Fever in young lambs: hypoxemia alters the febrile response to a small dose of bacterial pyrogen.

Experiments were done on eight young lambs to investigate the effects of hypoxemia on the body temperature, metabolic and cardiovascular responses to intravenous administration of a small dose of bacterial pyrogen (0.3 micrograms lipopolysaccharide extracted from Salmonella Abortus Equi; SAE). Each lamb was anaesthetized with halothane and prepared for sleep staging and measurements of cardiac output, arterial and mixed-venous haemoglobin oxygen saturations, body-core and ear-skin temperatures. Three experiments were done on each lamb, the first being done no sooner than three days after surgery. The first experiment consisted of establishing the thermal neutral environment during normoxemia (ie, environmental temperature at which total body oxygen consumption was minimal while body temperature was maintained) for each lamb. The second and third experiments were done at the lamb's thermoneutral environment as determined on day 1. One experiment was done during normoxemia (ie, control condition, SaO2 approximately 90%) and one experiment was done during hypoxemia (ie, experimental condition, SaO2 approximately 50%). Measurements were made during a control period and during one-minute experimental periods at 10 minute intervals for 120 minutes following administration of 0.3 micrograms of bacterial pyrogen in sterile saline. Administration of SAE produced a short-lived fever of about 0.8 degrees C in the normoxemic lambs, whereas no change in body-core temperature was observed in the hypoxemic lambs. During normoxemia, the increase in body-core temperature was preceded by peripheral vasoconstriction, the onset of shivering, and a surge in total body oxygen consumption. The increase in total body oxygen consumption was met primarily by an increase in total body oxygen extraction during the development of fever. Cardiac index, heart rate, and systemic oxygen transport increased during the peak body-core temperature response. Systemic arterial blood pressure did not change significantly during the febrile response; however, pulmonic arterial blood pressure increased. During hypoxemia, peripheral vasoconstriction and shivering occurred following administration of SAE, but there was no change in total body oxygen consumption or body-core temperature. Thus, our data provide evidence that hypoxemia alters the febrile response of young lambs to bacterial pyrogen. The precise mechanism remains to be determined.     

Vasodilator tone in the llama fetus: the role of nitric oxide during normoxemia and hypoxemia

The fetal llama responds to hypoxemia, with a marked peripheral vasoconstriction but, unlike the sheep, with little or no increase in cerebral blood flow. We tested the hypothesis that the role of nitric oxide (NO) may be increased during hypoxemia in this species, to counterbalance a strong vasoconstrictor effect. Ten fetal llamas were operated under general anesthesia. Mean arterial pressure (MAP), heart rate, cardiac output, total vascular resistance, blood flows, and vascular resistances in cerebral, carotid and femoral vascular beds were determined. Two groups were studied, one with nitric oxide synthase (NOS) blocker N(G)-nitro-L-arginine methyl ester (L-NAME), and the other with 0.9% NaCl (control group), during normoxemia, hypoxemia, and recovery. During normoxemia, L-NAME produced an increase in fetal MAP and a rapid bradycardia. Cerebral, carotid, and femoral vascular resistance increased and blood flow decreased to carotid and femoral beds, while cerebral blood flow did not change significantly. However, during hypoxemia cerebral and carotid vascular resistance fell by 44% from its value in normoxemia after L-NAME, although femoral vascular resistance progressively increased and remained high during recovery. We conclude that in the llama fetus: 1) NO has an important role in maintaining a vasodilator tone during both normoxemia and hypoxemia in cerebral and femoral vascular beds and 2) during hypoxemia, NOS blockade unmasked the action of other vasodilator agents that contribute, with nitric oxide, to preserving blood flow and oxygen delivery to the tissues.     

