Larger Increase In Cardiac Output Research Articles

Role of the Air-Blood Barrier Phenotype in Lung Oxygen Uptake and Control of Extravascular Water.

The air blood barrier phenotype can be reasonably described by the ratio of lung capillary blood volume to the diffusion capacity of the alveolar membrane (Vc/Dm), which can be determined at rest in normoxia. The distribution of the Vc/Dm ratio in the population is normal; Vc/Dm shifts from ∼1, reflecting a higher number of alveoli of smaller radius, providing a high alveolar surface and a limited extension of the capillary network, to just opposite features on increasing Vc/Dm up to ∼6. We studied the kinetics of alveolar-capillary equilibration on exposure to edemagenic conditions (work at ∼60% maximum aerobic power) in hypoxia (HA) (PIO2 90 mmHg), based on an estimate of time constant of equilibration (τ) and blood capillary transit time (Tt). A shunt-like effect was described for subjects having a high Vc/Dm ratio, reflecting a longer τ (>0.5 s) and a shorter Tt (<0.8 s) due to pulmonary vasoconstriction and a larger increase in cardiac output (>3-fold). The tendency to develop lung edema in edemagenic conditions (work in HA) was found to be directly proportional to the value of Vc/Dm as suggested by an estimate of the mechanical properties of the respiratory system with the forced frequency oscillation technique.

Abstract 16412: The Predictors of Hemodynamic Response to Phosphodiesterase-5a Inhibition in Advanced HFrEF

Introduction: In advanced HFpEF, acute phosphodiesterase 5 (PDE5) inhibition leads to favorable change in pulmonary vascular resistance (PVR) and to an increased cardiac output (CO) of variable degree. The determinants of the response are poorely understood. Methods: 47 HFrEF patients (85% males, 57±11 years, NYHA 2.9±0.5, 55% non-ischemic, PAmean 42±8 mmHg, 43% RV dysfunction) underwent clinical exam, echocardiography, biochemical tests and right heart catheterization (RHC) before and after I.V. administration of sildenafil (20 mg). Baseline predictors of absolute and relative (%diff) change of PVR and CO were studied. Results: PDE5i led to highly significant (p&lt;0.001) reduction of pulmonary artery (PA) mean pressure (-11±9 mmHg), PVR (-2.2±1.6 WU;-42±24%), PA wedge pressure (-5.2±7.3 mmHg), CVP (-3.2±2.3 mmHg) and to increase in cardiac output (+0.6±0.7 l/min; +18±23%). PVR decreased more than systemic resistance (PVR/SVR -27±30%diff). Predictors of high CO response (COdiff%) were: low BMI, no diabetes, low baseline CO and severity of mitral or tricuspid regurgitation (r=0.53 or =0.43, both p&lt;0.003). The strongest predictor of high PVR%diff was plasma potassium level. HF etiology, renal function, gender, RAAS inhibitor dose, renin or aldosterone levels were unelated to pulmonary vasoreactivity. Patients who dropped PVR&lt;3 WU after PDE5i had higher plasma K+ (4.1±0.5 vs 4.5±0.3 mmol/L, p=0.01) than those who did not, similar relation was found for K+ and PDE5i-induced change of transpulmonary gradient. Conclusions: The largest increase in CO after PDE5i is observed in HFrEF patients with severe mitral (or tricuspid) regurgitation, probably due to chamber unloading and reduction of regurgitant SV. Pulmonary vasodilator response to PDE5i may be influenced by plasma potassium level. High-normal plasma potassium levels may preserve normal pulmonary vasoreactivity in HFrEF, perhaps by influencing K-channels in pulmonary vascular smooth muscle cells.

Muscle metaboreflex-induced central blood volume mobilization in heart failure.

