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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of sustained hypercapnia on the acid-base balance and gill ventilation in rainbow trout, Salmo gairdneri, was studied. The response to an increase in PICO2 from 0.3 to 5.2 mm Hg was a five-fold increase in gill ventilation volume and a slight increase in breathing frequency. There was a concomitant rise in PACO2 and an immediate fall in pHa. If PICO2 was maintained at 5.2 mm Hg for several days, ventilation volume gradually returned to the initial, prehypercapnic level within three days. Arterial pH also returned to the initial level within 2-3 days. These results are consistent with the hypothesis that under these conditions fish regulate pH via HCO3/C1 exchange across the gills rather than by changes in ventilation and subsequent adjustment of PACO2. A reduction in environmental pH causes a reduction in pHa but only a slow gradual increase in VG. Injections of HC1 or NaHCO3 into the blood have opposite effects on pHa but both cause a marked increase in VG. It is concluded that a rise in PACO2 results in a rise in VG and that changes in pH in blood or water have little direct effect on VG in rainbow trout. Possible location for receptors involved in this reflex response are discussed.
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PMID:The effects of changes in pH and PCO2 in blood and water on breathing in rainbow trout, Salmo gairdneri. 0 Jul 53

To evaluate the metabolic adaptations of the brain to acute respiratory acid-base disturbances, a method was developed to measure intracellular pH (pHi) in the brain of dogs under conditions in which arterial pH is rapidly altered. Brain pHi was determined by measuring the distribution of 14C-labeled dimethadione (DMO) in brain relative to cortical CSF. Brain extracellular space (ECS) was evaluated as the 35SO4 = space relative to cortical CSF, and arterial Po2 was maintained at 82-110 mmHg. In normal dogs, brain (cerebral cortex) pHi was 7.05, and after 1 h of hypercapnia (arterial pH = 7.07) it fell to 6.93. However, after 3 h with arterial Pco2 maintained at 85 mmHg brain pHi was normal (7.06), and during this time brain bicarbonate had risen from 11.3 to 24.4 meq/kg H2O. These changes were not prevented by intravenous doses of acetazolamide,
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PMID:Intracellular pH of brain: alterations in acute respiratory acidosis and alkalosis. 0 79

Cardiac performance was assessed in 33 lambs less than 1 to 5 days of age by means of left ventricular function curves. Performance was quantified by determining stroke volume ejected at end diastolic pressure 10 cm H2O (SV10) with constant afterload. Coronary flow, myocardial O2 consumption (MVO2), blood gas tensions and pH were determined. Measurements were obtained before and at 30 min intervals following hemorrhage to 30 mm Hg arterial pressure, and in controls (arterial pressure 75 mm Hg). Effects of metabolic acidosis, hypercapnia and beta-blockade were determined. In control lambs acidosis and hypercapnia failed to reduce SV10 after two hours. In hemorrhaged animals both factors sharply reduced SV10 and lambs with prior beta-blockade showed no greater reduction. MVO2 fell following hemorrhage but did not differ with metabolic conditions and did not relate to SV10. It is concluded that beta-adrenergic function is critically important in preserving left ventricular performance in newborn exposed to acidosis or hypercapnia. With sustained hemorrhage this mechanism fails leading to a significant depression of ventricular function. MVO2 was not a determining factor in these studies.
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PMID:Cardiac function and metabolism following hemorrhage in the newborn lamb. 1 55

1. Blood O2 transport and acid-base balance were studied at 20 degrees C in rainbow trout (Salmo gairdneri) which had been kept in water of high CO2 content (15 mmHg) for at least a week. Also the blood gas chemistry of fish rapidly entering or leaving the hypercapnic environment was studied. 2. Fish entering high CO2 water suffered a sharp decrease in blood pH which significantly reduced O2 transport by the blood, but after a few hours considerable compensation was achieved. 3. After at least a week in high CO2 water, trout showed elevated plasma bicarbonate and PCO2 levels, and a decrease in plasma chloride, while pH was about 0 - 1 pH unit below the level for control fish. Oxygen transport by the blood was marginally reduced. 4. Hypercapnic fish rapidly entering fresh water showed a sharp increase in blood pH and a decrease in blood PO2. These parameters regained normal values after a few hours but plasma bicarbonate and chloride levels took much longer to regain control concentrations. 5. Acid-base balance in hypercapnic fish is discussed with particular reference to the role of the branchial ion exchanges.
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PMID:Blood respiratory properties of rainbow trout (Salmo gairdneri) kept in water of high CO2 tension. 1 48