Respiratory, cardiovascular, and metabolic adjustments to hypoxemia during sleep in piglets

The influence of sleep on ventilation, metabolic rate, cardiovascular function, and regional distribution of blood flow during hypoxemia (PaO2 of 45-50 mm Hg (1 mm Hg = 133.3 Pa)) was studied in piglets at 6+/-1 and 34+/-5 days (mean+/-SD). Measurement of ventilation and metabolic rate was done in a metabolic chamber, and blood flow was measured using the microsphere technique. A subgroup of animals was instrumented for cardiac output measurement (dye-dilution technique) and continuous monitoring of the hemoglobin saturation in oxygen (SaO2). We found that although sleep did not influence the metabolic and cardiac output response to hypoxemia, it affected the ventilatory response as well as the brain and the respiratory muscle blood flows. During active sleep in the older animals, the ventilatory response to hypoxemia was smaller than in the other two states; marked drops in SaO2 occurred with changes in the breathing pattern; and that state was associated with the highest rate of brain blood flow. As well, age affected the ventilatory and metabolic response, but not the cardiovascular response to hypoxemia. The age-dependent ventilatory changes with hypoxemia (smaller ventilatory response in the young than in the older animals) were related to the different levels of oxygen consumption. In summary, active sleep was responsible for all the sleep-dependent changes in the response to a moderate degree of hypoxemia.     

Cardiac output and regional blood flows during hypoxaemia in unanaesthetized newborn lambs

There is limited information available regarding the effects of hypoxemia on cardiac output and the distribution of blood flow and oxygen delivery in unanaesthetized newborns of any species. We measured these variables in 12 unanaesthetized newborn lambs during a control period and during 50% and 75% reductions in aortic blood oxygen content which were produced by placing each lamb in an environment of 8-10% and 5-6% oxygen, respectively. 1-2% carbon dioxide was added to the gas mixture and there were no significant changes in aortic blood PCO2 or pH. Hypoxaemia was associated with a 15-20% increase in cardiac output but total somatic oxygen delivery decreased. Cerebral, myocardial, adrenal and diaphragmatic blood flows increased and their oxygen deliveries were not diminished. Oxygen deliveries to the spleen, kidneys, gastrointestinal tract and carcass decreased when aortic blood oxygen content was reduced. This study demonstrates that the newborn lamb has a limited ability to increase its cardiac output during hypoaxemia, but that oxygen deliveries to the heart, brain, adrenals and diaphragm are maintained in association with a redistribution of blood flow.     

Age-dependent core temperature responses of conscious rabbits to acute hypoxemia.

Experiments were carried out on chronically instrumented newborn and older rabbits to characterize their core temperature (T(c)) responses to acute hypoxemia and to differentiate "forced" vs. "regulated" thermoregulatory responses. Three age ranges of kits were studied: 4-6, 9-11, and 28-30 days of age. During an experiment, T(c), selected ambient temperature (T(a)), and oxygen consumption were measured from kits studied in a thermocline during a control period of normoxemia, an experimental period of normoxemia or hypoxemia (fraction of inspired oxygen 0.10), and a recovery period of normoxemia. We reasoned that no change or a decrease in T(a) while T(c) decreased during hypoxemia would indicate a regulated thermoregulatory response, whereas an increase in T(a) while T(c) decreased during hypoxemia would indicate a forced thermoregulatory response. T(c) decreased during acute hypoxemia in the older kits but not in the 4- to 6-day-old kits; the decrease in T(c) was accentuated on postnatal days 28-30 compared with postnatal days 9-11. T(a) decreased or stayed the same during exposure to acute hypoxemia. Our data provide evidence that postnatal maturation influences the T(c) response of rabbits to acute hypoxemia and that the decrease in T(c) during hypoxemia in the older kits results from a regulated thermoregulatory response.     

Acidaemia reduces cardiac output and left ventricular contractility in conscious lambs