Underperfusion of active skeletal muscle causes metabolites to accumulate and stimulate group III and IV skeletal muscle afferents, which triggers a powerful pressor response termed the muscle metaboreflex. Muscle metaboreflex activation (MMA) during submaximal dynamic exercise in healthy individuals increases arterial pressure mainly via substantial increases in cardiac output (CO). The increases in CO occur via the combination of tachycardia and increased ventricular contractility. Importantly, MMA also elicits substantial central blood volume mobilization, which allows the ventricular responses to sustain the increases in CO. Otherwise preload would fall and the increases in CO could not be maintained. In subjects with systolic heart failure (HF), the ability to increase CO during exercise and MMA is markedly reduced, which has been attributed to impaired ventricular contractility. Whether the ability to maintain preload during MMA in HF is preserved is unknown. Using a conscious chronically instrumented canine model, we observed that MMA in HF is able to raise central blood volume similarly as in normal subjects. Therefore, the loss of the ability to raise CO during MMA in HF is not because of the loss of the ability to mobilize blood volume centrally. NEW & NOTEWORTHY In normal subjects during dynamic exercise muscle metaboreflex activation elicits large increases in cardiac output that occur via increases in heart rate, ventricular contractility, and, importantly, marked central blood volume mobilization that acts to maintain ventricular preload, thereby allowing the changes in cardiac function to maintain the increases in cardiac output. In subjects with heart failure, the ability to raise cardiac output during muscle metaboreflex activation is impaired. We investigated whether this is because of the inability to maintain ventricular preload. We found that this reflex is still able to elicit large increases in central blood volume, and therefore the limited ability to raise cardiac output likely stems from ventricular dysfunction and not the ability to maintain preload.

An Ovine Model for Studying the Pathophysiology of Septic Acute Kidney Injury.

The development of acute kidney injury (AKI) is both a significant and independent prognostic factor of mortality in patients with sepsis, but its pathophysiology remains unclear. Herein, we describe an ovine model of sepsis evoked by the administration of live Escherichia coli in which there is hypotension, peripheral vasodilatation with a large increase in cardiac output; a similar hyperdynamic state to that commonly reported in humans. Interestingly, in this sheep model of sepsis, despite an increase in global kidney blood flow, there is a progressive reduction in renal function. Although renal hyperperfusion develops, renal tissue hypoxia due to redistribution of intrarenal blood flow may contribute to the pathogenesis of septic AKI. We have, therefore, developed a novel methodology to chronically implant combination probes to monitor intrarenal tissue perfusion and oxygen tension during the development of septic AKI in conscious sheep with hyperdynamic sepsis.

Cardiovascular Responses to Psychosocial Stress Reflect Motivation State in Adults Born at Extremely Low Birth Weight.

Background. Adults born extremely preterm appear to have more difficulty managing the stresses of early adulthood than their term-born peers. Objective. To examine the effects of being born at extremely low birth weight (ELBW; birth weight < 1000 g) versus at full term on cardiovascular responses to stress. Method. Cardiovascular responses were elicited during administration of a widely used laboratory stressor, the Trier Social Stress Test (TSST). Results. Term-born adults exhibited a larger decrease in total peripheral resistance and larger increase in cardiac output for TSST performance, reflecting greater resilience, than did ELBW adults. Furthermore, in ELBW participants but not controls, cardiovascular responses were correlated with anxiety, suggesting that their responses reflected feelings of stress. Conclusions. Skills-training and practice with relevant stressors may be necessary to increase the personal resources of ELBW participants for managing stress as they transition to adulthood.

Gymnasium-based unsupervised exercise maintains benefits in oxygen uptake kinetics obtained following supervised training in type 2 diabetes

