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Biomedical subjects

S M Tenney

Publications and source records attributed to S M Tenney.

At least 37 records · Page 2Linked to original sources
PubMed1982

Comparative mechanics of mammalian respiratory system.

Compliances (C) of lung, thorax and respiratory system as well as resistances (R) of the respiratory system (lower airways + lung + chest wall) and of upper airway (primarily laryngeal and nasal) were measured in 5 species of mammals, spanning a 1000-fold range of body weights (mouse to dog), immediately following sacrifice with an overdose of sodium pentobarbital. The results indicate that compliance is proportional to BW1.0, while respiratory resistance and upper airway resistance have exponents of -0.819 and -0.702, respectively. The reciprocal of the time constant, tau -1 = (RC)-1 is proportional to BW-0.298 for respiratory resistance alone and BW-0.326 when upper airway resistance is included. Since breathing frequency varies as BW-0.28, these results indicate a proportional relationship between breathing frequency and passive emptying time. This suggests that passive respiratory mechanics play a major role in determining TE and therefore TTOT for animals during quiet breathing. Changes in volume history were found not to affect the slope of the relationships between compliance and body weight.

Airway Resistance↗
PubMed1981

Role of arginine vasopressin on fluid and electrolyte balance in rats exposed to high altitude.

Normal rats (N) and rats with hereditary hypothalamic diabetes insipidus (DI) were employed to examine the role of arginine vasopressin (AVP) in the reduction of water intake and urine output during hypoxic exposure. The pattern of reduced water intake followed by recovery was similar in both N and DI rats during 7 days of hypobaric hypoxia (inspired O2 pressure of 75 Torr). Water intake was markedly reduced during the first 6 h of hypoxic exposure in both groups, whereas urine output did not decrease significantly until after 6 h in DI rats and after 18 h in N rats. Total urinary excretion of AVP in N rats decreased and remained depressed during 7 days of hypoxia. (AVP excretion corrected for osmolar clearance was unchanged.) Plasma AVP of conscious N rats was 2.7 +/- 0.40 pg/ml plasma during normoxia and 2.4 +/- 0.74 pg/ml plasma after 2 h of exposure to inspired O2 fractional concentrations of 0.105 (paired samples). We conclude that AVP is not a major factor in the decreased water intake and urine output observed during hypoxia, and that the initial disturbance is a reduced water intake that leads to negative water balance, reduced urine volume, increased urine concentration, and hyperosmotic volume contraction. The reduced or unchanged AVP release in normal rats during hypoxia appears to be inappropriate.

Adaptation, Physiological↗
PubMed1981

Mechanism of reduced water intake in rats at high altitude.

Water intake was reduced during the 1st day of hypobaric hypoxia (inspired O2 pressure of 75 Torr) to 35-40% of the normoxic level in both normal rats (N) and rats with diabetes insipidus (DI). Analysis of water intake under graded saline loads at several inspired O2 levels (inspired O2 fractional concentrations of 0.105, 0.120, and 0.2095) indicated that hypoxia increased the threshold for osmotic stimulation of drinking without changing the sensitivity of the response in both N and DI rats. Nephrectomized N rats reduced water intake during hypoxia to 33% of the nephrectomized normoxic level of intake, and nephrectomized DI rats reduced intake to 47% of the nephrectomized normoxic intake. From these results it is concluded that reduced angiotensin II formation was not the factor responsible for reduced water intake during hypoxia. Polyethylene glycol-induced hypovolemia resulted in increased water intake during normoxia, but during hypoxia it was reduced to 29% of the normoxic rate. Reduced body temperature and hyperventilation were not the source of hypoxic attenuation of thirst. The mechanism may reside beyond the central integration of osmotic and nonosmotic information, or at the osmotic sensing mechanism itself.

Adaptation, Physiological↗
PubMed1980

Oxygen transport during progressive hypoxia in high-altitude and sea-level waterfowl.