We studied the effects of HCI-induced metabolic acidaemia on cardiac output, contractile function, myocardial blood flow, and myocardial oxygen consumption in nine unanaesthetized newborn lambs. Through a left thoracotomy, catheters were placed in the aorta, left atrium and coronary sinus. A pressure transducer was placed in the left ventricle. Three to four days after surgery, we measured cardiac output, dP/dt, left ventricular end diastolic and aortic mean blood pressures, heart rate, aortic and coronary sinus blood oxygen contents, and left ventricular myocardial blood flow during a control period, during metabolic acidaemia, and after the aortic pH was restored to normal. We calculated systemic vascular resistance, myocardial oxygen consumption and left ventricular work. Acidaemia was associated with reduction in cardiac output, maximal dP/dt, and aortic mean blood pressure. Left ventricular end diastolic pressure and systemic vascular resistance increased, and heart rate did not change significantly. The reduction in myocardial blood flow and oxygen consumption was accompanied by fall in cardiac work. Cardiac output returned to control levels after the pH had been normalized but maximal dP/dt was incompletely restored. Myocardial blood flow and oxygen consumption increased beyond control levels. This study demonstrates that HCI-induced metabolic acidaemia in conscious newborn lambs is associated with a reduction in cardiac output which could have been mediated by the reduction in contractile function and/or the increase in systemic vascular resistance. The decreases in myocardial blood flow and oxygen consumption appear to reflect diminished cardiac work. The restoration of a normal cardiac output after normalization of the pH appears to have resulted from the increases in heart rate and left ventricular filling pressures in conjunction with an incomplete restoration of contractile function.     

Role of glutamate as the central neurotransmitter in the hypoxic ventilatory response.

Recent data suggest that the increase in ventilation during hypoxia may be related to the release of the excitatory amino acid neurotransmitter glutamate centrally. To further investigate this, we studied the effects of MK-801, a selective noncompetitive N-methyl-D-aspartate receptor antagonist, on the hypoxic ventilatory response in lightly anesthetized spontaneously breathing intact dogs. The cardiopulmonary effects of sequential ventriculocisternal perfusion (VCP) at the rate of 1 ml/min with mock cerebrospinal fluid (CSF, control) and MK-801 (2 mM) were compared during normoxia and 8 min of hypoxic challenge with 12% O2. Minute ventilation (VE), tidal volume (VT), and respiratory frequency (f) were recorded continuously, and hemodynamic parameters [heart rate (HR), blood pressure (MAP), cardiac output (CO), pulmonary arterial pressure, and pulmonary capillary wedge pressure] were measured periodically. Each dog served as its own baseline control before and after each period of sequential VCP under the two different O2 conditions. During 15 min of normoxia, there were no significant changes in the cardiopulmonary parameters with mock CSF VCP, whereas with MK-801 VCP for 15 min, VE decreased by approximately 27%, both by reductions in VT and f (17 and 9.5%, respectively). HR, MAP, and CO were unchanged. During 8 min of hypoxia with mock CSF VCP, VE increased by 171% associated with increased VT and f (25 and 125%, respectively). HR, MAP, and CO were likewise augmented. In contrast, the hypoxic response during MK-801 VCP was characterized by an increased VE of 84%, mainly by a rise in f by 83%, whereas the VT response was abolished. The cardiovascular excitation was also inhibited.(ABSTRACT TRUNCATED AT 250 WORDS)     

Hypoxemia increases renin secretion rate in anesthetized newborn lambs

The response of renin secretion rate (RSR) to acute systemic hypoxemia (mean arterial p0₂ 34±8 torr) was studied in mechanically ventilated, anesthetized newborn lambs 5–10 days of age (n=6). Ventilation of these lambs with room air (normoxemia) was followed by administration of low oxygen inhaled gas mixture (f_i0₂ 0.11) which was associated with no change in arterial pC0₂, pH, mean arterial pressure (MAP), renal blood flow (RBF, measured by electromagnetic flow probe), and calculated renal vascular resistance (RVR). Arterial plasma renin activity (PRA_A 4.28±1.73 to 6.46±3.00 ng AI/ml · hr), renal vein plasma renin activity (PRA_RV, 6.26±3.79 to 11.44±7.11 ng AI/ml · hr) and renin secretion rate (RSR, 19.86±21.70 to 51.32±48.54 units/min · KgBW) increased significantly (p<0.05) in response to hypoxemia. Restoration of normoxemia (arterial p0₂ 100±18 torr) was associated with significant decline in MAP (to 65±14 mmHg) and RBF (to 9.0±2.1 ml/min · KgBW) and further increases in PRA_A (to 8.98±3.40 ng AI/ml · hr), PRA_RV (to 19.04±10.62 ng AI/ml · hr) and RSR (to 88.6±77.6 units/min · KgBW). PRA_A correlated strongly with PRA_RV (r=0.84) and RSR (r=0.60) in these lambs. These results suggest that PRA_A, PRA_RV and RSR increase in response to hypoxemia in anesthetized lambs by a mechanism other than renal arterial baroreceptor stimulation, although this mechanism may be active during recovery from hypoxemia. Furthermore, PRA_A closely approximates RSR in newborn lambs under these conditions.     