Supervised exercise (SE) in patients with type 2 diabetes improves oxygen uptake kinetics at the onset of exercise. Maintenance of these improvements, however, has not been examined when supervision is removed. We explored if potential improvements in oxygen uptake kinetics following a 12-week SE that combined aerobic and resistance training were maintained after a subsequent 12-week unsupervised exercise (UE). The involvement of cardiac output (CO) in these improvements was also tested. Nineteen volunteers with type 2 diabetes were recruited. Oxygen uptake kinetics and CO (inert gas rebreathing) responses to constant-load cycling at 50% ventilatory threshold (V(T)), 80% V(T), and mid-point between V(T) and peak workload (50% Δ) were examined at baseline (on 2 occasions) and following each 12-week training period. Participants decided to exercise at a local gymnasium during the UE. Thirteen subjects completed all the interventions. The time constant of phase 2 of oxygen uptake was significantly faster (p < 0.05) post-SE and post-UE compared with baseline at 50% V(T) (17.3 ± 10.7 s and 17.5 ± 5.9 s vs. 29.9 ± 10.7 s), 80% V(T) (18.9 ± 4.7 and 20.9 ± 8.4 vs. 34.3 ± 12.7s), and 50% Δ (20.4 ± 8.2 s and 20.2 ± 6.0 s vs. 27.6 ± 3.7 s). SE also induced faster heart rate kinetics at all 3 intensities and a larger increase in CO at 30 s in relation to 240 s at 80% V(T); and these responses were maintained post-UE. Unsupervised exercise maintained benefits in oxygen uptake kinetics obtained during a supervised exercise in subjects with diabetes, and these benefits were associated with a faster dynamic response of heart rate after training.

The Effects of Crystalloid and Colloid Preload on Cardiac Output in the Parturient Undergoing Planned Cesarean Delivery Under Spinal Anesthesia

Obstetric Anesthesia Digest: March 2011 - Volume 31 - Issue 1 - p 54-56 doi: 10.1097/01.aoa.0000393191.66961.a6

Gender differences in β‐adrenoceptor system in cardiac hypertrophy due to arteriovenous fistula

This study was undertaken to determine alterations in the β-adrenoceptor (β-AR) signaling system in male and female rats at 4 weeks after the induction of arteriovenous (AV) fistula or shunt. AV shunt produced a greater degree of cardiac hypertrophy and larger increase in cardiac output in male than in female animals. Increases in plasma levels of norepinephrine and epinephrine (EPI) due to AV shunt were also higher in male than females. While no difference in the β(1)-AR affinity was seen in males and females, AV shunt induced increase in β(1)-AR density in female rats was higher than that in males. Furthermore, no changes in basal adenylyl cyclase (AC) V/VI mRNA levels were seen; however, the increase in EPI-stimulated AC activities was greater in AV shunt females than in males. AV shunt decreased myocardial β(1)-AR mRNA level in male rats and increased β(2)-AR mRNA level in female hearts; an increase in G(i)-protein mRNA was detected only in male hearts. Although GRK2 gene expression was increased in both sexes, an increase in GRK3 mRNA was seen only in AV shunt female rats. β-arrestin1 mRNA was elevated in females whereas β-arrestin 2 gene expression was increased in both male and female AV shunt rats. While these data demonstrate gender associated differences in various components of the β-AR system in cardiac hypertrophy due to AV shunt, only higher levels of plasma catecholamines may account for the greater increase in cardiac output and higher degree of cardiac hypertrophy in males.

Metaboreflex control of the heart

Metaboreflex control of the heart

The Effects of Crystalloid and Colloid Preload on Cardiac Output in the Parturient Undergoing Planned Cesarean Delivery Under Spinal Anesthesia: A Randomized Trial

