ACUTE ESERINE POISONING IN THE MONKEY

1954 ◽  
Vol 32 (4) ◽  
pp. 446-451
Author(s):  
C. A. de Candole
Keyword(s):  
Intravenous Injection ◽  
Pulmonary Ventilation ◽  
Minute Volume ◽  
Before And After ◽  
Sublethal Doses ◽  
Respiratory Mechanism

The changes in pulmonary ventilation which follow the intravenous injection of lethal and sublethal doses of eserine in the urethanized monkey have been studied. A reduction in minute volume is the outstanding change; but periods of overventilation may occur both before and after the phase of underventilation.When death takes place within ten minutes respiration fails before the heart, whereas when death is delayed, both fail together.Different elements of the respiratory mechanism differ in their susceptibility to eserine. Thus diaphragmatic and intercostal function are rarely lost together, and gasping may continue for long periods after eupnoeic breathing has failed.

ACUTE ESERINE POISONING IN THE MONKEY

1954 ◽  
Vol 32 (1) ◽  
pp. 446-451
Author(s):  
C. A. de Candole
Keyword(s):  
Intravenous Injection ◽  
Pulmonary Ventilation ◽  
Minute Volume ◽  
Before And After ◽  
Sublethal Doses ◽  
Respiratory Mechanism

The changes in pulmonary ventilation which follow the intravenous injection of lethal and sublethal doses of eserine in the urethanized monkey have been studied. A reduction in minute volume is the outstanding change; but periods of overventilation may occur both before and after the phase of underventilation.When death takes place within ten minutes respiration fails before the heart, whereas when death is delayed, both fail together.Different elements of the respiratory mechanism differ in their susceptibility to eserine. Thus diaphragmatic and intercostal function are rarely lost together, and gasping may continue for long periods after eupnoeic breathing has failed.

Breathing in brief exercise

1960 ◽  
Vol 15 (4) ◽  
pp. 583-588 ◽  
Author(s):  
F. N. Craig ◽  
E. G. Cummings
Keyword(s):  
Carbon Dioxide ◽  
Oxygen Uptake ◽  
Respiratory Exchange Ratio ◽  
Metabolic Cost ◽  
Carbon Dioxide Tension ◽  
Minute Volume ◽  
Carbon Dioxide Output ◽  
Respiratory Minute Volume ◽  
Before And After

Two men ran for 20 or 60 seconds while inhaling air, oxygen or 4% carbon dioxide. Inspired respiratory minute volume was determined for each breath. Ventilation increased suddenly in the first breath with minimal changes in end-expiratory carbon dioxide tension and respiratory exchange ratio to a rate that remained constant for 20 seconds before increasing further. The rate of carbon dioxide output was uniform during the first 20 seconds. A 12% grade did not increase ventilation or oxygen uptake during runs of 20 seconds, but in the first minute of recovery, ventilation was 64% greater than after level runs. Inhalation of oxygen inhibited ventilation by 24% in the 20-second periods before and after the end of a 60-second run. Inhalation of carbon dioxide begun at rest produced increments in ventilation and end-expiratory carbon dioxide tension that varied little during running and recovery. In the 20-second runs ventilation varied with speed but appeared independent of ultimate metabolic cost. Submitted on January 21, 1960

Albumin synthesis in humans increases immediately following the administration of endotoxin

2002 ◽  
Vol 103 (5) ◽  
pp. 525-531 ◽  
Author(s):  
Hans BARLE ◽  
Anna JANUSZKIEWICZ ◽  
Lars HÅLLSTRÖM ◽  
Pia ESSÉN ◽  
Margaret A. MCNURLAN ◽  
...  
Keyword(s):  
Intravenous Injection ◽  
Early Phase ◽  
The Other ◽  
Synthesis Rate ◽  
Control Group ◽  
Albumin Synthesis ◽  
Fractional Synthesis Rate ◽  
Before And After ◽  
Fractional Synthesis ◽  
Absolute Synthesis

In order to investigate the immediate (i.e. within 3h) response of albumin synthesis to the administration of endotoxin, as a model of a moderate and well controlled catabolic insult, two measurements employing L-[2H5]phenylalanine were performed in 16 volunteers. One group (n = 8) received an intravenous injection of endotoxin (4ng/kg; lot EC-6) immediately after the first measurement of albumin synthesis, whereas the other group received saline. A second measurement was initiated 1h later. In the endotoxin group, the fractional synthesis rate of albumin was 6.9±0.6%/day (mean±S.D.) in the first measurement. In the second measurement, a significant increase was observed (9.6±1.2%/day; P<0.001). The corresponding values in the control group were were 6.6±0.6%/day and 7.0±0.6%/day respectively (not significant compared with first measurement and P<0.001 compared with the second measurement in the endotoxin group). The absolute synthesis rates of albumin were 148±35 and 201±49mg·kg-1·day-1 before and after endotoxin (P<0.01). In the control group, the corresponding values were 131±21 and 132±20mg·kg-1·day-1 (not significant compared with the first measurement and P<0.01 compared with the second measurement in the endotoxin group). In conclusion, these results indicate that albumin synthesis increases in the very early phase after a catabolic insult, as represented by the administration of endotoxin.