Integrative control of the skeletal muscle microcirculation in the maintenance of arterial pressure during exercise.

Skeletal muscle blood flow and vascular conductance are influenced by numerous factors that can be divided into two general categories: central cardiovascular control mechanisms and local vascular control mechanisms. Central cardiovascular control mechanisms are thought to be designed primarily for the maintenance of arterial pressure and central cardiovascular homeostasis, whereas local vascular control mechanisms are thought to be designed primarily for the maintenance of muscle homeostasis. To support the high metabolic rates that can be generated during muscle contraction, skeletal muscle has a tremendous capacity to vasodilate and increase oxygen and nutrient delivery. During whole body dynamic exercise at maximal oxygen consumption (VO2 max), the skeletal muscle receives 85-90% of cardiac output. Yet despite receiving such a large fraction of cardiac output during high-intensity exercise, a vasodilator reserve remains with the potential to produce further elevations in skeletal muscle vascular conductance and blood flow. However, because maximal cardiac output is reached during exercise at VO2 max, further elevations in muscle vascular conductance would produce a fall in arterial pressure. Therefore, limits on muscle perfusion must be imposed during whole body exercise to prevent such drops in pressure. Effective arterial pressure control in response to a potentially hypotensive challenge during high-intensity exercise occurs primarily through reflex-mediated increases in sympathetic nerve activity, which are capable of modulating vasomotor tone of the skeletal muscle resistance vasculature. Thus skeletal muscle vascular conductance and perfusion are primarily mediated by local factors at rest and during exercise, but other centrally mediated control systems are superimposed on the dominant local control mechanisms to provide an integrated regulation of both arterial pressure and skeletal muscle vascular conductance and perfusion during whole body dynamic exercise.     

Ventral medullary extracellular fluid pH and PCO2 during hypoxemia

We designed experiments to study changes in ventral medullary extracellular fluid (ECF) PCO2 and pH during hypoxemia. Measurements were made in chloralose-urethan-anesthetized spontaneously breathing cats (n = 12) with peripherial chemodenervation. Steady-state measurements were made during normoxemia [arterial PO2 (PaO2) = 106 Torr], hypoxemia (PaO2 = 46 Torr), and recovery (PaO2 = 105 Torr), with relatively constant arterial PCO2 (approximately 44 Torr). Mean values of ventilation were 945, 683, and 1,037 ml/min during normoxemia, hypoxemia, and recovery from hypoxemia, respectively. Ventilatory depression occurred in each cat during hypoxemia. Mean values of medullary ECF PCO2 were 57.7 +/- 7.2 (SD), 59.4 +/- 9.7, and 57.4 +/- 7.2 Torr during normoxemia, hypoxemia, and recovery to normoxemia, respectively; respective values for ECF [H+] were 60.9 +/- 8.0, 64.4 +/- 11.6, and 62.9 +/- 9.2 neq/l. Mean values of calculated ECF [HCO3-] were 22.8 +/- 3.0, 21.7 +/- 3.3, and 21.4 +/- 3.1 meq/l during normoxemia, hypoxemia, and recovery, respectively. Changes in medullary ECF PCO2 and [H+] were not statistically significant. Therefore hypoxemia caused ventilatory depression independent of changes in ECF acid-base variables. Furthermore, on return to normoxemia, ventilation rose considerably, still independent of changes in ECF PCO2, [H+], and [HCO3-].     