Hypotension after spinal anesthesia for cesarean delivery remains a major clinical problem. Fluid preloading regimens together with vasopressors have been used to reduce its incidence. Previous studies have used noninvasive arterial blood pressure measurement and vasopressor requirements to evaluate the effect of preload. We used a suprasternal Doppler flow technique to measure maternal cardiac output (CO) and corrected flow time (FTc, a measure of intravascular volume) before and after spinal anesthesia after 3 fluid preload regimens. We hypothesized that colloid solutions, compared with crystalloid, would produce the largest increase in CO and have the lowest incidence of hypotension. Sixty healthy term women scheduled for planned cesarean delivery under spinal anesthesia were recruited for this randomized, double-blind study. Baseline heart rate, systolic blood pressure (SBP), CO, and FTc were recorded in the left lateral tilt position. Patients were randomized to receive 1 of 3 fluid preload regimens given over 15 min: 1.5 L crystalloid (Hartman's solution), 0.5 L of 6% w/v hydroxyethyl starch (HES) solution (HES 0.5), or 1 L of 6% w/v HES solution (HES 1.0). Further measurements were made after fluid loading every 5 min for 30 min. After 30 min, spinal anesthesia was induced with hyperbaric bupivacaine 12.5 mg with fentanyl 15 microg and recordings were continued every 5 min for 20 min or until surgery started. The primary outcome, CO, was compared among groups. The incidence of hypotension (defined as a 20% reduction in SBP from the baseline), ephedrine use, and umbilical cord blood gases were also compared. Patient characteristics, heart rate, SBP, and cord gases were similar among groups. Although CO and FTc increased after preload in all groups (P < 0.005), this was only maintained with HES 1.0 after spinal anesthesia (P < 0.005). There were no differences among groups in the incidence of hypotension (70% vs 35% vs 65% for Hartman's solution, HES 0.5, and HES 1.0, respectively; P = 0.069) or mean ephedrine dose (10.4 vs 5.7 vs 9.7 mg; P = 0.26). Despite CO and FTc increases after fluid preload, particularly with HES 1.0 L, hypotension still occurred. The data suggest that CO increases after these preload regimens cannot compensate for reductions in arterial blood pressure after spinal anesthesia.

Regulation of Cerebral Blood Flow During Exercise

Constant cerebral blood flow (CBF) is vital to human survival. Originally thought to receive steady blood flow, the brain has shown to experience increases in blood flow during exercise. Although increases have not consistently been documented, the overwhelming evidence supporting an increase may be a result of an increase in brain metabolism. While an increase in metabolism may be the underlying causative factor for the increase in CBF during exercise, there are many modulating variables. Arterial blood gas tensions, most specifically the partial pressure of carbon dioxide, strongly regulate CBF by affecting cerebral vessel diameter through changes in pH, while carbon dioxide reactivity increases from rest to exercise. Muscle mechanoreceptors may contribute to the initial increase in CBF at the onset of exercise, after which exercise-induced hyperventilation tends to decrease flow by pial vessel vasoconstriction. Although elite athletes may benefit from hyperoxia during intense exercise, cerebral tissue is well protected during exercise, and cerebral oxygenation does not appear to pose a limiting factor to exercise performance. The role of arterial blood pressure is important to the increase in CBF during exercise; however, during times of acute hypotension such as during diastole at high-intensity exercise or post-exercise hypotension, cerebral autoregulation may be impaired. The impairment of an increase in cardiac output during exercise with a large muscle mass similarly impairs the increase in CBF velocity, suggesting that cardiac output may play a key role in the CBF response to exercise. Glucose uptake and CBF do not appear to be related; however, there is growing evidence to suggest that lactate is used as a substrate when glucose levels are low. Traditionally thought to have no influence, neural innervation appears to be a protective mechanism to large increases in cardiac output. Changes in middle cerebral arterial velocity are independent of changes in muscle sympathetic nerve activity, suggesting that sympathetic activity does not alter medium-sized arteries (middle cerebral artery).CBF does not remain steady, as seen by apparent increases during exercise, which is accomplished by a multi-factorial system, operating in a way that does not pose any clear danger to cerebral tissue during exercise under normal circumstances.

Heart failure attenuates muscle metaboreflex control of ventricular contractility during dynamic exercise

