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Query: UMLS:C0009443 (cold)
92,137 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of inspired CO2 on preoptic thermosensitive neurons were studied in urethanized rats. Most of the neurons changed their activities diversely while the rat breathed 4%, 7%, and 10% CO2 gas mixtures. Half of the neurons increased activity during CO2 inhalation, but activity was not necessarily intensified by elevating CO2 concentration. Thermosensitive neurons tended to increase activity more than thermally insensitive neurons. The effect of CO2 on sensitivity of thermosensitive neurons was also examined by regression of neuronal activity on preoptic temperature. The slopes of the regression lines during CO2 inhalation did not differ significantly from those during air inhalation in either warm-sensitive or cold-sensitive neurons, but CO2 did elevate the intercepts in most instances (P less than 0.01). However, if P less than 0.05 is accepted as a significance level, the slopes of the regression lines for warm-sensitive neurons tended to decrease during CO2 inhalation (9/39 pairs). The present results indicate that preoptic thermosensitive neurons generally increase their activities and modify their thermosensitivities during CO2 inhalation.
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PMID:Effects of carbon dioxide inhalation on preoptic thermosensitive neurons. 309 May 15

A simple and standardized test has been developed to measure airway responsiveness to cold dry air. This consists of stepwise increases in ventilation of dry subfreezing air at 10, 20, 40 and 60% of predicted indirect maximum breathing capacity (IMBC). For each step, the inhalation time was 3 min. The optimal time between the steps was 5 min. Exposure ceased when either a fall in forced expiratory volume in one second (FEV1) of more than 20% of baseline occurred or when there was no response after breathing cold air at 60% predicted IMBC. Moderate isocapnic hyperventilation with cold air beyond 3 min induced no further bronchoconstriction. Varying the interval (0, 2 and 5 min) between the steps produced no significant differences in test results. Changing the pattern of breathing had no effect on airway responsiveness, provided that the patient maintained a constant minute-ventilation. This implies that it is not necessary to monitor the rate and depth of respiration continuously in order to achieve a given minute-ventilation, making the technique simpler. In addition, a "CO2 requirement graph" has been constructed at different levels of ventilation. This allows the inspired CO2 concentration to be preset, eliminating the need for elaborate equipment and monitoring of end-tidal CO2 to keep the subject isocapnic during hyperventilation.
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PMID:Cold air test: a simplified standard method for airway reactivity. 309 6

The purpose of this study was to assess the relationship between the breathing pattern response to CO2 and the severity of mechanical impairment in twenty patients with COLD. The CO2 response was compared to that of a control group of twelve normal subjects. All patients had airway obstruction (FEV1 = 40 +/- 14% of predicted; means +/- SD) and hyperinflation (FRC = 154 +/- 23% of predicted). Tidal volume (VT), inspiratory and total cycle duration (TI, TT), occlusion pressure (P0.1) and endtidal PCO2 were measured at rest and during hyperoxic CO2 rebreathing. On the same day, in all patients, arterial blood gas analysis, spirometric and plethysmographic measurements were made. The slope (S) of the P0.1 response (SP 0.1) to increasing endtidal PCO2 was negatively correlated with airway resistance (r = -0.59; p less than 0.01). Although the flow response, S(VT/TI), was positively and closely correlated with SP 0.1 (r = 0.88; p less than 0.001), it also appeared to be independently influenced by obstruction (p less than 0.01). The tidal volume response, SVT, was principally correlated with inspiratory capacity (r = 0.90; p less than 0.001) and also, independently, with Vmax50 (p less than 0.01). SVT was diminished in seventeen patients, ten of whom only had a decreased S(VT/TI). The shortening in TI during hypercapnia was most marked in patients with the greatest S(P0.1), who did not have arterial hypercapnia at rest. These results suggest: that the poor VT response to CO2 in COLD patients is principally caused by a limitation in inspiratory volume expansion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of the mechanical impairment on the ventilatory response to CO2 in chronic airway obstruction. 310 31

The effects of hypoxia (10% O2) on the thermosensitivities of preoptic neurons were studied in urethanized rats and compared to the effects of hypercapnia (10% CO2). This was examined by regression of neuronal activity on preoptic temperature. During hypoxia, the slope of the regression line increased significantly in 8 (23%) of 35 warm-sensitive neurons and decreased in eight other neurons (P less than 0.05). During hypercapnia, the slope of the regression line decreased significantly in 7 (30%) of the 23 warm-sensitive neurons (P less than 0.05). No neuron was found that significantly increased the slope of the regression line. The effects of hypoxia on thermosensitivities (i.e. the slope of the regression line) of PO neurons differed from those of hypercapnia in chi-square analysis (P less than 0.05). Responses of the cold-sensitive neurons to hypoxia or hypercapnia did not generally differ from those of the warm-sensitive neurons. During hypoxia and hypercapnia, arterial blood pressure, respiratory frequency, heart rate, and EEG were recorded to examine their relations to neuronal activity. The present results indicate that the thermosensitivities of preoptic neurons are modified by both hypoxia and hypercapnia, but that hypoxic differ from hypercapnic effects.
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PMID:Effects of air constituents on thermosensitivities of preoptic neurons: hypoxia versus hypercapnia. 311 32

