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This paper reports on our attempts to demonstrate potential failure modes under combined thermal and transverse loading of unidirectional composites and to validate the predictions of an analytical model through careful design and testing of composite specimens. Several fiber/matrix combinations are being considered with appropriate variations of the fiber-matrix interfacial bond strength and processing conditions. The interfacial bond strength is reduced in one set of specimens by applying a release agent to the surface of the fiber prior to its incorporation in the matrix. Curing is done both at room and at elevated temperature to account for thermal residual stresses induced from the mismatch in the coefficients of thermal expansion of the constituents. The experimental technique including specimen preparation, test procedures and detection of the sequence of failure events is described. The correlation between the experimental and analytical results is fairly reasonable.

Modeling of the consolidation of ceramic and metal powders by sintering, hot pressing, and hotisostatic pressing (HIP) was conducted using a continuum yield function and associated-flow rule modified to incorporate microstructure effects such as grain growth, pore size, and pore geometry. It was shown that consolidation behavior can be described over the entire range of densities through two parameters, the stress intensification factor and Poisson’s ratio, which are readily measured using uniaxial upset tests. Both parameters are functions of relative density, whose exact dependence varies from one material to another. Furthermore, it was demonstrated that in sinter forging of ceramics, an “apparent” Poisson’s ratio depending on stress level (relative to the sintering stress) gives a quantitative measure of the compctition between sintering and creep deformation. The accuracy of the microstructure-sensitive yield function was established through finite-element modeling (FEM) simulations of the isothermal sintering of a soda-lime glass, sinter forging of alumina, and die pressing of an alpha-two titanium aluminide alloy.

The effect of inclusions on the composite creep viscosity was investigated for a model glass-matrix composite consisting of a soda-lime glass matrix and nickel inclusions of various sizes. The effect of inclusion on the creep viscosity of glass-matrix composites has been modelled both analytically and numerically

The transverse tensile strength of the fiber-matrix interface plays an important role in controlling a number of failure modes in polymer matrix composites (PMCs). These include the transverse failure of 90° plies, as well edge delamination in PMC laminates. On the other hand, while significant attention has been focused in the PMC literature on interface shear failure, such as under pull-out conditions, little attention has been focused on the interface tensile strength. In order to avoid edge effects, a cruciform geometry was selected for evaluating the tensile strength. SiC fibers with different types of coatings were evaluated inside an epoxy matrix, and the bond strength was estimated from the mechanical test data. Interface failure was confirmed using optical, dye penetrant, and an ultrasonic shear wave back reflection technique. Tests using straight sided specimens confirmed that singularities at specimen edges have significant influence on interface failure, and hence must be avoided for obtaining valid interface strength data.

The concept of an oxidation resistant fiber-matrix interphase that deflects cracks by cleavage is explored. Sols with the nominal composition CaAl12O19 were used to coat single-crystal alumina fiber and plates and yttrium-aluminum garnet fiber. Subsequent annealing, or consolidation in a matrix, results in strong texturing of the hibonite coating with basal planes parallel to the interface. Texture development within the hibonite interphase occurs by a complex series of phase transformations and reactions. Fiber pushout tests indicate high sliding resistance; however, strain-energy release rates of hibonite-bonded alumina laminates were found to be adequate to provide for crack deflection within the interphase via cleavage. Model composites containing hibonite-coated fibers were tested and showed evidence of crack deflection within the interphase.

The response of the ventilatory system of dogs to transient step and pulse train hypoxia at the carotid bodies is an abrupt increase in tidal volume during the first few seconds of stimulation Subsequent to the initial pulses of pulse trains, ventilation either slowly rises (2 s on - 2 s off pulses) or is sustained (3 s on - 3 s off pulses) at a new steady state intermediate between control and step perfusion ventilation. Data during the 2 s on - 2 s off pulse trains was not obtained for a sufficient length of time to determine the equilibrium level. Recovery from hypoxic perfusion is characterized by a slow return to control ventilation. A mathematical model of the carotid body control system based on these data was developed in the form of nonlinear differential equations. This model indicates that carotid body chemoreceptor mediation of the respiratory controller is a nonlinear system that contains linear dynamics with proportional and rate-sensitve elements in each of two parallel pathways.

