBJECTIVES: To determine whether patients with clinically identified infection have the same outcome as patients with apparent sepsis but no identified infectious source. DESIGN: Retrospective analysis of patient data. PATIENTS: All patients treated with septic shock in a 31-bed intensive care unit (ICU) over a 3-year period. RESULTS: Data from 227 patients were analysed. Eighty-seven percent had a clinically identified source of infection. ICU mortality was higher in septic shock patients without a clinically identified source of infection than in those with an identified source of infection (86% versus 66%, p < 0.05). CONCLUSIONS: A small number of patients presenting with septic shock have no clinically identified infection. These patients have a higher mortality rate than patients in whom an infection is identified.

Partitioning of pulmonary vascular resistance in primary pulmonary hypertension.

OBJECTIVES: This study sought to determine the site of increased pulmonary vascular resistance (PVR) in primary pulmonary hypertension by standard bedside hemodynamic evaluation. BACKGROUND: The measurement of pulmonary vascular pressures at several levels of flow (Q) allows the discrimination between active and passive, flow-dependent changes in mean pulmonary artery pressure (Ppa), and may detect the presence of an increased pulmonary vascular closing pressure. The determination of a capillary pressure (Pc') from the analysis of a Ppa decay curve after balloon occlusion allows the partitioning of PVR in an arterial and a (capillary + venous) segment. These approaches have not been reported in primary pulmonary hypertension. METHODS: Ppa and Pc' were measured at baseline and after an increase in Q induced either by exercise or by an infusion of dobutamine, at a dosage up to 8 microg/kg body weight per min, in 11 patients with primary pulmonary hypertension. Reversibility of pulmonary hypertension was assessed by the inhalation of 20 ppm nitric oxide (NO), and, in 6 patients, by an infusion of prostacyclin. RESULTS: At baseline, Ppa was 52+/-3 mm Hg (mean value+/-SE), Q 2.2+/-0.2 liters/min per m2, and Pc' 29+/-3 mm Hg. Dobutamine did not affect Pc' and allowed the calculation of an averaged extrapolated pressure intercept of Ppa/Q plots of 34 mm Hg. Inhaled NO had no effect. Prostacyclin decreased Pc' and PVR. Exercise increased Pc' to 40+/-3 mm Hg but did not affect PVR. CONCLUSIONS: ns. These findings are compatible with a major increase of resistance and reactivity at the periphery of the pulmonary arterial tree.

Effects of pulmonary embolism on pulmonary vascular impedance in dogs and minipigs.

Pigs have been reported to present with a stronger pulmonary vascular reactivity than many other species, including dogs. We investigated the pulmonary vascular impedance response to autologous blood clot embolic pulmonary hypertension in anesthetized and ventilated minipigs (n = 6) and dogs (n = 6). Before embolization, minipigs, compared with dogs, presented with higher mean pulmonary arterial pressure (Ppa; by an average of 9 mmHg), a steeper slope of Ppa-flow (Q) relationships, and higher 0-Hz impedance (Z0) and first-harmonic impedance (Z1), without significant differences in characteristic impedance (Zc), and a lower ratio of pulsatile hydraulic power to total hydraulic power. Embolic pulmonary hypertension (mean Ppa: 40-55 mmHg) was associated with increased Z0 and Z1 in both species, but the minipigs had a steeper slope of Ppa/Q plots and an increased Zc. At identical Q and Ppa, minipigs still presented with higher Z1 and Zc and a lower ratio of pulsatile hydraulic power to total hydraulic power. The energy transmission ratio, defined as the hydraulic power in the measured waves divided by the hydraulic power in the forward waves, was better preserved after embolism in minipigs. No differences in wave reflection indexes were found before and after embolism. We conclude that minipigs, compared with dogs, present with a higher pulmonary vascular resistance and reactivity and adapt to embolic pulmonary hypertension by an increased Zc without earlier wave reflection. These differences allow for a reduced pulsatile component of hydraulic power and, therefore, a better energy transfer from the right ventricle to the pulmonary circulation.