Under conditions of progressive hypoxia, oxygen transport was compared in bar-headed geese (Anser indicus), a species which breeds on the Tibetan Plateau and migrates at altitudes up to 9200 m, and Pekin ducks (Anas platyrhynchos, forma domestica), a similarly sized, sea-level water fowl that does not fly. Pekin ducks showed no altitude-induced behavioral effects (e.g., restlessness) up to 7620 m, while bar-headed geese tolerated 10,668 m with no observable behavioral changes. Ventilatory and cardiac responses to hypoxia as functions of PaO2 followed a typical hyperbolic contour, but the response began at almost 20 Torr lower in the bar-headed goose. Both ventilation and cardiac output appeared to follow a common response curve for the two species, when the independent variable was expressed as arterial oxygen content. The goose had a high oxygen affinity hemoglobin, compared with the duck; the oxyhemoglobin curves of both shifted slightly to the right as a result of acclimation to 5640 m; but only the duck developed erythrocytosis as a consequence of acclimation. Under sea level conditions the duck maintained a higher mixed venous PO2, but with acute hypoxic exposures PVO2 was higher in the goose. Following acclimation, cardiac output in the duck was lower than in pre-acclimatized state, but in the goose it was higher up to the altitude at which it migrates. The selective pressures leading to the evolution of favorable oxygen transport in the bar-headed goose are discussed.

Adaptation, Physiological↗
PubMed1980

Is there localized cerebral cortical influence on hypoxic ventilatory response?

A cortical inhibitory influence on net ventilatory response to hypoxia is inferred from the hyperexcitable response of decorticate cats. Electrical stimulus exploration of the cortex localizes the regions inhibitory to breathing predominantly on the orbital gyrus of the frontal lobes. The present experiments were designed to determine whether ablations of those regions of the orbital gyrus would replicate the effect of total decortication on hypoxic ventilatory response. Steady state hypoxic ventilatory response curves were determined in 8 cats under both hypocapnic and eucapnic conditions, first in the control state and second at various times after regional ablations of the orbital gyrus. Only 3 of the 8 cats showed a hyperexcitable response under hypoxia after lesioning, and they all recovered to the control state by 10 days. The isocapnic and hypocapnic responses were affected similarly. No unique contribution of this region of the brain to hypoxic ventilatory control can be documented.

Animals↗
PubMed1979

Adrenocortical function in rats chronically exposed to high altitude.

In rats exposed to a simulated altitude of 5,486 m for 3 mo, pituitary and adrenal glands hypertrophied and plasma levels of corticosterone increased more than threefold over sea-level controls. The in vitro rates of corticosterone production by the quartered adrenal gland were significantly enhanced, but the responsiveness of the adrenal gland to ACTH remained normal.

Acclimatization↗
PubMed1977

Hypoxic ventilatory response of cats at high altitude: an interpretation of 'blunting'.

Cats acclimatized to a simulated altitude of 5500 m developed attenuated ventilatory response in the hypoxic test range of PAO2 = 60-45 torr, but their CO2 response remained normal, although the curve was shifted to a lower PACO2 range. The acclimatized cats a high respiratory frequency and maintained hyperventilation under normoxia. Cats from 3100 m altitude had hypoxic reponses which were, on the average, slightly below sea level standards, but the difference was not statistically significant. Two cats raised at 4640 m had a normal hypoxic ventilatory response even though the frequency response was 'blunted'. These data suggest the possibility of hypoxic 'threshold' near 5500 m to produce an attenuation effect. Another series of cats acclimatized to 5500 m were tested with more severe hypoxia, and they exhibited brisk ventilatory response in range PAO2, 40-25 torr, although they showed typical 'blunting' in the range PAO2, 60-45 torr. These results suggested that the phenomenon of attenuated hypoxic response at high altitude was a reflection of shift of hypoxic set point to a lower PAO2. Finally, it was shown that the hypoxic responses of 'blunted' animals were restored to normal after mid-collicular decerebration; and that decortication resulted in a typical hyperexcitability of the hypoxic response. These results are discussed in terms of hypothesized suprapontine modulating influences on the control of breathing, and possiblities for a contribution of these mechanisms in pathogenesis of hypoxic 'blunting' are raised.

Acclimatization↗
PubMed1977

Ventilatory response of decorticate and decerebrate cats to hypoxia and CO2.