Oxygen consumption and ventilation of dogs during passive and active exercise

1977 ◽  
Vol 42 (6) ◽  
pp. 923-927 ◽  
Author(s):  
A. K. Russo ◽  
J. Tarasantchi ◽  
M. A. Griggio
Keyword(s):  
Minute Volume ◽  
O2 Consumption ◽  
Experimental Conditions ◽  
Pentobarbital Sodium ◽  
Passive Exercise ◽  
Respiratory Parameters ◽  
Ventilatory Equivalent ◽  
Before And After ◽  
Proportional Increase ◽  
Passive Muscle

A comparison was made between the influence of passive and active exercise on the energy metabolism (EM) and respiratory parameters (RP) of dogs: respiratory minute volume and ventilatory equivalent for O2. Passive exercise was performed in 24 dogs, anesthetized with pentobarbital sodium and morphine or ketamine hydrochloride and pentobarbital sodium, by moving the four limbs at constant frequencies of 25, 45, or 80 movements/min before and after curarization. Active exercise was induced in 35 animals by electric stimulation of the quadriceps and triceps muscles or of the distal ends of femoral and radial nerves at the same frequencies previously indicated. Values obtained for EM and RP during passive exercise were not significantly different from those obtained during resting conditions; active exercise caused a significant increase which was directly proportional to the frequencies of limb movement. Our results indicate that passive muscle movement induces no alteration in O2 consumption and the possible relfexes generated in these experimental conditions were not apparently important on ventilatory control. In active movements, over the range of the frequencies studied, there is a proportional increase in O2 consumption followed by a corresponding increase in ventilation.

Hypothalamus and respiratory minute volume

1960 ◽  
Vol 198 (6) ◽  
pp. 1304-1306 ◽  
Author(s):  
Edward S. Redgate
Keyword(s):  
Blood Pressure ◽  
High Frequency ◽  
Muscle Tone ◽  
Minute Volume ◽  
Reflex Pathways ◽  
Before And After ◽  
Significant Depression ◽  
Volume Decrease ◽  
Frequency Current ◽  
Respiratory Reflex

Minute volume of respiration was measured in 21 cats. Hypodermic tubing and electrodes were implanted in the hypothalamus. Minute volume of respiration was measured before and after depression of the hypothalamus by coagulation with high frequency current or by microinjection of 4% thiopental into sites in the hypothalamus. Depression of the hypothalamus was followed by a 20–30% decrease in minute volume. The results were statistically significant. Depression of the thalamus by coagulation or microinjection of thiopental was not followed by a significant change in minute volume. Intravenous injection of the amount of thiopental injected into the hypothalamus did not alter minute volume. Minute volume decrease was often associated with blood pressure and muscle tone decreases, but in several cases, minute volume decreases were independent of blood pressure and muscle tone. The evidence supports the argument that tonic discharges from the hypothalamus increase the excitability of respiratory reflex pathways and effect increased minute volume.

Failure of tracheal distension to inhibit breathing in anesthetized dogs

1980 ◽  
Vol 48 (5) ◽  
pp. 794-798 ◽  
Author(s):  
T. C. Lloyd ◽  
J. A. Cooper
Keyword(s):  
Tidal Volume ◽  
Lung Volume ◽  
Potential Role ◽  
Minute Volume ◽  
Abdominal Compression ◽  
Frequency Increase ◽  
Before And After ◽  
Anesthetized Dogs ◽  
Spontaneously Breathing

Using anesthetized spontaneously breathing dogs, we compared the respiratory effects of tracheal distension with the effects of changes in lung volume before and after vagotomy. We used an endotracheal tube with a long cuff to distend the trachea to pressures of 10, 20, and 40 cmH2O. Lung volume increases were imposed by expiratory threshold loading, and volume was decreased by abdominal compression, both of which caused outward rib cage displacement. During expiratory loading, the tidal volume was unchanged but respiratory frequency and minute volume fell and an active expiratory effort appeared; whereas frequency and minute volume rose, but tidal volume fell during abdominal compression. Tracheal distension evoked no discernible change in breathing. Following vagotomy, tidal volume and minute volume fell, and frequency rose slightly, during expiratory loading but abdominal compression was without effect. After vagotomy, 40 cmH2O tracheal distension caused a slight frequency increase. We concluded that the potential role of tracheal deformation in the reflex control of breathing is insignificant in comparison with the other airways.