False-positive diagnosis of pulmonary hypertension by Doppler echocardiography.

A 37-yr-old female presented with a history of several months of exertional dyspnoea. A diagnosis of primary pulmonary hypertension was suspected on the basis of a negative extensive cardiorespiratory work-up with a systolic pulmonary artery pressure of 41-46 mmHg calculated from repeated measurement of the maximum velocity of tricuspid regurgitation jets at 2.8-3 m x s(-1) by continuous-wave Doppler echocardiography. However, a right heart catheterization with a high-fidelity transducer-tipped catheter revealed pulmonary artery pressures of 22/8 mmHg at rest, which remained within normal limits at exercise. This case indicates a possible misleading overestimation of pulmonary artery pressures from Doppler echocardiographic studies of tricuspid regurgitation.

Effects of positioning and exercise on intracranial pressure in a neurosurgical intensive care unit.

BACKGROUND AND PURPOSE: The purpose of the study was to assess the safety of physical therapy by investigating its effects on intracranial pressure (ICP) and cerebral perfusion pressure. SUBJECTS: The subjects were 65 patients in a neurosurgical intensive care unit who had normal ICP (< 15 mm Hg) or increased ICP (> 15 mm Hg). METHODS: Intraventricular ICP was measured in a 30-degree head-up position (all patients) and in supine and 45-degree head-up positions (patients with normal ICP) during passive range of motion (comatose patients) and exercises involving limb movement (awake patients). RESULTS: In patients with normal ICP, passive range of motion decreased mean ICP by 1 mm Hg in the supine position but not in the head-up position. In patients with high ICP, it decreased ICP by 2 mm Hg. Limb exercises left the mean ICP essentially unchanged in both the patients with normal ICP and the patients with high ICP. Isometric hip adduction increased mean ICP by 4 mm Hg in patients with normal ICP. It did not affect ICP in patients with high ICP. Limb movement was associated with suppression of abnormal ICP waves and improvement of consciousness in 13 patients. CONCLUSION AND DISCUSSION: Physical therapy can be used safely in patients with normal or increased ICP provided that Valsalva-like maneuvers are avoided. [Brimioulle S, Moraine J-J, Norrenberg D, Kahn RJ. Effects of positioning and exercise on intracranial pressure in a neurosurgical intensive care unit.

Sympathetic modulation of hypoxic pulmonary vasoconstriction in intact dogs.

BACKGROUND: The effects of the sympathetic nervous system on hypoxic pulmonary vasoconstriction (HPV) have been reported variably. We studied the effects of adrenergic receptor blockade and epidural blockade on HPV in 32 pentobarbital-anaesthetised intact dogs. METHODS: Pulmonary arterial flow-pressure relationships were determined in hyperoxia and hypoxia, at baseline and after alpha-blockade (phentolamine 2 mg/kg + 50 micrograms.kg-1.-1), beta-blockade (propranolol 2 mg/kg), alpha beta-blockade, epidural blockade (lignocaine 20 mg/kg), and alpha beta-plus epidural blockade. RESULTS: At reference flow of 3.5 1.min-1.m-2, the mean hypoxic response (hypoxia-induced increase in transpulmonary pressure gradient, each n = 8) changed from 6.0 +/- 0.9 to 3.5 +/- 1.0 mmHg after alpha-blockade, from 5.8 +/- 0.9 to 0.7 mmHg after beta-blockade, from 4.1 +/- 0.8 to 0.9 +/- 1.4 mmHg after alpha beta-blockade from 3.4 +/- 1.0 to 4.3 +/- 0.9 mmHg after epidural blockade (all P < 0.05), and was not affected by epidural blockade after alpha beta-blockade. CONCLUSIONS: In pentobarbital-anaesthetised dogs, (1) HPV is attenuated by alpha- and enhanced by beta-, alpha beta- and epidural blockade, and (2) epidural blockade has no significant adrenergic-unrelated effect on the pulmonary vasculature.