Underperfusion of active skeletal muscle elicits a reflex pressor response termed the muscle metaboreflex (MMR). In normal dogs during mild exercise, MMR activation causes large increases in cardiac output (CO) and mean arterial pressure (MAP); however, in heart failure (HF) although MAP increases, the rise in CO is virtually abolished, which may be due to an impaired ability to increase left ventricular contractility (LVC). The objective of the present study was to determine whether the increases in LVC seen with MMR activation during dynamic exercise in normal animals are abolished in HF. Conscious dogs were chronically instrumented to measure CO, MAP, and left ventricular (LV) pressure and volume. LVC was calculated from pressure-volume loop analysis [LV maximal elastance (E(max)) and preload-recruitable stroke work (PRSW)] at rest and during mild and moderate exercise under free-flow conditions and with MMR activation (via partial occlusion of hindlimb blood flow) before and after rapid ventricular pacing-induced HF. In control experiments, MMR activation at both workloads [mild exercise (3.2 km/h) and moderate exercise (6.4 km/h at 10% grade)] significantly increased CO, E(max), and PRSW. In contrast, after HF was induced, CO, E(max), and PRSW were significantly lower at rest. Although CO increased significantly from rest to exercise, E(max) and PRSW did not change. In addition, MMR activation caused no significant change in CO, E(max), or PRSW at either workload. We conclude that MMR causes large increases in LVC in normal animals but that this ability is abolished in HF.

Muscle Metaboreflex (MMR) Responses During Recovery From Pacing‐Induced Heart Failure

We studied MMR responses in eight chronically instrumented dogs before and after modest pacing-induced heart failure (HF; 225 bpm for ~30 days; ~Class II HF) and during recovery from HF. The MMR was activated during mild and moderate exercise via imposed graded reductions in hindlimb blood flow (HLBF). In control experiments, decreases in HLBF were necessary to evoke the MMR suggesting that it is not tonically active. MMR activation led to a rise mean arterial pressure (MAP) that was mediated almost solely via a large increase in cardiac output (CO). During HF, the levels of HLBF at both workloads were at or near the threshold for the MMR determined during control experiments, which suggests that the MMR may already have been tonically active. Even small reductions in HLBF induced a pressor response; however, CO remained largely unchanged and the rise in MAP was mediated via peripheral vasoconstriction. With recovery from HF ( 18 days after disconnecting the pacemaker), during free-flow dynamic exercise at both workloads, CO and HLBF tended to be higher than during control experiments. Reductions in HLBF were necessary to evoke the MMR (i.e., there was again a clear threshold) and the mechanisms of the pressor response reverted back to CO, as observed in control experiments. In conclusion, dynamic exercise during recovery from pacing induced HF was accompanied by increased CO and HLBF which likely relieved the metabolic stimulus that led to tonic MMR activation during HF. Supported by NIH HL55473 and VA-DoD Grant.

Point: The muscle metaboreflex does restore blood flow to contracting muscles

Imposed reductions in oxygen delivery to active skeletal muscle during dynamic exercise in conscious dogs evoke a powerful pressor response, termed the muscle metaboreflex. During submaximal work rates, the major mechanism used by this reflex is to increase cardiac output (CO), which generates a

Impaired muscle metaboreflex-induced increases in ventricular function in heart failure.

We investigated to what extent heart failure alters the ability of the muscle metaboreflex to improve ventricular function. Dogs were chronically instrumented to monitor mean arterial pressure (MAP), cardiac output (CO), heart rate (HR), stroke volume (SV), and central venous pressure (CVP) at rest and during mild treadmill exercise (3.2 km/h) before and during reductions in hindlimb blood flow imposed to activate the muscle metaboreflex. These control experiments were repeated at constant heart rate (ventricular pacing 225 beats/min) and at constant heart rate coupled with a beta-adrenergic blockade (atenolol, 2 mg/kg iv) in normal animals and in the same animals after the induction of heart failure (HF, induced via rapid ventricular pacing). In control experiments in normal animals, metaboreflex activation caused tachycardia with no change in SV, resulting in large increases in CO and MAP. At constant HR, large increases in CO still occurred via significant increases in SV. Inasmuch as CVP did not change in this setting and that beta-adrenergic blockade abolished the reflex increase in SV at constant HR, this increase in SV likely reflects increased ventricular contractility. In contrast, after the induction of HF, much smaller increases in CO occurred with metaboreflex activation because, although increases in HR still occurred, SV decreased thereby limiting any increase in CO. At constant HR, no increase in CO occurred with metaboreflex activation even though CVP increased significantly. After beta-adrenergic blockade, CO and SV decreased with metaboreflex activation. We conclude that in HF, the ability of the muscle metaboreflex to increase ventricular function via both increases in contractility as well as increases in filling pressure are markedly impaired.