The ventilatory response and amino acid levels in dog brain and cerebrospinal fluid (CSF) were determined after one hour of respiratory acidosis at a narcotic level of 25–35% CO2, balance O2, that raised PaCO2 greater than 24 kPa, lowered pH of arterial blood to 6.66 ± 0.03 and pH of cisternal cerebrospinal fluid to 6.70 ± 0.03. Ventilation was 36 ± 4 liters/min (room air normal

The effect of β-adrenoceptor blockade on the carotid body chemoreceptor response to hypoxia was assessed in anesthetized and paralyzed cats. Propranolol, atenolol and ICI 118,551 each abolished the enhancement of chemoreceptor activity produced by i.v. infusion of exogenous isoproterenol; however the blocking durgs did not significantly diminish the increase in chemoreceptor neural discharge induced by hypoxia. These results do not support the hypothesis that β-adrenergic receptors play an essential role in the chemoreceptor response to oxygen deprivation.

The carotid body impulse generator has been previously characterized as a Poisson-type random process. We examined the validity of this characterization by analyzing sinus nerve spike trains for interspike interval dependency. Fifteen single chemoreceptive afferents were recorded in vivo under hypoxic-hypercapnic conditions, and approximately 1,000 consecutive interspike intervals for each fiber were timed and analyzed for serial dependence. The same set of intervals placed in shuffled order served as a control series without serial dependence. The original spike interval trains showed significantly negative first-order serial correlation coefficients and less variability in joint interval distributions than did the shuffled interval trains. These results suggest that the chemoreceptor afferent train is not random and may reflect a negative feedback system operating within the carotid body that limits variation about a mean frequency.

As a means of probing the chemotransducer, impulse sequences from in vitro, superfused sinus nerve-carotid body preparations were analyzed for departures from randomness. Twelve of 17 spike trains showed interval histograms that did not differ significantly from exponential. Thus these sequences resembled a Poisson (random) process with respect to time-independence of probability of occurrence of an event. However, 5 spike trains departed significantly from the exponential distribution forcing rejection of the Poisson model in these cases. Furthermore, mean interval vs standard deviation analysis revealed a significant positive correlation among intervals. These data suggest that the carotid body impulse generator possesses an intrinsic regularity and that the Poisson model does not accurately describe the in vitro sinus nerve interspike interval sequence.

Dogs anesthetized with 30 mg/kg pentobarbital were artificially respired after differential cannulation of the main stem bronchi. Following median sternotomy. blood flow was monitored by electromagnetic flow probes on Ihe left pulmonary artery (Q L ) and on the pulmonary trunk or aorta, Q-p Following 10 min of bilateral 100% O 2 , Q L was 42.5 ± 7% of Qr. When 6 % O 2 was substituted as the gas mixture inspired by the left lung while the right lung remained on 100% O 2 , Pa o , was above 70 mm Hg and Q, tell to 24.5+5% of Qr. Room air was then used to ventilate the right lung while the left lung remained on 6% O 2 . This caused Pa O2 to fall to 42.3 ± 3 mm Hg and Q L to rise to 38.3+6% Qr. This increase in blood flow to the unilaterally hypoxic lung during systemic hypoxemia did not occur in dogs after peripheral chemoreceptor denervation. Therefore, interference with the local response to alveolar hypoxia during systemic hypoxemia appears to be mediated by the arterial chemoreceptors.

The hemodynamic and respiratory effects of spontaneous ventilation with continuous positive airway pressure (CPAP) and mechanical ventilation with positive end-expiratory pressure (PEEP) were compared in nine patients who had adult respiratory distress syndrome. These patients were capable of maintaining spontaneous ventilation (tidal volume above 300 ml. and PaCO2 below 45 torr). Arterial and mixed venous blood gases, cardiac output, oxygen delivery and consumption, pulmonary artery pressure, and pulmonary wedge pressure were measured in 11 instances, with each patient on 5 or 10 cm. H2O CPAP or PEEP, and in nine instances, with each patient on the ventilator but without PEEP (O PEEP). During CPAP, when compared to PEEP at the same level of end-expiratory pressure, mean PaO2 increased significantly (p less than 0.05) and mean physiological shunt decreased (p less than 0.05). In nine of 11 instances, cardiac output was higher on CPAP than on a corresponding level of PEEP. Thus CPAP was more effective than the same amount of PEEP in improving arterial oxygenation by the lung without adversely affecting cardiac output.

