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  • 1
    Online Resource
    Online Resource
    American Physiological Society ; 1977
    In:  Journal of Applied Physiology Vol. 43, No. 2 ( 1977-08-01), p. 379-381
    In: Journal of Applied Physiology, American Physiological Society, Vol. 43, No. 2 ( 1977-08-01), p. 379-381
    Abstract: A semicontinuous but noninvasive blood pressure monitoring system is described. It consists of a commercial electronic sphygmomanometer which utilizes a microphone under an occluding arm cuff to detect the Korotkoff sounds, a pressure transducer, and a simple gating circuit. The gate passes the cuff pressure signal to a recorder only when a proper Korotkoff sound is detected. The cuff is rapidly inflated to just above the anticipated systolic pressure, then deflated at a steady rate of 2–6 Torr/heartbeat. When diastolic pressure is passed, the cuff is fully deflated momentarily before repeating the cycle. Systolic and diastolic pressures can be recorded up to 3 or 4 times/min. Spurious signals are rejected by the electronics which process the output of the microphone. This allows the use of the system in experiments on exercising man and in environments where unwanted signals exist. The system offers greater versatility than commercial semiautomatic pressure monitors, at less than half the cost.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    RVK:
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1977
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 2
    Online Resource
    Online Resource
    American Physiological Society ; 1979
    In:  Journal of Applied Physiology Vol. 47, No. 2 ( 1979-08-01), p. 352-359
    In: Journal of Applied Physiology, American Physiological Society, Vol. 47, No. 2 ( 1979-08-01), p. 352-359
    Abstract: Receptor sites for the ventilatory response to isoproterenol were investigated in anesthetized rabbits with bolus injections in the common carotid artery (ia) and in the vena cava (iv). The delay from injection to the increase in ventilation (TVE) was significantly shorter following ia (1.5 s) compared to iv injections (about 5 s). The delay to the increase in heart rate (THR) was significantly shorter after iv (about 4.5 s) than after ia injections (12.5 s). When isoproterenol and NaCN injections were compared, there was no difference in TVE. Following carotid body resection, the VE response to isoproterenol was greatly reduced after iv and ia injections; however, THR was unaffected. In intact animals breathing 100% O2 the VE response to isoproterenol was significantly reduced with no change in TVE or in the heart rate response. We conclude that the ventilatory increase following the injection of isoproterenol is due primarily to direct stimulation of the carotid bodies.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    RVK:
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1979
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 3
    Online Resource
    Online Resource
    American Physiological Society ; 1982
    In:  Journal of Applied Physiology Vol. 53, No. 5 ( 1982-11-01), p. 1071-1079
    In: Journal of Applied Physiology, American Physiological Society, Vol. 53, No. 5 ( 1982-11-01), p. 1071-1079
    Abstract: Functional residual capacity (FRC), tidal volume (VT), and frequency (f) were compared in 23 rats while either awake and unrestrained or anesthetized. FRC was determined from gas compression with closed airway inside a cone-shaped body plethysmograph. In the awake state (mean +/- SD), FRC was 1.02 +/- 0.22 ml/100 g, VT was 0.38 +/- 0.06 ml/100 g, and f was 142 +/- 22 breaths/min. During anesthesia, FRC decreased (P less than 0.01) to 52.9% of awake values, VT increased (P less than 0.01) to 147.4%, and f decreased (P less than 0.01) to 71.8%, leaving minute ventilation almost unchanged. An additional seven rats were used to examine postural effects on FRC during anesthesia, and in another seven animals pleural pressure changes were monitored. Dynamic lung compliance (0.80 ml . kg-1 X cmH2O-1) was not altered by anesthesia, but the pressure-volume curve was shifted 6 cmH2O higher. Thoracic compression, followed by a time-dependent effect of volume history, may account for the major change in FRC. The remainder of the decrease in FRC may be due to lower breathing frequency, loss of inspiratory muscle activity, and/or less airway resistance after anesthesia. Peak diaphragmatic electromyogram per unit VT was shown to increase almost linearly