The present studies were performed in order to determine whether "filtration edema" will develop as a consequence of cerebral vasoparalysis, vasoparalysis in combination with arterial hypertension or arterial hypertension alone. A series of dogs, anaesthetised with i.v. Chloralose-Urethane were exposed 1) to cerebral vasoparalysis, produced by hypercapnia (PaCO2 about 150 mm Hg) and hypoxaemia (PaO2 40-60 mm Hg); 2) to arterial hypertension and 3) to a combination of cerebral vasoparalysis and arterial hypertension. Following cerebral vasoparalysis and arterial hypertension, a significant decrease of total cerebrovascular resistance and moderate increase of venous resistance was observed. Regional cerebral blood flow (133Xe), intracranial pressure, as well as the pressure in postcapillary venous outflow (sinus sagittalis wedge pressure and confluence sinuum pressure) were increased. Neither normotonic vasoparalysis nor vasoparalysis in combination with slight arterial hypertension (MABP more than 90 min above 180 mm Hg) resulted in cerebral edema. In contrast, cerebral vasoparalysis in combination with severe arterial hypertension (MABP more than 90 min above 220 mm Hg) resulted in a statistically significant increase in the water content in the white matter without evidence of protein extravasation. Multiple small foci of Evans blue extravasates, however, were found in the cortex following arterial hypertension in combination with vasodilation, indicating a damage of the blood brain barrier. In these blue stained cortical areas the water content was significantly in creased. The following conclusions were drawn from the results. Vasoparalysis during normotension does not produce brain edema despite the slightly elevated hydrostatic pressure gradient between intravasal and extracellular space. Only considerable increase of this hydrostatic pressure gradient caused by a combination of vasoparalysis with severe arterial hypertension is able to produce brain edema in the white matter. In addition, acute hypertension may cause minor multifocal damage of the blood brain barrier in the cerebral cortex. It is concluded that so-called brain swelling, which has been described by several authors in states of cerebral vasoparalysis, is not predominantly caused by brain edema but by vascular congestion. The clinical aspects of the result are discussed.
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PMID:[Cerebral vasoparalysis, arterial hypertension and brain edema (author's transl)]. 5 29

The study of electrocardiogram and opercular movement records, from eels exposed for prolonged periods to hypercarbic water (saturation by the gaseous mixture 2% CO2, 98% air) shows that 1) heart rate is not significantly changed; 2) the duration of spontaneous apnea phases and the magnitude of opercular movements during ventilatory phases are increased under hypercapnic conditions. Because the integrated records of opercular movements only give an arbitrary estimate of changes in ventilation rate, direct measurements of the ventilation volume were performed in order to state the way of the dominant action of CO2. This method allows us to conclude that exogenous hypercapnia significantly decreases the ventilatory rate in eels.
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PMID:[Cardiorespiratory effects of exogenous hypercapnia in eels]. 13 81

The effects of sustained constriction of the rib cage (RCC), constriction of the abdomen (AC) and of breathing against a positive pressure of 10 cms of water (PPB) were studied in four normal subjects with moderate constant hypercapnia. Intercostal electrical activity (Eic) was measured by implanted wire electrodes and diaphragmatic electrical activity (Edia) by oesophageal electrodes. There was no fixed relation between Edia and VT. VT was unaltered during AC and RCC: Edia was unaltered during AC but increased during RCC. The response to PPB without constriction varied: three subjects increased end-expiratory VL with increase in Edia and inspiratory Eic. One subject initially, and one subject after training, maintained end-expiratory VL constant with no change in Edia and an increase in expiratory Eic. When PPB was applied during AC and RCC there was an increase in Edia proportional to end-expiratory lung volume. The overall response to distortion was determined by voluntary choice, but muscle electrical activity reflected chest wall configuration: when the diaphragm was shorter and at a mechanical disadvantage its electrical activity increased. This was compatible with a reflex with afferent information from diaphragm tendon organ and muscle spindle receptors.
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PMID:Muscle activity during chest wall restriction and positive pressure breathing in man. 36 29