Role of hypoxemia for the cardiovascular responses to apnea during exercise

We sought to define the role of hypoxemia in eliciting the cardiovascular responses to apnea during exercise. Eleven men performed repeated apneas during 100-W steady-state exercise, either with normoxic gas (air) or 95% oxygen (oxygen). Beat-by-beat arterial blood pressure, arterial oxygen saturation, and heart rate (HR) were determined, and stroke volume (SV) was estimated from impedance cardiography calibrated with soluble gas rebreathing. There were large interindividual variabilities of HR, mean arterial pressure (MAP), and total peripheral resistance (TPR) at end-apnea (ea). However, for each individual, HR(ea), MAP(ea), and TPR(ea) were highly correlated between air and oxygen (R = 0.94, 0.78, and 0.93). HR decreased and MAP increased faster during apnea with air than with oxygen (ANOVA, P < 0.05), but MAP(ea) was not different between conditions. Cardiac output was reduced by 33% with air and by 11% with oxygen (P < 0.001 for air vs. oxygen). We conclude that the hypoxemia component cannot account for the wide interindividual differences of HR and TPR responses to apnea. However, hypoxemia augments the HR and TPR responses and may limit the MAP response to apnea by preventing a bradycardia-associated increase of SV.     

Baroreceptor control of pressure-flow relationships during hypoxemia

In the absence of peripheral chemoreceptors, the effects of graded hypoxemia on the carotid sinus control of central and regional hemodynamics were studied in anesthetized mongrel dogs. Baroreceptor stimulation was effected by carotid sinus isolation and perfusion under controlled pressure. Blood flows were measured in the aorta and the celiac, mesenteric, left renal, and right iliac arteries. Carotid sinus reflex set-point pressures were well maintained until hypoxemia was severe. Carotid sinus reflex set-point gain was maximal during mild hypoxemia. Reflex operating point regional flows were unaffected by hypoxemia. A factorial analysis of overall reflex increases in mean aortic pressure, flow, and power during reduced baroreceptor stimulation showed potentiation by increasing hypoxemia. Corresponding effects of baroreceptor stimulation and hypoxemia on aortic resistance and heart rate were additive. Celiac, renal, and iliac blood flows increased during both hypoxemia and reduced baroreceptor stimulation. Only in the celiac bed were blood flow changes independent of concomitant changes in cardiac output. Thus, at maximum sympathetic stimulation (low carotid sinus pressure) during hypoxemia, the cardiovascular system maintained both central and regional blood flows at high systemic blood pressures independent of the peripheral chemoreceptors.     

Influence of sleep on the cardiovascular and metabolic responses to a decrease in ambient temperature in lambs

Experiments were done on seven lambs between the ages of 10 and 24 days to investigate the effects of sleep on the cardiovascular and metabolic responses to a decrease in ambient temperature. Each lamb was anesthetized and instrumented for recordings of electrocorticogram, electro-oculogram, and nuchal electromyograms and measurements of cardiac output, systemic and pulmonic pressures and hemoglobin oxygen saturations as well as body core temperature. No sooner than three days after surgery, measurements were made during periods of quiet wakefulness, quiet sleep and active sleep at ambient temperatures of 25 degrees C and 18 degrees C. Decreasing the environmental temperature from 25 degrees C to 18 degrees C elicited a similar thermogenic response during quiet wakefulness, quiet sleep and active sleep as evidenced by an increase in total body oxygen consumption. The increased metabolic oxygen demand was met by an increase in systemic oxygen transport as well as by an increase in total body oxygen extraction. Since shivering was absent during active sleep, it is likely that nonshivering thermogenesis played a major role in the metabolic response. Our data provide evidence that sleep does not significantly alter the cardiovascular and metabolic responses to a modest decrease in ambient temperature in young lambs.     

Acute hypoxemia does not increase the oxidative stress in resting and contracting muscle in humans

In healthy humans sustaining static handgrip at 60% of maximal voluntary contraction (MVC) until exhaustion, we measured the venous blood concentration of reduced ascorbic acid (RAA) and thiobarbituric acid reactive substances (TBARS), respectively, used as markers of the post-exercise oxidative stress and lipid peroxidation. Measurements were conducted in normoxemia, then during a 30-min period of hypoxemia (PaO 2 =56 mmHg) produced by inhalation of an hypoxic gas mixture. Compared to normoxemia, hypoxemia did not significantly modify the resting concentrations of TBARS and RAA, and did not affect the consumption of ascorbic acid after 60% MVC but suppressed the post-exercise TBARS increase. We conclude that acute hypoxemia does not modify the production of oxygen free radicals after strenuous static efforts and even seems to attenuate the lipid peroxidation.     