The steady state ventilatory response of normal, fully awake cats was studied under graded hypoxia (at PAO2 = 110, 55, 45 torr) with PACO2 controlled throughout at the resting, normoxic level and at +5 torr. Subsequently, either a mid-collicular decerebration or a decortication was performed, and the ventilatory studies were repeated. Respiratory frequency, tidal volume, and ventilation in the decerebrate state responded to hypoxia and hypercapnia in a manner indistinguishable from the control. The decorticate cats, however, exhibited an exaggerated response to hypoxia, principally the result of increased frequency. The negative hypoxic, hypercapnic interaction, characteristic of awake cats, was demonstrable in both the decerebrate and decorticate animals. The findings are interpreted as revealing coupled descending influences on the medullary respiratory centers in hypoxia--one that is facilitatory and originates in the diencephalon, and the other, inhibitory, from the cerebrum. The significance of this suprapontine system in normal hypoxic ventilatory control is discussed.

Animals↗
PubMed1976

The role of brief hypocapnia in the ventilatory response to CO2 with hypoxia.

In conscious cats the ventilatory response curve to physiological range of CO2 is displaced upward by hypoxia (about 45 torr), but it rises, either parallel with, or convergent on, the normoxic curve. Thus, a positive interaction of hypoxia and hypercapnic stimuli is not observed under these circumstances. However, if during the hypoxic exposure, hypocapnia is allowed to develop, the subsequently determined CO2 ventilatory response curve will shift to the left, rise steeply, particularly in the early phase, and demonstrate a positive hypoxic hypercapnic interaction. A demonstrable interactive effect was dependent on a conditioning period of hypocapnia, and this was shown to be associated with an elevated level of lactic acid to a greater degree in cerebral venous blood than in CSF or arterial blood. The interpretation is discussed without reaching a firm conclusion of mechanism, but the results emphasize how a minor change of experimental protocol affects a basic phenomenon in the chemical control of breathing.

Animals↗
PubMed1976

Hypoxia and carbon dioxide as separate and interactive depressants of ventilation.

The respiratory frequency, tidal volume and ventilization responses of 20 conscious cats to hypoxia, at controlled levels of alveolar CO2, revealed a characteristic steady state response in the majority of animals which indicated a negative interaction of stimuli on tidal volume and minute volume of ventilation, but a positive interaction on frequency. Another series of studies, conducted on seven conscious cats, sought to identify hypoxic response thresholds and depression thresholds, by determining responses over a wide range of hypoxic stimulus intensities, and at different controlled alveolar PCO2. Response threshold was at about 65 torr PAO2. Under eucapnic conditions, ventilation began to fail at PAO2 about 30 torr due to failure of tidal volume. The frequency continued to increase even in the lowest range of PAO2. With hypocapnia no failure of ventilation, frequency, or tidal volume was seen even at the lowest PAO2, but with hypercapnia, the tidal volume began to fail at PAO2 about 50 torr. The minute volume however, continued to increase into the lowest range of PAO2, because the frequency continued to respond at a rate greater than the tidal volume was failing. The results are discussed in terms of interactive depression manifest through the coupled responses of peripheral and central mechanisms.

Animals↗
PubMed1976

Effect of potassium depletion on cerebrospinal fluid bicarbonate homeostasis.

We have examined the effect of K depletion on CSF [HCO3-] homeostasis in awake rats. The relationship of CSF [HCO3-] to arterial [HCO3-] in metabolic acid-base disturbances is displaced is an upward direction and has a significantly increased slope in K-depleted vs. control rats (0.51 +/- 0.02 vs. 0.42 +/- 0.02). Results of partial K-repletion experiments, with peripheral acid-base balance held constant, suggest that the effect is K specific. The K-depleted animals also exhibit a wider (CSF-arterial) PCO2 difference than controls (11.1 vs. 8.4 mmHg). When CSF [HCO3-] is shown as a function of CSF PCO2 the data of K-depleted rats are no longer displaced when compared to controls but still have a significantly greater slope (1.21 +/- 0.23 vs. 0.89 +/- 0.08). This increased slope is interpreted to reflect enhanced HCO3- movement from blood to CSF at high arterial [HCO3-]. Analysis of our data and observations from the literature in conditions of mixed acid-base disturbances suggest that CSF [HCO3-] is determined by a) CSF PCO2 and b) the level of arterial [HCO3-] when the latter is greater than the normal CSF [HCO3-].

