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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Seventeen (39%) of 44 patients with chest pain but without significant ST depression on treadmill exercise had their usual chest pain reproduced during or after 3 min of voluntary hyperventilation (VHV) at rest. These patients with hyperventilation positive tests had not only significantly more hyperventilation-related symptoms and respiratory complaints but also shorter breath-holding times, lower mean resting end-tidal pCO2 and higher mean respiratory rates than those with negative tests and normal controls. Of the psychological variables, only phobic avoidance scores for agoraphobia were higher in patients with positive tests. These findings suggest that in two fifths of patients with exercise tests negative for ischaemia, chest pain is associated with HV, but abnormalities of breath control and relative hypocapnia are present even in the absence of chest pain. It is possible that a chronic abnormality of respiratory control may interact with attitudinal factors in the experience of non-cardiac chest pain.
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PMID:Hyperventilation provocation in patients with chest pain and a negative treadmill exercise test. 202 44

This study was designed to examine the influence of carotid body (CB) hypocapnia on ventilation by selectively perfusing the CB through an extracorporeal circuit in 19 goats. When PcbCO2 was decreased from normocapnic levels in 14 awake goats (delta PcbCO2 = 10.9 Torr), PaCO2 increased 5.6 Torr (P less than 0.05) and VE decreased 24% (P less than 0.001) (mean values). The ventilatory sensitivity to inspired CO2 was not changed by CB hypocapnia in 5 of these goats, but the response was shifted to the right. During CB hypocapnia, ventilatory instability, including apnea, was observed in 4 of 14 goats; this irregular breathing continued at elevated levels of PaCO2. In 5 anesthetized goats, CB hypocapnia (delta PcbCO2 = 18.0 Torr) decreased VE by 70% in the intact state, but produced no significant ventilatory depression after CB denervation. We conclude that CB hypocapnia depresses ventilation in both awake and anesthetized goats mostly through CB chemoreceptor effects, and suggest that this hypoventilation may predispose to ventilatory instability in some animals.
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PMID:The effects of carotid body hypocapnia on ventilation in goats. 211 Jun 82

After voluntary hyperventilation, normal humans do not develop a significant ventilatory depression despite low arterial CO2 tension, a phenomenon attributed to activation of a brain stem mechanism referred to as the "afterdischarge." Afterdischarge is one of the factors that promote ventilatory stability. It is not known whether physiological stimuli, such as hypoxia, are able to activate the afterdischarge in humans. To test this, breath-by-breath ventilation (VI) was measured in nine young adults during and immediately after a brief period (35-51 s) of acute hypoxia (end-tidal O2 tension 55 Torr). Hypoxia was terminated by switching to 100% O2 (end-tidal O2 tension of first posthypoxic breath greater than 100 Torr). Brief hypoxia increased VI and decreased end-tidal CO2 tension. In all subjects, termination of hypoxia was followed by a gradual ventilatory decay; hyperoxic VI remained higher than the normoxic baseline for several breaths and, despite the negative chemical stimulus of hyperoxia and hypocapnia, reached a new steady state without an apparent undershoot. We conclude that brief hypoxia is able to activate the afterdischarge mechanism in conscious humans. This contrasts sharply with the ventilatory undershoot that follows relief of sustained hypoxia, thereby suggesting that sustained hypoxia inactivates the afterdischarge mechanism. The present findings are of relevance to the pathogenesis of periodic breathing in a hypoxic environment. Furthermore, brief exposure to hypoxia might be useful for evaluation of the role of afterdischarge in other disorders associated with unstable breathing.
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PMID:Hypoxic exposure and activation of the afterdischarge mechanism in conscious humans. 212 78

Autoregulation of blood flow denotes the intrinsic ability of an organ or a vascular bed to maintain a constant perfusion in the face of blood pressure changes. Alternatively, autoregulation can be defined in terms of vascular resistance changes or simply arteriolar caliber changes as blood pressure or perfusion pressure varies. While known in almost any vascular bed, autoregulation and its disturbance by disease has attracted particular attention in the cerebrovascular field. The basic mechanism of autoregulation of cerebral blood flow (CBF) is controversial. Most likely, the autoregulatory vessel caliber changes are mediated by an interplay between myogenic and metabolic mechanisms. Influence of perivascular nerves and most recently the vascular endothelium has also been the subject of intense investigation. CBF autoregulation typically operates between mean blood pressures of the order of 60 and 150 mm Hg. These limits are not entirely fixed but can be modulated by sympathetic nervous activity, the vascular renin-angiotensin system, and any factor (notably changes in arterial carbon dioxide tension) that decreases or increases CBF. Disease states of the brain may impair or abolish CBF autoregulation. Thus, autoregulation is lost in severe head injury or acute ischemic stroke, leaving surviving brain tissue unprotected against the potentially harmful effect of blood pressure changes. Likewise, autoregulation may be lost in the surroundings of a space-occupying brain lesion, be it a tumor or a hematoma. In many such disease states, autoregulation may be regained by hyperventilatory hypocapnia. Autoregulation may also be impaired in neonatal brain asphyxia and infections of the central nervous system, but appears to be intact in spreading depression and migraine, despite impairment of chemical and metabolic control of CBF. In chronic hypertension, the limits of autoregulation are shifted toward high blood pressure. Acute hypertensive encephalopathy, on the other hand, is thought to be due to autoregulatory failure at very high pressure. In long-term diabetes mellitus there may be chronic impairment of CBF autoregulation, probably due to diabetic microangiopathy.
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PMID:Cerebral autoregulation. 220 48