Acute Hypoxemia Does Not Increase the Oxidative Stress in Resting and Contracting Muscle in Humans

In healthy humans sustaining static handgrip at 60% of maximal voluntary contraction (MVC) until exhaustion, we measured the venous blood concentration of reduced ascorbic acid (RAA) and thiobarbituric acid reactive substances (TBARS), respectively, used as markers of the post-exercise oxidative stress and lipid peroxidation. Measurements were conducted in normoxemia, then during a 30-min period of hypoxemia (PaO 2 =56 mmHg) produced by inhalation of an hypoxic gas mixture. Compared to normoxemia, hypoxemia did not significantly modify the resting concentrations of TBARS and RAA, and did not affect the consumption of ascorbic acid after 60% MVC but suppressed the post-exercise TBARS increase. We conclude that acute hypoxemia does not modify the production of oxygen free radicals after strenuous static efforts and even seems to attenuate the lipid peroxidation.     

Canine renal vascular response to bilateral carotid occlusion during hypoxia

Chloralose-urethane anesthetized dogs were utilized to determine if hypoxemic potentiation of the baroreceptor-mediated increase in renal sympathetic nerve activity (RSNA) results in sufficient renal vascular vasoconstriction to reduce renal blood flow (RBF) during bilateral carotid occlusion (BCO). Additionally, hypercapnia and mechanical ventilation were randomly combined with hypoxemia during BCO to determine if further augmentation of renal vasoconstriction could be accomplished. BCO resulted in a similar increase in blood pressure (renal perfusion pressure) in all periods. RBF was not reduced significantly by BCO during any period even though renal vascular resistance was significantly increased by BCO during each period. When hypoxemia was combined with hypercapnia and mechanical ventilation simultaneously, there was a greater percentage increase in renal resistance with BCO. During BCO, when renal perfusion pressure was returned to control values by suprarenal aortic constriction, RBF remained unchanged and renal resistance decreased to control values. These results indicate that the BCO-induced increase in RSNA is relatively moderate and, even when potentiated by hypoxemia, hypercapnia, and mechanical ventilation, is not sufficient to reduce RBF in the presence of an increase in blood pressure and renal autoregulation.     

Abolition of ventilatory response to caffeine in chemodenervated lambs

In this study we have evaluated the role of the peripheral chemoreceptors in the ventilatory response to caffeine at a dose currently used in human infants for treatment of central apneas (10 mg/kg). Twelve lambs were studied; six had carotid body denervation (CBD) and six had a sham denervation (intact). The denervation was done the 2nd wk of life, and the study of the response to caffeine infusion was carried out at a mean age of 82 days. The awake and nonsedated animals received 10 mg/kg of caffeine, and caffeine blood levels were, respectively, 8.8 and 9.0 mg/l in the intact and in the CBD lambs. The intact lambs responded to caffeine by a significant immediate increase in minute ventilation (VE) of 46% from 274 to 400 ml X min-1 X kg-1 (P less than 0.001), 1 min after caffeine infusion. This response rapidly faded, but VE was still increased at 2 h, 314 ml X min-1 X kg-1. The increase in ventilation was brought about by a change in mean inspiratory flow (VT/TI), which increased from 9.9 to 14.0 ml X s-1 X kg-1 within 1 min (P less than 0.01); VT/TI was still increased at 11.2 ml X s-1 X kg-1 2 h later. In contrast, for the CBD lambs there was no response to caffeine infusion as measured by VE or VT/TI. We conclude that bolus caffeine infusion produces a rapid response in VE followed by a fall in VE that remained above base line until at least 2 h postinfusion, and the intact chemoreceptor function appears as an essential mediator for these increases in ventilation, since the peripheral chemodenervation has completely abolished the VE response to this particular dose of caffeine.     