with FRC, indicating that diaphragmatic efficiency was decreased as lung volume was elevated. Functional residual capacity (FRC), tidal volume (VT), and frequency (f) were compared in 23 rats while either awake and unrestrained or anesthetized. FRC was determined from gas compression with closed airway inside a cone-shaped body plethysmograph. In the awake state (mean +/- SD), FRC was 1.02 +/- 0.22 ml/100 g, VT was 0.38 +/- 0.06 ml/100 g, and f was 142 +/- 22 breaths/min. During anesthesia, FRC decreased (P less than 0.01) to 52.9% of awake values, VT increased (P less than 0.01) to 147.4%, and f decreased (P less than 0.01) to 71.8%, leaving minute ventilation almost unchanged. An additional seven rats were used to examine postural effects on FRC during anesthesia, and in another seven animals pleural pressure changes were monitored. Dynamic lung compliance (0.80 ml . kg-1 X cmH2O-1) was not altered by anesthesia, but the pressure-volume curve was shifted 6 cmH2O higher. Thoracic compression, followed by a time-dependent effect of volume history, may account for the major change in FRC. The remainder of the decrease in FRC may be due to lower breathing frequency, loss of inspiratory muscle activity, and/or less airway resistance after anesthesia. Peak diaphragmatic electromyogram per unit VT was shown to increase almost linearly with FRC, indicating that diaphragmatic efficiency was decreased as lung volume was elevated. Functional residual capacity (FRC), tidal volume (VT), and frequency (f) were compared in 23 rats while either awake and unrestrained or anesthetized. FRC was determined from gas compression with closed airway inside a cone-shaped body plethysmograph. In the awake state (mean +/- SD), FRC was 1.02 +/- 0.22 ml/100 g, VT was 0.38 +/- 0.06 ml/100 g, and f was 142 +/- 22 breaths/min. During anesthesia, FRC decreased (P less than 0.01) to 52.9% of awake values, VT increased (P less than 0.01) to 147.4%, and f decreased (P less than 0.01) to 71.8%, leaving minute ventilation almost unchanged. An additional seven rats were used to examine postural effects on FRC during anesthesia, and in another seven animals pleural pressure changes were monitored. Dynamic lung compliance (0.80 ml . kg-1 X cmH2O-1) was not altered by anesthesia, but the pressure-volume curve was shifted 6 cmH2O higher. Thoracic compression, followed by a time-dependent effect of volume history, may account for the major change in FRC. The remainder of the decrease in FRC may be due to lower breathing frequency, loss of inspiratory muscle activity, and/or less airway resistance after anesthesia. Peak diaphragmatic electromyogram per unit VT was shown to increase almost linearly with FRC, indicating that diaphragmatic efficiency was decreased as lung volume was elevated. Functional residual capacity (FRC), tidal volume (VT), and frequency (f) were compared in 23 rats while either awake and unrestrained or anesthetized. FRC was determined from gas compression with closed airway inside a cone-shaped body plethysmograph. In the awake state (mean +/- SD), FRC was 1.02 +/- 0.22 ml/100 g, VT was 0.38 +/- 0.06 ml/100 g, and f was 142 +/- 22 breaths/min. During anesthesia, FRC decreased (P less than 0.01) to 52.9% of awake values, VT increased (P less than 0.01) to 147.4%, and f decreased (P less than 0.01) to 71.8%, leaving minute ventilation almost unchanged. An additional seven rats were used to examine postural effects on FRC during anesthesia, and in another seven animals pleural pressure changes were monitored. Dynamic lung compliance (0.80 ml . kg-1 X cmH2O-1) was not altered by anesthesia, but the pressure-volume curve was shifted 6 cmH2O higher. Thoracic compression, followed by a time-dependent effect of volume history, may account for the major change in FRC. The remainder of the decrease in FRC may be due to lower breathing frequency, loss of inspiratory muscle activity, and/or less airway resistance after anesthesia. Peak diaphragmatic electromyogram per unit VT was shown to increase almost linearly with FRC, indicating that diaphragmatic efficiency was decreased as lung volume was elevated.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    RVK:
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1982
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 4
    Online Resource
    Online Resource
    Elsevier BV ; 1979
    In:  Respiration Physiology Vol. 38, No. 1 ( 1979-9), p. 83-92
    In: Respiration Physiology, Elsevier BV, Vol. 38, No. 1 ( 1979-9), p. 83-92