The avian respiratory system is a crosscurrent gas exchange system. One of the aspects of this type of gas exchange system is that end-expired PCO2 is greater than arterial PCO2, the highest possible value being equal to mixed venous PCO2. We made steady-state measurements of arterial, mixed venous, and end-expired PCO2 in anesthetized, spontaneously breathing chickens during inhalation of room air or 4–8% CO2. We found end-expired PCO2 to be higher than both arterial and mixed venous PCO2, the sign of the differences being such as to oppose passive diffusion. The observation that end-expired PCO2 was higher than arterial PCO2 can be explained on the basis of crosscurrent gas exchange. However, the observation that end-expired PCO2 exceeded mixed venous PCO2 must be accounted for by some other mechanism. The positive end-expired to mixed venous PCO2 gradients can be explained if it is postulated that the charged membrane mechanism suggested by Gurtner et al. (Respiration Physiol. 7: 173–187, 1969) is present in the avian lung.

The carotid chemoreceptor increases its discharge with increases in CO 2 and H ion though the CO 2 response may be greater than that attributed to concomitant pH changes alone. We attempted to study this increased CO 2 responsiveness. However, in 9 of 10 single fibers studied, once a 20–40 min equilibration period elapsed, the response to CO 2 -dependent H ion increases was comparable to increases due to acid infusion. Thus, we conclude that H ion changes alone can completely account for chemoreceptor CO 2 stimulation.

Neurological aberrations occurring in patients with advanced chronic obstructive pulmonary disease (COPD) and in patients with hepatic encephalopathy have many similarities. These similarities include changes in the level of consciousness varying from restlessness to coma1, 2 and alterations in neuromuscular tone, including dyskinetic movements3, 4. There may be a common biochemical derangement in these diseases, for Valero et al.5 have demonstrated that elevations of both cerebrospinal fluid (CSF) and arterial blood ammonia levels to concentrations equivalent to those seen in hepatic insufficiency can occur in COPD.

Six dogs anesthetized with 30 mg/kg pentobarbital were ventilated after differential cannulation of the main stem bronchi. Following sternotomy, blood flow was monitored byelectromagnetic flow probes on the left pulmonary artery (Q l ) and on the pulmonary truck or aorta (Q t ). Following 10 min of bilateral 100% O 2 , Q l was 37.4 ± 5.8% of Q t . When left lung actelectasis was induced whiel the right lung remained on 100% O 2 , Pa O 2 remained above 75 mm Hg and Q l fell to 26.1 ± 5.0% of Q t . However, when the right lung was ventilated with room air while the left lung remained atelectatic, Pa O 2 fell to 50.0 ± 2.6 mm Hg and Q l rose to 36.7 ± 6.2% of Q t . Six dogs which had undergone peripheral chemoreceptor denervation prior to these experiments showed a similar decrease in perfusion of the atelectatic left lung when the right lung was ventilated with 100% O 2 , but did not increase blood flow to the atelectatic lung during systemic hypoxemia. Thus, the increased blood flow to the atelectatic lung which occurs during systemic hypoxemia appears to be mediated by the arterial chemoreceptors.

Pharmacologic doses of methylprednisolone sodium succinate were administered to 10 critically ill patients when the steroid was the only variable. Measurements of respiratory and circulatory physiologic parameters were obtained in all patients prior to injection and at 30 and 90 minutes following injection of methylprednisolone sodium succinate. A significant increase in Cardiac Index was seen (P less than .01) which appeared to be in association with a decrease in pulmonary vascular resistance (P less than .01) at a time when physiologic shunting of blood through the lungs increased (P less than .01). These changes imply improved perfusion of non- or poorly ventilated portions of the lungs. Four of ten patients demonstrated removal of lactate by the lung during the control period. Following methylprednisolone sodium succinate injection, 9 of 10 patients demonstrated production or a washout of lactate from the lungs.