Pelvic visceral input into the nucleus gracilis is largely mediated by the postsynaptic dorsal column pathway

1996 ◽  
Vol 76 (4) ◽  
pp. 2675-2690 ◽  
Author(s):  
E. D. Al-Chaer ◽  
N. B. Lawand ◽  
K. N. Westlund ◽  
W. D. Willis
Keyword(s):  
Intravenous Injection ◽  
Visceral Pain ◽  
Background Activity ◽  
Dorsal Column ◽  
Mustard Oil ◽  
Medial Lemniscus ◽  
Afferent Pathways ◽  
Nucleus Gracilis ◽  
Before And After ◽  
Postsynaptic Dorsal Column

1. The purpose of this study was to investigate a proposed role for the postsynaptic dorsal column (PSDC) pathway in mediating visceral nociceptive input into the dorsal column (DC) nuclei. 2. In one group of animals, the hypogastric nerves were sectioned, thereby restricting colorectal input into the cord to pelvic afferent pathways known to coverage on lower lumbar and sacral segments. Extracellular recording were made from 41 nucleus gracilis (NG) cells that responded to colorectal distension (CRD). Results reported are from 15 NG cells that were tested before and after the administration of morphine into the sacral cord by microdialysis. 3. The responses of 11 NG cells to CRD were dramatically reduced by morphine infused into the sacral cord through a microdialysis fiber. This reduction was reversed by an intravenous injection of naloxone. Microdialysis administration of 6-cyano-7-nitro-quinoxaline-2,3-dione (CNQX) or a lesion of the DC also abolished the responses of the NG cells to CRD. 4. Four NG cells that responded to CRD showed an increase in their background activity approximately 25 min after an injection of mustard oil (MO). This increase in activity was counteracted by morphine or by a lesion of the DC. 5. In a second group of animals, recordings were made from 28 PSDC cells in the L0-S1 segments of the cord. These units were antidromically activated by stimulation of the upper cervical fasciculus gracilis. The projections of five PSDC neurons into the NG were traced with the use of antidromic mapping. Results are reported for the responses of 12 PSDC cells to CRD and to cutaneous stimuli before and after morphine administration into the sacral cord by microdialysis. 6. Morphine given spinally reduced the responses of 12 PSDC cells to CRD. This reduction was reversed by an intravenous injection of naloxone. CNQX administered spinally also abolished the responses to CRD of the PSDC cells tested. 7. Four other PSDC cells were studied before and after an injection of MO into the colon. Their background activity started to increase within 25 min after the injection. Morphine suppressed this increase in background activity and this effect of morphine was reversed by naloxone. 8. The responses of NG cells to cutaneous stimuli were not significantly affected by morphine in the dose used. On the other hand, morphine significantly reduced the responses of PSDC cells to noxious cutaneous stimuli although this effect was not as dramatic as that on responses to visceral stimuli. 9. From the results of the studies described in this and the companion paper, we conclude that there is an important pelvic visceral nociceptive pathway involving PSDC neurons that synapse in the NG. The NG in turn activates neurons in the ventral posterolateral (VPL) nucleus of the thalamus. We presume that activation of VPL neurons by noxious visceral stimulation contributes to visceral pain sensation and thus that pelvic visceral pain depends largely on activity in the DC-medial lemniscus system.

scholarly journals Role of nitric oxide in systemic vasopressin-induced hypothermia

1998 ◽  
Vol 275 (4) ◽  
pp. R937-R941 ◽  
Author(s):  
Alexandre A. Steiner ◽  
Evelin C. Carnio ◽  
José Antunes-Rodrigues ◽  
Luiz G. S. Branco
Keyword(s):  
Nitric Oxide ◽  
Intravenous Injection ◽  
Induced Hypothermia ◽  
Basal Body Temperature ◽  
Systemic Injection ◽  
The Third ◽  
Before And After ◽  
Injection Control ◽  
Synthase Inhibitor

It has been reported that arginine vasopressin (AVP) plays a thermoregulatory action, but very little is known about the mechanisms involved. In the present study, we tested the hypothesis that nitric oxide (NO) plays a role in systemic AVP-induced hypothermia. Rectal temperature was measured before and after AVP, AVP blocker, or N G-nitro-l-arginine methyl ester (l-NAME; NO synthase inhibitor) injection. Control animals received saline injections of the same volume. The basal body temperature (Tb) measured in control animals was 36.53 ± 0.08°C. We observed a significant ( P < 0.05) reduction in Tb to 35.44 ± 0.19°C after intravenous injection of AVP (2 μg/kg) and to 35.74 ± 0.10°C after intravenous injection ofl-NAME (30 mg/kg). The systemic injection of the AVP blocker [β-mercapto-β,β-cyclopentamethylenepropionyl1, O-Et-Tyr2,Val4,Arg8]vasopressin (10 μg/kg) caused a significant increase in Tb to 37.33 ± 0.23°C, indicating that AVP plays a tonic role by reducing Tb. When the treatments with AVP and l-NAME were combined, systemically injected l-NAME blunted AVP-induced hypothermia. To assess the role of central thermoregulatory mechanisms, a smaller dose ofl-NAME (1 mg/kg) was injected into the third cerebral ventricle. Intracerebroventricular injection ofl-NAME caused an increase in Tb, but when intracerebroventricular l-NAME was combined with systemic AVP injection (2 μg/kg), no change in Tb was observed. The data indicate that central NO plays a major role mediating systemic AVP-induced hypothermia.

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