To investigate the effect on the pattern of breathing of cooling receptors in the nose, eight normal male volunteers underwent a steady-state CO2 stimulation by nasal inhalation. The inhaled gas temperature was randomly switched between "warm" (32 degrees C) and "cold" (2 degrees C) at each of three levels of inspired CO2 fraction (FICO2). Breathing cold air through the nose reduced the mean slope of the ventilatory response to CO2 by 27% (P less than 0.05) and the mean intercept at PCO2 of 45 Torr by 6.6 l/min (P less than 0.01). This was due mainly to a reduction in tidal volume (VT). Analysis of the breathing pattern recorded at a high level of minute ventilation (VE) (end-tidal partial pressure of CO2 approximately 52 Torr) showed a reduction of VE that was due almost entirely to a reduction in VT (P less than 0.05) associated with a reduction in inspiratory time (TI) as a fraction of total respiratory cycle time (P less than 0.05) but little change in VT/TI. In a separate experiment conducted with five subjects, there was no significant difference in inspired nasal resistance between warm and cold runs during CO2-stimulated breathing. The results confirm the previous observation that cold air breathed through the nose inhibits ventilation in normal subjects and show that this is not related to an increase in flow resistance. The reduction in ventilation is due to reduction in VT associated with shortening of the duty cycle.
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PMID:Effects of nasal cold receptors on pattern of breathing. 312 27

To test the hypothesis that the reduction of ventilatory response to CO2 during nasal breathing of cold air is due to cooling of the hypothalamus, four adult male volunteers breathed either cold air (3 degrees C) or warm air (33 degrees C) through the nose by means of a face mask. Ventilation was increased to a mean of 30 l/min by increasing inspired CO2 concentration, which was adjusted so as to match ventilation in the two conditions. Cold air through the nose reduced the ventilatory response to CO2 so that with cold, higher inspired CO2 concentrations were required to produce the same ventilation as during warm air breathing. Rectal temperature was used as a measure of "core temperature", and tympanic membrane temperature as an indirect index of brain temperature. A hand immersion water calorimeter was used to measure the peripheral vascular response to hypothalamic regulatory changes. There was no measurable change in hand heat loss, rectal, or tympanic membrane temperature. This suggests that the depressant effect of cold air breathing is mediated by skin and mucosal temperature receptors connected to the respiratory centres rather than by direct cooling of the hypothalamus.
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PMID:No evidence for hypothalamic cooling during nasal cold air breathing in man. 313 35

A good result from the heart-lung transplantation depends on the quality of the preservation of cardiopulmonary transplants. To determine the functional and pathological status of the heart-lung block after preservation for several hours, we performed 10 heterologous heart-lung transplantations in Beagle dogs (weight 13.5 kg) under extracorporeal circulation. Weight and length compatibility between donor and receiver was ensured. Measurements of hemodynamics, lung mechanics and blood gases were performed in the donor and in the receiver before the transplantation, and in the receiver after heart-lung reimplantation. Histological studies were carried out by biopsy on the heart and on the lung of the donor before removal, at the beginning of the preservation at low temperature, after 3 h of ischemia in cold, and every hour after recirculation in the heart-lung block. Myocardial preservation was conducted with cold cardioplegia at 4 degrees C (Ringer lactate solution with high potassium). Lung preservation was achieved by injecting a Euro-Collins solution at 4 degrees C, with addition of dog plasma, into the pulmonary artery; during the whole ischemic phase, the lung parenchyma was maintained at 0 degrees C, and inflated at a 10 cm H2O pressure. After transplantation, we observed that cardiac output was low in all cases, with normal or subnormal pulmonary arterial pressure. Dynamic lung compliance was very low immediately after transplantation, and increased when restarting the circulation, but deteriorated again after several hours. At the same time alveolo-arterial O2 pressure difference and arterio-alveolar CO2 pressure difference progressively increased, due to the extensive gas exchange impairment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardiorespiratory function and pathological findings in heart-lung block reimplanted after hypothermic preservation. 313 46