The hemodynamic and respiratory effects of spontaneous ventilation with continuous positive airway pressure (CPAP) and mechanical ventilation with positive end-expiratory pressure (PEEP) were compared in nine patients who had adult respiratory distress syndrome. These patients were capable of maintaining spontaneous ventilation (tidal volume above 300 ml. and PaCO2 below 45 torr). Arterial and mixed venous blood gases, cardiac output, oxygen delivery and consumption, pulmonary artery pressure, and pulmonary wedge pressure were measured in 11 instances, with each patient on 5 or 10 cm. H2O CPAP or PEEP, and in nine instances, with each patient on the ventilator but without PEEP (O PEEP). During CPAP, when compared to PEEP at the same level of end-expiratory pressure, mean PaO2 increased significantly (p less than 0.05) and mean physiological shunt decreased (p less than 0.05). In nine of 11 instances, cardiac output was higher on CPAP than on a corresponding level of PEEP. Thus CPAP was more effective than the same amount of PEEP in improving arterial oxygenation by the lung without adversely affecting cardiac output.

13 previously untreated patients suffering from early pulmonary sarcoidosis (stages II and III) were studied radiologically and physiologically after 4 months of corticosteroid treatment. The results of airway function studies before and after corticosteroid treatment were compatible with small airway disease that did not improve after treatment. Before steroids, the main abnormalities were decreased diffusion and compliance, increased alveolar-arterial oxygen tension gradients, and the presence of frequency-dependent compliance. After steroids, significant improvement was found in diffusion and alveolar-arterial oxygen tension gradients, but compliance as well as frequency-dependent compliance did not improve.

In 16 dogs ventilated with 100% O2, control blood flow to the left lung was 35 +/- 2% of aortic flow. When left lung atelectasis was induced, left pulmonary artery flow fell to 19 +/- 2% of aortic flow. A large retrograde component of flow developed in this pulmonary artery, suggesting that blood flows into the pulmonary arteries of both lungs during systole, but flows back out of the collapsed lung and into the uncollapsed lung during diastole. Systemic PaO2 remained above 78 mmHg. Subsequently, when the ventilation of the right lung was changed from oxygen to room air, systemic PaO2 fell to 64 +/- 3 mmHg and atelectatic left lung flow rose from 19 +/- 2% to 28 +/- 2% f aortic flow. This was associated with a reduction in reflux from the atelectatic lung. These results suggest that the attenuation of flow to an atelectatic lung is more pronounced if systemic normoxemia is maintained by adequate oxygenation of the normal lung.

This study evaluates the effects of 30 mg/kg methylprednisolone (MP) administered to eight trauma patient over a 30-minute period during initial resuscitation. Vascular pressures, cardiac index (CI), left ventricular stroke work index (LVSWI), systemic (SVR) and pulmonary (PVR) vascular resistance, oxygen delivery (OD), oxygen consumption (VO2), physiological shunt (shunt), limb blood flow (LBF), limb-oxygen delivery (LOD), and limb oxygen consumption (VLO2) were calculated at control and 1, 2, 4 and 6 hours following MP administration. At 1 hour there was an increase in CI from 2.9 +/- 0.3 to 3.5 +/- 0.3 liters/min/m2 (P less than 0.01), in OD from 961 +/- 172 to 11067 +/- 148 ml/min (P less than 0.05), in VO2 from 178 +/- 16 to 220 +/- 16 ml/min (P less than 0.01), in shunt from 25 +/- 3% to 33 +/- 3% (P less than 0.05), and a decrease in SVR from 1187 +/- 98 to 1945 +/- 87, and in PVR form 222 +/- 22 to 178 +/- 18 dyne sec/cm5 (P less than 0.05). These values returned to control by 4 hours. In spite of a pulmonary wedge pressure (PWP) that did not increase form a control of 5 +/- 2 mm Hg, and a mean arterial blood pressure (MABP) that did not decrease from a control of 86 +/- 5 mm Hg, LVSWI increased significantly at 1 hour (P less than 0.01). LBF, LOD, and VLO2 decreased at 1 hour (P less than 0.05). Since increased cardiac output was associated with increased stroke volume and left ventricular stroke work index, but without an increase in preload (PWP) or a decrease in afterload (MABP), methylprednisolone(MP), in pharmacologic dosage appears to have a positive inotropic effect on the myocardium of trauma patients during resuscitation.