新理论CPET指导个体化精准运动整体方案有效改善“虚弱症”的整体功能状态*

目的: 探讨整体整合生理学医学新理论指导下,根据心肺运动试验（CPET）制定个体化精准运动整体方案对整体功能状态的影响。方法: 李xx,女,31岁,自幼心率快（90~100 bpm）,平时手脚冰凉,秋冬季为甚,既往体健。2019年9月底在阜外医院签署知情同意书后行CPET,峰值摄氧量、无氧阈（AT）和峰值心排量分别为（69~72）%pred,摄氧通气效率和二氧化碳排出通气效率基本正常（96~100）%pred。静息心率快、血压偏低,运动过程中血压反应弱,以心率升高为主。整体整合生理学医学理论认为其自身虚弱,且以心脏弱为主。以CPET指导个体化精准运动强度进行滴定,结合连续逐搏血压、心电、脉搏和血糖动态监测制定个体化定量运动整体方案,实施8周强化管理后复查CPET等。结果: 经整体强化管理8周后四肢温暖,发凉症状消失。复查CPET峰值摄氧量、无氧阈和峰值心排量分别为（90~98）%pred,分别提高30%~36%,虚弱的整体功能状态得到显著提升;基本正常的摄氧通气效率和二氧化碳排出通气效率也分别提高10%~37%;静息心率和血压基本恢复正常,运动中血压和心率反应均正常。连续动态血糖监测提示血糖平均水平略下降,更趋于平稳,连续心电、逐搏血压等的重复测定结果也提示静息、运动全程和睡眠期间的心率降低、血压提升,桡动脉脉搏波的重搏波幅度加大,变得更加明显。结论: 新理论体系指导CPET制定个体化精准运动整体方案可以安全有效增强心肌收缩力、增加每搏输出量,提升血压、降低心率,稳定并略降低血糖,提高整体功能状态。     

Reflex control of vascular capacitance during hypoxia, hypercapnia, or hypoxic hypercapnia

We tested the hypothesis that the changes in venous tone induced by changes in arterial blood oxygen or carbon dioxide require intact cardiovascular reflexes. Mongrel dogs were anesthetized with sodium pentobarbital and paralyzed with veruronium bromide. Cardiac output and central blood volume were measured by indocyanine green dilution. Mean circulatory filling pressure, an index of venous tone at constant blood volume, was estimated from the central venous pressure during transient electrical fibrillation of the heart. With intact reflexes, hypoxia (arterial PaO2 = 38 mmHg), hypercapnia (PaCO2 = 72 mmHg), or hypoxic hypercapnia (PaO2 = 41; PaCO2 = 69 mmHg) (1 mmHg = 133.32 Pa) significantly increased the mean circulatory filling pressure and cardiac output. Hypoxia, but not normoxic hypercapnia, increased the mean systemic arterial pressure and maintained the control level of total peripheral resistance. With reflexes blocked with hexamethonium and atropine, systemic arterial pressure supported with a constant infusion of norepinephrine, and the mean circulatory filling pressure restored toward control with 5 mL/kg blood, each experimental gas mixture caused a decrease in total peripheral resistance and arterial pressure, while the mean circulatory filling pressure and cardiac output were unchanged or increased slightly. We conclude that hypoxia, hypercapnia, and hypoxic hypercapnia have little direct influence on vascular capacitance, but with reflexes intact, there is a significant reflex increase in mean circulatory filling pressure.     

Cardiorespiratory effects of rapid saline infusion in normal man.

We have studied the cardiorespiratory effects of the rapid infusion (100 ml/min) of 2 liters of saline in four normal seated subjects. Cardiac output and pulmonary arterial pressure increased, while vital capacity (VC) and total lung capacity (TLC) decreased. There was an increase in closing volume (CV) without any detectable change in lung compliance or flow-volume characteristics. There was an increase in Pao2 during infusion period which can be related to better matching of ventilation to perfusion and to improved hemoglobin transport. In the recovery stage as cardiac output, pulmonary arterial pressure, TLC, and VC all returned toward control values CV remained high. In two subjects CV occurred within the normal tidal range of ventilation and in these two subjects Pao2 fell significantly below values obtained in the control period. The results suggest that rapid saline infusion in man can cause interstitial edema and lead to premature airway closure and hypoxemia.