    Type of Medium: Online Resource
    ISSN: 0034-5687
    Language: English
    Publisher: Elsevier BV
    Publication Date: 1979
    detail.hit.zdb_id: 2010715-8
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  • 5
    Online Resource
    Online Resource
    Georg Thieme Verlag KG ; 2006
    In:  Zeitschrift für Klassische Homöopathie Vol. 50, No. S 1 ( 2006-12), p. S35-S48
    In: Zeitschrift für Klassische Homöopathie, Georg Thieme Verlag KG, Vol. 50, No. S 1 ( 2006-12), p. S35-S48
    Type of Medium: Online Resource
    ISSN: 0935-0853 , 1439-4308
    Language: German
    Publisher: Georg Thieme Verlag KG
    Publication Date: 2006
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  • 6
    Online Resource
    Online Resource
    American Physiological Society ; 1981
    In:  Journal of Applied Physiology Vol. 51, No. 6 ( 1981-12-01), p. 1574-1580
    In: Journal of Applied Physiology, American Physiological Society, Vol. 51, No. 6 ( 1981-12-01), p. 1574-1580
    Abstract: We have attempted to determine the membrane parameters, permeability-surface area product (PS) and reflection coefficient (sigma), necessary to describe solute exchange in the pulmonary circulation. Experimental lymph-to-plasma ratios were obtained for total protein (Rtot) and albumin (Ralb) using lung lymph collected from goats with chronic lung lymph fistulae. Lymph flow (QL) and solute flow (QS) were varied by increasing microvascular pressure in a stepwise manner by inflating a balloon in the left atrium. The increased QL and decreased Ralb from multiple experiments in four goats were used to plot PS vs. sigma using the equation of Patlak et al. (J. Theor. Biol. 5: 426–442, 1963). The region of intersection of two or more such curves should identify the two membrane constants. However, these curves rarely intersected suggesting that perhaps the lung barrier was not adequately represented by a single homoporous membrane. To evaluate heteroporosity, the three-pore model of Blake and Staub (Microvasc. Res. 12: 197–220, 1976) was investigated. By use of their pore sizes and relative pore distributions, values for the fluid filtration coefficient, PS, and sigma of each pore type were calculated, and finally QL and R were predicted at various microvascular pressures. When these calculated values of QL and R were plotted using the equation of Patlak et al., an equivalent homoporous PS and sigma could still be found. Therefore, a heteroporous membrane does not appear to explain the failure of our data plots to intersect. Possible alternative models are suggested.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    RVK:
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1981
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 7
    Online Resource
    Online Resource
    Walter de Gruyter GmbH ; 1991
    In:  Clinical Chemistry and Laboratory Medicine Vol. 29, No. 10 ( 1991)
    In: Clinical Chemistry and Laboratory Medicine, Walter de Gruyter GmbH, Vol. 29, No. 10 ( 1991)
    Type of Medium: Online Resource
    ISSN: 1434-6621 , 1437-4331
    Language: Unknown
    Publisher: Walter de Gruyter GmbH
    Publication Date: 1991
    detail.hit.zdb_id: 1492732-9
    SSG: 15,3
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  • 8
    Online Resource
    Online Resource
    American Physiological Society ; 1984
    In:  Journal of Applied Physiology Vol. 56, No. 4 ( 1984-04-01), p. 979-985
    In: Journal of Applied Physiology, American Physiological Society, Vol. 56, No. 4 ( 1984-04-01), p. 979-985
    Abstract: Lung injuries were produced by instilling 2.5 ml/kg of 0.1 N HCl into the trachea of lightly anesthetized goats with previously implanted lung lymph fistulas. Lymph flow (QL), lymph-to-plasma protein concentration ratio (L/P), pulmonary arterial and wedge pressures (Ppa, Pw), percent shunt (Qs/QT), and postmortem extravascular lung water (EVLW) were then measured for up to 48 h. QL began to increase within 15 min of injury from a baseline value of 7.2 ml/h to reach a peak of 231% of base line by 1.5 h, then decreased to 160% at 24 h and returned to base line by 48 h. Average L/P increased from 0.66 to a peak of 0.73 at 2 h. Ppa increased from 17.0 cmH2O to a first peak of 25.3 cmH2O at 15 min, then decreased to base line by 75 min. There was a second rise that peaked at 3 h before returning to base line at 24–48 h; Pw was unchanged throughout. Qs/QT increased from 8.5 to a peak of 34% at 1 h, then decreased to 15% at 4 h, and stabilized at 17–20% at 48 h. EVLW was 237% of base line at 4 h and declined somewhat but remained elevated at 194% of base line at 24 and 48 h. Qs/QT was less than expected based on the reduction in lung volume after aspiration. We conclude that microvascular permeability was increased after acid and that a protective vasoconstriction, probably due to local hypoxia, directed blood away from nonventilated alveoli.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    RVK:
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1984
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 9
    Online Resource
    Online Resource
    American Physiological Society ; 1984
    In:  Journal of Applied Physiology Vol. 56, No. 2 ( 1984-02-01), p. 308-314
    In: Journal of Applied Physiology, American Physiological Society, Vol. 56, No. 2 ( 1984-02-01), p. 308-314
    Abstract: A special phenomenon (difficult to inflate and deflate) occurring in the postmortem guinea pig lungs was studied in 40 animals. Thirty minutes after excision of the lungs or exsanguination, less than 50% of the lungs could be inflated even at high inflation pressure (34 cmH2O), and most gas was trapped during deflation. The amount of trapped gas volume at 30 min was related to the degree of lung inflation maintained during the 5- to 30-min period after exsanguination. Since stiffness of the lung tissue was unlikely to explain the phenomenon, we speculated airway obstruction as the major factor. No foam or bubbles were found in larger airways and we thus hypothesized that the obstruction was due to bronchoconstriction. This was confirmed histologically in that the lumina of both bronchi and bronchioles were constricted. The latent period to the onset of this constriction was short (approximately 5 min). It was not associated with O2 availability but was delayed an additional 15 min by a thromboxane inhibitor (dazoxiben). Neither maintaining lung temperature at 37 degrees C nor vagotomy and/or cervical transection prevented the constriction. Without exsanguination, onset of bronchoconstriction was delayed by about 1 h. We conclude that postmortem bronchoconstriction may be caused by release of an endogenous constrictor agent.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    RVK:
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1984
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 10
    Online Resource
    Online Resource
    American Physiological Society ; 1984
    In:  Journal of Applied Physiology Vol. 57, No. 3 ( 1984-09-01), p. 692-697
    In: Journal of Applied Physiology, American Physiological Society, Vol. 57, No. 3 ( 1984-09-01), p. 692-697
    Abstract: To examine endogenous factors affecting the development of the massive bronchoconstriction in the postmortem guinea pig lung, 58 anesthetized open-chest animals were divided into three groups: 1) exsanguination only (n = 13), 2) pulmonary perfusion with 5% dextran and 1% bovine serum albumin (BSA) in Tyrode's solution (Ca2+ perfusate) (n = 21), and 3) pulmonary perfusion with 5% dextran and 1% BSA in saline (Ca2+-free perfusate) (n = 24). These groups were further divided into several subgroups according to treatments: 1) substance P depletion by chronic administration of capsaicin, 2) acute capsaicin treatment to release substance P, 3) dazoxiben treatment to block endogenous synthesis of thromboxane A2, 4) diethylcarbamazine treatment to eliminate leukotriene (LT) synthesis, and 5) FPL 55712 treatment to antagonize actions of LT. Vital capacity from the deflation pressure-volume (PV) curve of the lung was used as the indicator of bronchoconstriction. Most PV curves were performed for 30 min following exsanguination or artificial perfusion. Ca2+-free perfusate enhanced the airway spasm at 5–10 min, but the spasm disappeared gradually after 10 min. Substance P depletion significantly decreased (P less than 0.01) the bronchial constriction at 20–30 min, whereas substance P release induced severe airway spasm (P less than 0.01) during the entire study. In addition, FPL 55712 reduced the bronchospasm (P less than 0.05) in Ca2+ perfusate at 30 min. Thus Ca2+ and several endogenous mediators may be involved with the airway spasm of the postmortem guinea pig lung.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    RVK:
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1984
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
    Library Location Call Number Volume/Issue/Year Availability
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