1. Whole-body, hind-limb and uterine tissue metabolism of glucose was studied using a combination of isotopic and arterio-venous difference techniques in shorn and unshorn pregnant sheep over the final 4 weeks of pregnancy. This was combined with the measurement of the concentrations of oxygen and carbon dioxide in arterial blood and plasma concentrations of lactate, acetate, non-esterified fatty acids, 3-hydroxybutyrate, glycerol, growth hormone (GH), insulin, glucagon, cortisol, thyroxine and 3,5,3'-triiodothyronine (T3). 2. Glucose entry rate was 28% higher in shorn ewes compared with unshorn controls, even though there was no difference in the arterial plasma concentration of glucose. This effect may have been caused by a decrease in the molar rate, insulin: glucagon (I:G), which was 40% lower in shorn ewes as a result of a significant decrease in the plasma concentration of insulin. There was no difference in the plasma concentration of cortisol or GH. 3. Blood flow across the hind-limb or uterine tissues was not significantly different between shorn and unshorn groups, neither were the net glucose uptake, glucose oxidation rate or contribution of glucose to O2 consumption across these tissues. 4. Insulin-tolerance tests performed on a separate group of shorn and unshorn ewes showed an increased sensitivity to the hypoglycaemic effects of insulin in the shorn group. 5. There was no significant difference between shorn and unshorn animals in the contribution of glucose to CO2 output or in the proportion of glucose entry rate oxidized. CO2 entry rate was 18% higher in shorn ewes compared with unshorn controls which resulted in a 26% higher estimated value for heat production. There was a 47% increase in glucose oxidation rate in shorn ewes but there was no significant difference in the proportion of total heat production which was derived from glucose. The arterial concentrations of O2 and CO2 were significantly higher in shorn ewes, which may be an indication of the higher metabolic rate in these animals. This effect may be mediated via a significant rise in plasma T3 concentration in the shorn group. 6. It is concluded that as a result of long-term cold exposure there is a significant increase in whole-body glucose entry and oxidation rates in the shorn pregnant ewe. The increase in insulin sensitivity at the same time as a decrease in plasma insulin concentration may represent a mechanism to ensure continued glucose supply to insulin-sensitive tissues while the concomitant decrease in plasma I:G stimulates hepatic gluconeogenesis.
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PMID:Glucose metabolism in shorn and unshorn pregnant sheep. 314 99

The objective of this study in 5 selected volunteer subjects was to see whether the circulatory diving response which is elicited by breath holding and by cold water on the face would affect the duration of maximal-effort breath holds. Compared to control measurements (breath holding during resting, breathing with 35 degrees C water on the face) breath holding with the face cooled by 20 degrees C water caused a 12% reduction of heart rate, 6% reduction of cardiac output, 33% reduction in [corrected] forearm blood flow, and 9% rise in mean arterial blood pressure, but there was no difference in breath-hold duration (control and experimental both 94 s). There were also no differences in time of appearance of the first involuntary respiratory efforts during breath holding, in alveolar gas exchange, or in breaking-point alveolar O2 and CO2 tensions. When the diving response was magnified by a brief bout of exercise so that there was a 19% [corrected] reduction in heart rate, 23% reduction in cardiac output, and 48% reduction in forearm blood flow, breath-hold duration was still unaffected by face cooling. Compared to intermittent immersions, continuous exposure of the face to cold water abolished the diving response, probably by a cold adaptation of facial thermal receptors. These results with cooling of the face only are consistent with our earlier finding that there was a negative correlation between the duration of a maximal-effort breath hold and the diving response during whole-body submersion in cold water.
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PMID:Breath-hold duration in man and the diving response induced by face immersion. 320 33

We examined temperature-gradient and evaporative energy losses during cold gas inhalation challenges in patients with exercise-induced asthma by using gases with similar water-carrying capacities but significantly different volume heat capacities. Seven subjects were asked to hyperventilate mixtures of 80% helium/20% oxygen (HeO2) or 80% sulfur hexafluoride/20% oxygen (SF6O2) for 5 min at a fixed target minute ventilation of 20 x FEV1 and an inspired gas temperature of 0 degrees C. Each subject equilibrated his or her lungs with the appropriate gas mixture prior to testing: PETCO2 and FIO2 were monitored and maintained at constant values (CO2 = 0.05; O2 = 0.20) by CO2 scrubbing and addition of compressed gas to the system. Gas composition, inspired and expired flow rates, and gas temperatures at the airway opening were recorded in real time using a computer-based data collection system that calculated respiratory heat loss on a per breath basis. Bronchoconstriction was quantitated using specific airway conductance measured before and serially after each challenge. The degree of bronchoconstriction correlated closely with evaporative respiratory heat loss (r = 0.658 p less than 0.05), but poorly with both temperature-gradient (r = 0.114, p greater than 0.20) and total (r = 0.268, p greater than 0.15) heat loss. These findings suggest that total respiratory heat loss is not the primary stimulus in exercise-induced asthma, and further suggest that total water loss, or focal heat/water loss, may be important in inducing bronchospasm in this subset of asthmatics.
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PMID:Dissociation of temperature-gradient and evaporative heat loss during cold gas hyperventilation in cold-induced asthma. 320 10


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