Water balance is tightly regulated within a tolerance of less than 1 percent by a physiologic control system located in the hypothalamus. Body water homeostasis is achieved by balancing renal and nonrenal water losses with appropriate water intake. The major stimulus to thirst is increased osmolality of body fluids as perceived by osmoreceptors in the anteroventral hypothalamus. Hypovolemia also has an important effect on thirst which is mediated by arterial baroreceptors and by the renin-angiotensin system. Renal water loss is determined by the circulating level of the antidiuretic hormone, arginine vasopressin (AVP). AVP is synthesized in specialized neurosecretory cells located in the supraoptic and paraventricular nuclei in the hypothalamus and is transported in neurosecretory granules down elongated axons to the posterior pituitary. Depolarization of the neurosecretory neurons results in the exocytosis of the granules and the release of AVP and its carrier protein (neurophysin) into the circulation. AVP is secreted in response to a wide variety of stimuli. Change in body fluid osmolality is the most potent factor affecting AVP secretion, but hypovolemia, the renin-angiotensin system, hypoxia, hypercapnia, hyperthermia and pain also have important effects. Many drugs have been shown to stimulate the release of AVP as well. Small changes in plasma AVP concentration of from 0.5 to 4 muU per ml have major effects on urine osmolality and renal water handling.
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PMID:The clinical physiology of water metabolism. Part I: The physiologic regulation of arginine vasopressin secretion and thirst. 39 80

Most of the previous literature concerning otologic problems in compressed gas environments has emphasized middle ear barotrauma. With recent increases in commercial, military, and sport diving to deeper depths, inner ear disturbances during these exposures have been noted more frequently. Studies of inner ear physiology and pathology during diving indicate that the causes and treatment of these problems differ depending upon the phase and type of diving. Humans exposed to simulated depths of up to 305 meters without barotrauma or decompression sickness develop transient, conductive hearing losses with no audiometric evidence of cochlear dysfunction. Transient vertigo and nystagmus during diving have been noted with caloric stimulation, resulting from the unequal entry of cold water into the external auditory canals, and with asymmetric middle ear pressure equilibration during ascent and descent (alternobaric vertigo). Equilibrium disturbances noted with nitrogen narcosis, oxygen toxicity, hypercarbia, or hypoxia appear primarily related to the effects of these conditions upon the central nervous system and not to specific vestibular end-organ dysfunction. Compression of humans in helium-oxygen at depths greater than 152.4 meters results in transient symptoms of tremor, dizziness, and nausea plus decrements in postural equilibrium and psychomotor performance, the high pressure nervous syndrome. Vestibular function studies during these conditions indicate that these problems are due to central dysfunction and not to vestibular end-organ dysfunction. Persistent inner ear injuries have been noted during several phases of diving: 1) Such injuries during compression (inner ear barotrauma) have been related to round window ruptures occurring with straining, or a Valsalva's maneuver during inadequate middle ear pressure equilibration. Divers who develop cochlear and/or vestibular symptoms during shallow diving in which decompression sickness is unlikely or during compression in deeper diving, should be placed on bed rest with head elevation and avoidance of maneuvers which result in increased cerebrospinal fluid and intralabyrinthine pressure. With no improvement in symptoms after 48 hours, exploratory tympanotomy and repair of a possible labyrinthine window fistula should be considered. Recompression therapy is contraindicated in these cases...
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PMID:Diving injuries to the inner ear. 40 82

Steady-state responses to hyperoxic hypercapnia and eucapnic hypoxia were measured both as minute ventilation (VE) and as inspiratory mouth occlusion pressure (P0.1) with and without 25 cm H2O/I/s added resistance (R). Reduction in slope of the ventilatory response to CO2 with R was highly significant in all 3 subjects whereas the response to hypoxia was barely significantly reduced in 1 subject and not significantly decreased in two. Although P0.1 was higher with than without R under all conditions, the slope of the P0.1 response to CO2 with R was not increased in two subjects and only slightly increased in the third. The slope of the P0.1 response to hypoxia was significantly greater in all subjects with R. Expiratory reserve volume was increased with R but the change was the same with hypoxia and hypercapnia. We conclude that ventilation is better maintained with resistive loading during hypoxia than during hypercapnia and that this results from a greater force output of inspiratory muscles as reflected by a higher P0.1. This suggests a greater neural output to these muscles.
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PMID:Ventilatory and occlusion pressure response to CO2 and hypoxia with resistive loads. 42 14


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