Pulmonary function was measured in 24 sarcoidosis patients, 17 nonsmokers and 7 smokers. 12 (4 smokers) had evidence of small airway disease and 6 patients (3 smokers) had evidence of large airway disease. A significantly greater proportion of smokers had an increased closing volume, and closing volume appears to be the most sensitive test for small airway disease in sarcoidosis. However, 3 patients with normal closing volumes had evidence of small airway disease by forced expiratory flow rates or frequency dependence of compliance. We conclude that there is a high incidence of small airway disease in patients with sarcoidosis. There also appears to be a synergism between sarcoidosis and smoking that leads to a significant degree of hyperinflation of the lung.

Dogs anesthetized with 30 mg/kg pentobarbital were artificially respired after differential cannulation of the main stem bronchi. Following median sternotomy, blood flow was monitored by electromagnetic flow probes on the left pulmonary artery (QL) and on the pulmonary trunk or aorta, QT. Following 10 min of bilateral 100% O2, QL was 42.5 +/- 7% of QT. When 6% O2, was substituted as the gas mixture inspired by the left lung while the right lung remained on 100% O2, PaO2 was above 70 mm Hg and QL fell to 24.5 +/- 5% of QT. Room air was then used to ventilate the right lung while the left lung remained on 6% O2. This caused PaO2 to fall to 42.3 +/- 3 MM Hg and QL to rise to 38.3 +/- 6% QT. This increase in blood flow to the unilaterally hypoxic lung during systemic hypoxemia did not occur in dogs after peripheral chemoreceptor denervation. Therefore, interference with the local response to alveolar hypoxia during systemic hypoxemia appears to be mediated by the arterial chemoreceptors.

The role of endogenous carotid body dopamine in the afferent chemoreceptor circuit was studied by means of haloperidol-induced dopamine antagonism. In 19 cats that were anesthetized with pentobarbital sodium and paralyzed, single carotid body nerve fibers were dissected free and placed on unipolar platinum wire electrodes. In 10 of these cats, the neural response to room air and the last 2 min of 6-min inhalations of 3, 6, and 9% CO2 were recorded, and blood samples were drawn for gas tension measurements. Haloperidol was administered at a dose (250 micrograms/kg) shown to block the inhibitory effect of injected dopamine. Following a 15-min equilibration, the CO2 response was again tested. In four other cats the CO2 response was tested with a hyperoxic background. In the remaining five cats the response to isocapnic hypoxia was recorded during administration of 15, 12, and 8% O2 before and following haloperidol. There was a significant increase in room air discharge activity and in hypoxic sensitivity following haloperidol. However, there was no significant change in hypercapnic sensitivity. These results suggest that there is a modulatory role for endogenous dopamine only in the hypoxic response.

Effects of antagonism of endogenous dopamine with haloperidol on single-unit frequency, interspike interval distribution, and interval serial dependency of the cat sinus nerve were tested using an in vitro carotid body-sinus nerve superfusion technique. A dose dependency of inhibition by haloperidol (0.05–2.0 microgram/ml) was observed. Superfusion with 1–2 microgram/ml haloperidol significantly reduced frequency within 5 min (P less than 0.05) and caused a complete cessation of firing within 25 min in 5 of 10 chemoreceptor units. Frequency recovered to control during drug washout. Acetylcholine (10-micrograms/ml superfusion or 500-micrograms bolus) increased sinus nerve activity under control conditions but not during superfusion with haloperidol. No effect of haloperidol on impulse serial dependency was detected. However, interval distribution was significantly altered by haloperidol in five of six chemoreceptor units. Our results suggest an excitatory role for dopamine in carotid chemoreception.

Much of the recent work evaluating the role of the carotid body chemoreceptors in the control of ventilation has involved the application of transient stimuli. The response of ventilation to a sustained step decrease in Po 2 from 90 mm Hg to 32 mm Hg of blood perfusing the carotid bodies of dogs indicated an abrupt increase in ventilation to nearly the final steady-state levels. The similarity of this response to the classic linear second-order system response prompted the investigation of a mathematical model that could be used to simulate the ventilatory control loop. It has been determined that the response of the ventilatory system of the dog to step, ramp, pulse, and pulse train inputs of hypoxia can be simulated with good accuracy by a nonlinear closed-loop feedback system that contains linear second-order dynamics. The input to this system is proportional to the magnitude and the rate of change of Po 2 at the carotid bodies.