1. Synchronization of spontaneous sympathetic discharge during the respiratory cycle was studied in the cervical and renal nerves of vagotomized, normotensive Wistar-Kyoto rats (WKYs) and age-matched spontaneously hypertensive rats (SHRs). Phrenic nerve discharge was used as an index of central inspiratory activity. 2. In normotensive Wistar-Kyoto rats depression of sympathetic activity appeared at the onset of inspiration reaching a minimum at mid-inspiration. Peak maximal sympathetic discharge corresponded to postinspiratory phase; a second increase sometimes appeared in late expiration. Variations of respiratory frequency over wide range of experimental conditions by hypoxia, hyperoxia, hyper- or hypocapnia and transection of carotid sinus nerves did not affect this pattern. 3. In SHRs the respiratory-phase-related timing of sympathetic discharge was variable. In normoxia, the maximal sympathetic activity occurred in late inspiration, preceded by short depression at early inspiration and followed by postinspiratory depression. A second increase in sympathetic activity was observed in mid-expiration. 4. The pattern of respiratory phase modulated sympathetic activity in SHRs was altered by hypoxic stimulation of the peripheral chemoreceptors. The early inspiratory depression of sympathetic activity was substantially prolonged and the maximal sympathetic discharge was shifted from inspiration to early expiration. This effect was abolished after carotid sinus nerves had been cut. 5. Hypercapnic stimulation of central chemoreceptors in SHRs with carotid sinus nerves cut did not influence the timing of the sympathetic activity in relation to the respiratory phase, though the magnitude of rhythmical sympathetic discharges was increased. 6. We discuss the possibility that altered synchronization between central respiratory drive and sympathetic neuronal system may contribute to the neurogenic mechanisms of arterial hypertension in SHRs.
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PMID:Respiratory-related discharge pattern of sympathetic nerve activity in the spontaneously hypertensive rat. 223 3

Apnea and desaturation following nitrous oxide inhalation were studied in seven adult volunteers breathing spontaneously. Arterial oxygen saturation (SpO2), end-tidal CO2 concentration in the nasal cavity and respiratory patterns were measured in volunteers breathing air after N2O (50% or 67%) + O2. SpO2 was measured with Biox 3700 and end-tidal CO2 concentration was measured with Normocap, and respiratory patterns were recorded with RESPIGRAPH. After breathing N2O, two volunteers had frequent apnea (greater than 20 sec) accompanied by desaturation (SpO2 less than 90%). The lowest value of SpO2 was 82%. When the apnea occurred, the airway seemed to be open and end-tidal CO2 concentration values were lower than those before N2O inhalation. The authors considered that this kind of apnea was due to several factors, such as hypocapnia caused by hyperventilation during N2O anesthesia, dilution of alveolar O2 and CO2 during N2O excretion, loss of consciousness by N2O, and depression of CO2 ventilatory response by N2O. Inhalation of O2 at high concentrations for five minutes could improve the hypocapnia and prevent the apnea.
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PMID:[Apnea and oxygen desaturation following nitrous oxide inhalation]. 223 28