Acid-Base Equilibrium↗
PubMed1976

Effects of potassium depletion on control of breathing in awake rats.

Possible mechanisms for the variable ventilatory response to metabolic acid-base disturbances have been examined in normal and K-depleted rats. Ventilatory measurements are correlated with CSF acid-base data. The ratios VE/VO2 and 1/PaCO2 are utilized as indices of alveolar ventilation. The log of these indices correlates closely with CSF [H+] independent of [K+] except at very low CSF [H+] where the change in log 1/PaCO2 and log VE/VO2 per change in CSF [H+] is much diminished in low-K rats. This finding suggests the presence of an additional stimulus to breathing in the low-K rat opposing the inhibitory effect of low CSF [H+]. Otherwise the chemical control of ventilation appears to be normal. However, low-K rats always breath with a low-flight-Vt pattern and occasionally with abnormal rhythms. The similarity of the low K breathing pattern to that reported in awake animals with vagotomy and pneumotaxic center (PC) lesions suggests that the altered breathing pattern in depletion involves vagal and/or PC pathways. The similarity of the low-K breathing pattern to that observed with reserpine administration together with the known relationships of K and catecholamine metabolism lead to the speculation that K depletion alters breathing via an effect on central catecholamine metabolism. However, other mechanisms involving changes in membrane excitability and intracellular pH in K depletion might also be involved.

Acid-Base Imbalance↗
PubMed1975

Hyperoxic hyperventilation in carotid-deafferented cats.

Ventilation when breathing air and during exposure to hyperoxia (PAO2 equal to 400-450 mm Hg) was studied in unanesthetized cats before and after carotid sinus nerve section (chemo-deafferentation). Chemo-deafferentation resulted in lowered values of measured ventilation, tidal volume, and respiratory frequency, during air breathing PACO2 increased by an average of 7.9 mm Hg. In intact animals, ventilation after 10 minutes of exposure to hyperoxia was similar in magnitude and pattern to that measured during air breathing. Exposure of chemo-deafferented animals to hyperoxia resulted in an increased ventilation, due entirely to augmented tidal volume. Increased ventilation was accompanied by a decrease in PACO2. This response to hyperoxia developed gradually duringa 3-4-minute period, the rise in ventilation and fall in PACO2 invariably stabilizing by 5 minutes. It is concluded that carotid body chemoreceptor activity is essential for the maintenance of normal values of ventilation and PACO2 in unanesthetized cats. In addition, central mechanisms responsible for tidal volume production may, in the absence of carotid body afferent input, be depressed by the PO2 characteristic of normal arterial blood. The significance of these findings to the chemical control of breathing is discussed.

Air↗
PubMed1975

Hypoxia-induced tachypnea in carotid-deafferented cats.

Ventilation while breathing air and in response to hypoxia was studied in unanesthetized cats after carotid body chemo-defferentation. Hypoxic exposure (FIO2 equal to 0.07-0.12) of chemo-deafferented animals rapidly produced a high frequency, low tidal volume tachypnea. Tachypneic breathing, although usually associated with an increased expired ventilation, was accompanied by an increase in PACO2. In contrast to intact cats, behavioral arousal during hypoxic exposure was not observed after chemo-deafferentation. The response to milder hypoxia (FIO2 equal to 0.14-0.16) occurred with an increased latency, and there resulted a less marked depression of tidal volume and stimulation of respiratory frequency. Elevation of PACO2 to 5 mm Hg above the resting value, by addition of CO2 to the inspired gas, prevented the appearance of tachypnea upon subsequent reduction of FIO2 from 0.21 to 0.07. Depletion of central catecholamine stores, by administration of reserpine, did not prevent the tachypneic response to hypoxia. Following administration of anesthesia (pentobarbital, 30 mg/kg, IP), hypoxic exposure (FIO2 equal to 0.10) led to depression of both respiratory frequency and tidal volume, resulting in apnea within 1.5 minutes. It is concluded that hypoxia (FLO2 equal to 0.07-0.16) acts, in a concentration-related manner, as a powerful stimulant to central respiratory frequency generation and as a depressant of the tidal volume in the unanesthetized cat.

Anesthesia, Local↗