Nine of 105 cats with hyperthyroidism treated with propylthiouracil developed a serious immune-mediated drug reaction during treatment. Adverse clinical signs, which developed after 19 to 37 days (mean, 24.8 days) of propylthiouracil administration, included lethargy, weakness, anorexia, and bleeding diathesis. Physical examination revealed pale mucous membranes, and petechial hemorrhages of the skin and oral cavity. Results of hematologic testing revealed severe anemia and thrombocytopenia. The direct antiglobulin (Coombs') test was positive in all 7 cats evaluated, whereas the serum antinuclear antibody titer was greater than or equal to 1:10 in 5 of the 8 cats tested. In 4 of the cats, treatment included appropriate supportive therapy and cessation of propylthiouracil; in these cats, anemia and thrombocytopenia resolved and Coombs' and antinuclear antibody tests became negative within 2 weeks.

To investigate the role of ventilation-perfusion (VA/Q) imbalance in the hypoxemia observed after head injury, 5 male subjects (17 to 26 years of age) with isolated head trauma and subsequent hypoxemia were studied. Disturbances of ventilation and perfusion were assessed using the steady-state elimination of six inert gases of different solubilities. Paired studies were conducted during mechanical ventilation with a volume-cycled ventilator and during spontaneous ventilation. Distributions recovered from studies of spontaneous ventilation show a mode of ventilation and perfusion near a VA/Q of 1.0. In addition, 41% of the cardiac output was distributed to a second population of lung units with low VA/Q (less than 0.1) and shunt. During mechanical ventilation, perfusion to these regions of low VA/Q decreased to 21% of the cardiac output, whereas shunt fraction was unchanged. This was associated with a marked broadening of the VA/Q mode near 1.0, relative to the studies during spontaneous ventilation. Mean functional residual capacity during mechanical ventilation was not different from that during spontaneous ventilation. These results suggest that head injury can lead to hypoxemia through a failure of VA/Q regulatory mechanisms.

The ventilatory responses to step changes in vertebral artery P CO 2 were investigated in intact and carotid body denervated dogs. The steady-state ventilatory responses of the denervated dogs were less than those of intact dogs. However, when expressed as a ratio to the control ventilation there was no difference between the two groups. While the arterial P CO 2 was held at 56 mm Hg by adding CO 2 to the inspiref air the perfusion of the vertebral arteries was switched from the dog's own arterial supply to hypocapnic blood. The ventilation of the denervated dogs decreased at a faster rate (half time = 130 ± 9 sec) to a level less than the room air control ventilation. The ventilation in the intact dogs decreased at a slower rate (half time = 184 ± 23 sec) and was maintained above the room air control level after ten minutes of hypocapnic perfusion. Increasing the medullary blood flow, as measured with radiolabeled microspheres, augmented the rate of decline of ventilation in intact dogs. We conclude, (1) the influence of the peripheral chemoreceptors appears to increase as central drive is decreasing, and (2) the remaining time course of the decrease in ventilation is related to the rate of brain stem perfusion.

The hypothesis that cyclic variation of CO2 tension of the arterial blood (PaCOCO2) about its mean produces an additional stimulus to ventilation was tested in the dog. Oscillations of alveolar carbon dioxide tension were produced by the intermittent administration of 20% CO2 for 1 breath every 7–12 breaths. The increment in ventilation per mm Hg rise in mean PaCOCO2 during the intermittent administration of 20% CO2 was compared to that during continuous administration of 3% CO2 in nine adult dogs anesthesized with sodium pentobarbital. Thirteen experiments with oscillating CO2 and eighteen with steady CO2 were performed. In all except one animal the increase in ventilation per mm Hg change in mean PaCOCO2 was greater during intermittent CO2 than during steady CO2. In three experiments intermittent administration of CO2 caused a ventilatory response sufficient to lower the mean PaCOCO2 below control values. The increment in total ventilation per mm Hg rise in arterial carbon dioxide tension for steady CO2 breathing was 0.58 liters/min per mm Hg and for intermittent CO2 was 2.00 liters/min per mm Hg. These findings support the concept that chemoreceptors are stimulated by oscillations of PaCOCO2 as well as by the mean level of PaCOCO2. The oscillatory stimulus appears not to be related to the amplitude of the oscillation or to the peak Pco2 attained, but rather to the rate of increase of arterial Pco2. respiration control; ventilation Submitted on October 17, 1963