The effects of mild hypocapnia (PaCO2 22 mm Hg) and hypercapnia (PaCO2 59 mm Hg) on the splanchnic circulation and hepatic function were studied in six pentobarbital anesthetized, laparotomized, mechanically ventilated beagles. Tidal volume and respiratory frequency were held constant throughout the measurements. Hepatic artery blood flow (HABF) and portal vein blood flow (PVBF) were measured by electromagnetic flowmeters. Hepatic function was assessed by indocyanine green (ICG) elimination kinetic analysis after intravenous injection of the dye. Hypocapnia caused a decrease in HABF without affecting the systemic circulation. Hypercapnia, on the other hand, caused a significant increase in cardiac output without changing mean arterial pressure. There was a significant increase in PVBF and total hepatic blood flow (THBF = PVBF + HABF). Despite the increases in PVBF and THBF, the half-life of ICG was significantly longer during hypercapnia (9.09 +/- 0.79 min) than during hypocapnia (7.16 +/- 0.37 min), and plasma ICG clearance was smaller during hypercapnia (4.79 +/- 0.44 ml.min-1) than during hypocapnia (5.44 +/- 0.33 ml.min-1) or normocapnia (5.27 +/- 0.50 ml.min-1), indicating the depressed hepatic function during hypercapnia. We conclude that mild hypocapnia decreases HABF without affecting hepatic function and that mild hypercapnia is associated with a depression of hepatic function in spite of the increases in PVBF and THBF.
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PMID:Effects of hypocapnia and hypercapnia on splanchnic circulation and hepatic function in the beagle. 250 78

High-frequency jet ventilation (HFJV) is used in respiratory distress syndrome (RDS) to avoid high airway pressures and barotrauma. This study was designed to find rational strategies to regulate oxygenation and alveolar ventilation at HFJV and to determine appropriate monitoring methods. Seven dogs were subjected to total lung lavage with saline to induce RDS. PEEP was increased at conventional intermittent positive-pressure ventilation until re-expansion was indicated by a PaO2 of 300 torr at an FIO2 of 1.0 HFJV at 4 and 15 Hz was each tried at 0 and 10 cm H2O PEEP. Intermittent low-frequency inflations were also added to HFJV at 0 PEEP. Lung expansion was maintained without circulatory depression by adjustment of minute ventilation (VE) delivered by the HFJ ventilator; external PEEP was a useful complement. PaCO2 was controlled by frequency adjustment. HFJV at 4 Hz resulted in hypocapnia; intermittent low-frequency inflations had no effect. VE monitoring, CO2 elimination monitoring, and PEEP adjustment was done with a standard ventilator during HFJV. This study illustrates that HFJV is efficient in RDS; VE and external PEEP strongly influence oxygenation and may be used to regulate this factor, and frequency affects CO2 elimination, thus suggesting a method of PaCO2 control.
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PMID:Setting and monitoring of high-frequency jet ventilation in severe respiratory distress syndrome. 267 44

In pentobarbitalized rats, hypoxia induced by inhalation of O2 8%-N2 92%, produces a transient hyperventilation which is followed by a respiratory depression and an apnea. A cardiovascular collapse is then observed. Correction of the hypocapnia depending on the initial hyperventilation, by inhalation of a gas mixture containing 4% CO2 maintains the hyperventilation and suppresses the cardiovascular collapse. Carbon dioxide activity is both a direct one by stimulation of respiratory centers and an indirect one by increasing the sensitivity of the peripheral arterial chemoreceptors to hypoxia. Four percent carbon dioxide just compensating hypocapnia are sufficient to prevent apnea and vascular collapse. The increase of this concentration up to hypercapnia complicates the interpretation of the results by addition of hypoxic and hypercapnic effects.
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PMID:[Effects of the addition of carbon dioxide on manifestations of acute hypoxia in rats]. 297 Feb 83

The end tidal partial pressure of carbon dioxide (PCO2) was measured during treadmill exercise in 30 normal controls and 113 patients referred for assessment of chest pain. Among the 92 patients without significant ST depression hypocapnia occurred more often in those reporting "typical" than "atypical" chest pain (17 of 22 patients compared with 29 of 70; p less than 0.01). Hypocapnia was uncommon in patients with significant ST depression whether reporting typical or atypical chest pain (one of 10 patients and two of 11, respectively). Hypocapnia at rest (PCO2 less than 4 kPa) occurred in 16 (14%) patients but in only one control. Hypocapnia occurred during or after exercise in only one control and three of the 21 patients with significant ST depression on exercise (group 1). The remaining 92 patients were divided into those with a history suggestive of hyperventilation (group 2; n = 30) and those without (group 3; n = 62). Hypocapnia developed significantly more often in both these groups (21 and 25 patients respectively) than in controls or patients with significant ST depression. An abnormal response of the PCO2 to exercise provided objective data to support a clinical suspicion of chest pain induced by hyperventilation in 24 cases, suggested a cause for equivocal ST depression other than coronary stenosis in five patients, and led to the diagnosis of previously unsuspected respiratory disease in 14 patients. Measurement of end tidal PCO2 gives additional valuable diagnostic information during the conventional treadmill exercise test in patients with both typical and atypical chest pain.
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PMID:Value of measuring end tidal partial pressure of carbon dioxide as an adjunct to treadmill exercise testing. 313 51


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