Ventilatory and cardiovascular modulation associated with burying behaviour in two sympatric crab species, Cancer magister and Cancer productus

Physiological parameters associated with burying were investigated in the Dungeness crab, Cancer magister, and the red rock crab, Cancer productus. Ventilation frequency of the branchial chambers increased while the crabs were burying, this was associated with the greater oxygen demand of the tissues. The number of ventilatory reversals in C. magister increased in number as well as in duration and magnitude when the crabs were buried, which functioned to clear the branchial chambers of sediment. In contrast, the number of ventilatory reversals in C. productus decreased. On the surface of the sand, cardiac parameters (heart rate, stroke volume, cardiac output) of both species remained stable. During the burial process, there was a large increase in cardiac output which was afforded primarily by an increased stroke volume of the heart. Once buried, cardiac output declined in both species; this was due to a decrease in stroke volume in C. productus, but a decreased heart rate in C. magister. There were also differences in haemolymph flows through each arterial system. During the burying process, both species increased haemolymph flow to the muscles of the limbs via the sternal artery. Once buried haemolymph flows to the limbs decreased, and increased flow to eyestalks and antennae via the anterior aorta occurred. Perfusion of the digestive organs via the anterolateral and hepatic arteries did not change when the crabs were buried. There was an increase in flow through the posterior aorta, of C. magister, but flow through this artery did not change in C. productus. Periods of spontaneous cardiac arrest were observed in both species while resting on the surface. These increased in duration in C. productus when buried, but there was no change in C. magister. Changes in ventilatory and cardiac variables were closely linked on the surface, but tended to uncouple when the animals were buried. The physiological responses of C. magister resembled those of true sand-dwelling crabs, whereas the responses of C. productus paralleled those of crabs that only bury occasionally in the substrate. Although these two species often occur sympatrically, they employ different physiological mechanisms when buried in the sediment.

Release of atrial natriuretic factor prohormone peptides 1-30, 31-67 and 99-126 from freshwater- and seawater-acclimated perfused trout (Oncorhynchus mykiss) hearts

Atrial natriuretic factor (ANF), a 28-amino-acid peptide hormone produced in the heart, circulates in both freshwater and seawater rainbow trout. In mammals, two other peptide hormones, proANF 1-30 and proANF 31-67, derived from the same 126-amino-acid prohormone as ANF (amino acids 99&shyp;126), circulate and have natriuretic and diuretic properties. It has never been determined whether these peptides circulate in fish. The present investigation was designed to determine (1) whether proANF 1-30 and/or proANF 31-67 circulate in perfused hearts from freshwater- and seawater-acclimated rainbow trout (Oncorhynchus mykiss) in situ, and (2) if they do, to determine whether increasing the filling pressure of the heart causes their release in trout as it does in mammals. High-performance gel-permeation chromatography of fish plasma revealed that both proANF 1-30 and 31-67 circulate in freshwater- and seawater-acclimated trout plasma at threefold higher concentrations than does ANF. The basal rates of release of ANF and proANF 1-30 and 31-67 were similar in both freshwater and seawater trout, with the rate of release of proANF 1-30 being 10 times higher and that of proANF 31-67 20 times higher than that of ANF. When the filling pressure was increased to the peak of the Starling curve (max), the rate of release of ANF and proANFs 1-30 and 31-67 increased fivefold for each peptide in the freshwater trout, while in seawater trout the rates of release increased six- to ninefold. We conclude that proANF 1-30 and 31-67, as well as ANF, circulate in both freshwater-and seawater-acclimated trout and do so at concentrations higher than that of ANF. Increasing the filling pressure to the trout heart was found to cause a similar increase in the release rates for each of these peptides, but the maximal increase was higher in the seawater-acclimated trout, apparently because they showed a larger increase in cardiac output.

Release of atrial natriuretic factor prohormone peptides 1-30, 31-67 and 99-126 from freshwater- and seawater-acclimated perfused trout (Oncorhynchus mykiss) hearts

Atrial natriuretic factor (ANF), a 28-amino-acid peptide hormone produced in the heart, circulates in both freshwater and seawater rainbow trout. In mammals, two other peptide hormones, proANF 1-30 and proANF 31-67, derived from the same 126-amino-acid prohormone as ANF (amino acids 99&shyp;126), circulate and have natriuretic and diuretic properties. It has never been determined whether these peptides circulate in fish. The present investigation was designed to determine (1) whether proANF 1-30 and/or proANF 31-67 circulate in perfused hearts from freshwater- and seawater-acclimated rainbow trout (Oncorhynchus mykiss) in situ, and (2) if they do, to determine whether increasing the filling pressure of the heart causes their release in trout as it does in mammals. High-performance gel-permeation chromatography of fish plasma revealed that both proANF 1-30 and 31-67 circulate in freshwater- and seawater-acclimated trout plasma at threefold higher concentrations than does ANF. The basal rates of release of ANF and proANF 1-30 and 31-67 were similar in both freshwater and seawater trout, with the rate of release of proANF 1-30 being 10 times higher and that of proANF 31-67 20 times higher than that of ANF. When the filling pressure was increased to the peak of the Starling curve (max), the rate of release of ANF and proANFs 1-30 and 31-67 increased fivefold for each peptide in the freshwater trout, while in seawater trout the rates of release increased six- to ninefold. We conclude that proANF 1-30 and 31-67, as well as ANF, circulate in both freshwater-and seawater-acclimated trout and do so at concentrations higher than that of ANF. Increasing the filling pressure to the trout heart was found to cause a similar increase in the release rates for each of these peptides, but the maximal increase was higher in the seawater-acclimated trout, apparently because they showed a larger increase in cardiac output.

Adrenergic innervation of the heart of the bat, Miniopterus schreibersii.

The adrenergic innervation of the heart of the bat (Miniopterus schreibersii) was studied with a fluorescence histochemical technique. The appearance and distribution pattern of the terminal adrenergic nerve fibers demonstrated in the atria, sinoatrial and atrioventricular nodes, and ventricles is typically mammalian. Fine varicose adrenergic fibers run in and parallel to the ventricular muscle where they are common and uniformly distributed. Indian ink perfusion of the coronary vasculature demonstrates the high density of vessels in the ventricles, but obscures the terminal innervation of the ventricular muscle. This alone, or in combination with the apparent seasonal change in the terminal innervation of the ventricles, may explain the inability of previous workers to identify an adrenergic ventricular innervation in the bat Nyctalus noctula. The adrenergic ventricular innervation might be involved in the large increases in cardiac output associated with the commencement of flight and in the massive sympathetic activation that mediates arousal from torpor.

Effect of Tidal Volume on Gas Exchange and Oxygen Transport in the Adult Respiratory Distress Syndrome

The effect of tidal volume (VT) on gas exchange and oxygen delivery (DO2) was studied in nine patients with adult respiratory distress syndrome (ARDS) and in 10 postoperative open-heart surgery patients (CABG). During controlled mechanical ventilation, VT was initially 10 to 12 ml/kg, followed by an increase and reduction of 25% (1.25 VT and 0.75 VT, respectively). In both groups of patients, dead space (VD) correlated strongly with VT (p < 0.001), while the VD/VT ratio was independent of VT. PaO2 tended to increase in CABG patients and decrease in ARDS patients at 1.25 VT. Arterial oxygen saturation (SaO2) did not change at 1.25 VT but decreased at 0.75 VT (p < 0.001) in the ARDS group. Venous admixture (QS/QT) decreased with 1.25 VT and increased with 0.75 VT (p < 0.001). A relatively larger increase in cardiac output compensated for the increased QS/QT and the reduced SaO2, resulting in significantly higher DO2 with 0.75 VT (p < 0.01). A lower VT resulted in improved balance between pulmonary gas exchange and whole body oxygen supply.