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

Prolonged normoxic hypercapnia initially caused an increase in canine cerebral blood flow, as measured by the radioactive microsphere technique, accompanied by a decrease in cerebrovascular resistance. These effects persisted for 3 hours. An adaptive decrease in cerebral blood flow and increase in cerebrovascular resistance were seen when hypercapnia was maintained for an additional 3 hours. Regional variations occurred; those areas with the greatest initial hypercapnic blood flow (cortex, caudate nucleus) showed a greater rate of decay of flow over time. Cerebrospinal fluid pH, initially acidotic during hypercapnia, increased over the subsequent 5 hours from 6.99 +/- 0.02 to 7.13 +/- 0.02. This was accompanied by an increase in the cerebrospinal fluid bicarbonate ion concentration from a normocapnic baseline of 19.6 +/- 0.6 to 26.2 +/- 4 mEq/l. Total and regional cerebral blood flow were linearly related to cerebrospinal fluid pH (R2 = 0.97). Extrapolation of a full adaptive return of flow to baseline indicated a shift in the cerebrovascular sensitivity to extracellular hydrogen ion concentration during prolonged hypercapnia.
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PMID:Time-dependent effects of prolonged hypercapnia on cerebrovascular parameters in dogs: acid-base chemistry. 381 Jul 47

The purpose of this investigation was to examine the effects of norepinephrine cardiomyopathy (NE-CM) on left ventricular (LV) performance in diabetic rabbits. Diabetes mellitus was produced in 11 rabbits by giving them alloxan monohydrate, 120 mg/kg. Cardiomyopathy was produced in five animals by a 90-min infusion of norepinephrine (2 micrograms/min/kg). Left ventricular contractility and pump function (VF) were examined 2 days later. The effects of hypercapnia and inotropic responsiveness to NE were also determined. VF was assessed by means of left ventricular function curves obtained with constant mean aortic pressure and heart rate and quantified by determining stroke volume (SV) at a left ventricular pressure of 10 cm H2O (SV10). Mean SV10 was 1.22 +/- 0.08 ml in control diabetics but averaged only 0.95 +/- 0.08 ml in diabetics with NE-CM (P less than 0.05). NE-CM markedly reduced LV dP/dt max responses to NE infusion but the increments in SV10 did not differ. Hypercapnia caused significantly greater ventricular depression in NE-CM than in control diabetic rabbits (P less than 0.001). The depressive effect of hypercapnia can be countered in part by the administration of NE in both groups, but differential depression in VF to hypercapnia was persistent between the two groups.
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PMID:Ventricular performance in diabetic rabbits with norepinephrine cardiomyopathy. 394 45

Acute occlusion of one common carotid artery in the anesthetized normocapnic rat results in a moderate cerebral blood flow (CBF) decrease in both cerebral hemispheres. No asymmetrical perfusion is observed when the overall flow in each hemisphere is considered. The increase in blood flow which normally occurs in hypercapnia is strongly impaired in the cerebral hemisphere on the occluded side resulting in an important asymmetrical hemispheric perfusion. The days (1, 5, 15, 30) following unilateral carotid occlusion normal control CBF values are found in both hemispheres in normocapnic conditions. Hemispheric perfusion asymmetry in hypercapnia also becomes progressively less pronounced with time but a slight asymmetry still persists one month after unilateral carotid occlusion.
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PMID:Hemispheric blood flow in the rat after unilateral common carotid occlusion: evolution with time. 396 69

The lumen diameters of the main cortical surface arteries were continuously monitored through a closed cranial window in spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto rats (WKY). The arterial diameter was significantly smaller in SHR (55 +/- 1 micron) than in WKY (87 +/- 1 micron) during resting conditions as well as during hypercapnic dilatation (87 +/- 2 micron compared to 117 +/- 5 micron). The per cent increase in diameter induced by hypercapnia was larger in SHR (54%) than in WKY (36%), presumably a consequence of the altered vascular wall to lumen ratio. Alpha-adrenoreceptor blockade with yohimbine and phenoxybenzamine had no significant effect on arterial diameter during hypercapnia. The diameters of the largest pial surface veins increased to the same extent in SHR and WKY during hypercapnia (about 10%).
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PMID:Reaction of pial arteries and veins to hypercapnia in hypertensive and normotensive rats. 397 71

One hundred twenty-four patients had 155 carotid endarterectomies for the relief of stroke symptoms. General hypercarbia anesthesia and arterial pco2 monitoring were used, without resort to internal bypass shunt or hypothermia. Significant permanent post-operative complications developed in three patients (1.9 percent) and there were two postoperative deaths, one of which was caused by a massive myocardial infarction.
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PMID:A safe approach to carotid endarterectomy. 513 26

It has been proposed that sympathetic activation may prevent maximum dilatation of extra-parenchymal cerebral vessels during hemorrhagic hypotension and hypercapnia. In the present study, the effect of alpha-adrenoreceptor antagonists (phenoxybenzamine 1.5 mg kg-1 or phentolamine 8 mg kg-1) on pial vessel diameter was studied in the cat during hypotension and hypercapnia alone or in combination. Two levels of hypercapnia were used (mean PaCO2 74 and 122 mm Hg respectively). Pial arterial vessels (resting diameter 40--184 micrometers) were observed by means of a closed cranial window technique using a Leitz intravital microscope, an image splitting eyepiece, and a videoangiometer, the latter giving continuous data on changes of the inspected vessel diameters. Alpha-adrenoreceptor antagonists did not further increase the arterial diameter in any of the situations studied.
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PMID:Alpha-adrenoreceptor antagonists and pial vessel diameter during hypercapnia and hemorrhagic hypotension in the cat. 611 57

1. Almitrine, an agonist of peripheral chemoreceptors, has been shown to be effective in lowering PaCO2 in patients with chronic obstructive lung disease. The aim of this investigation was to evaluate the pulmonary haemodynamic response to almitrine in clinically stable patients with chronic airflow obstruction and chronic hypercapnia (PaCO2 7.1 +/- 0.5 kPa, mean +/- SD). 2. Seven men, aged from 55 to 64 years, had the following values for pulmonary function (means +/- SD): FEV1.0 0.67 +/- 0.16 litre; VC 2.12 +/- 0.52 litres; FEV1.0/VC 33 +/- 8%. They had haemodynamic monitoring during 1 h of almitrine (1 mg/kg intravenously) and solvent (placebo) in a random fashion while receiving 28% oxygen. Before infusion, six patients had evidence of pulmonary hypertension and the mean pulmonary artery pressure (PAP) for all seven patients was 4.3 +/- 1.6 kPa (mean +/- SD); the pulmonary vascular resistance (PVR) was 0.61 +/- 0.22 kPa 1(-1)s (mean +/- SD). 3. There were no significant changes from baseline values during placebo. During almitrine, however, the PAP and right ventricular stroke work (mean +/- SD) increased significantly at 30 min (6.0 +/- 2.1 kPa, P less than 0.001, 0.38 +/- 0.12 J, P less than 0.05, respectively) with maximum increase of PVR at 45 min (1.01 +/- 0.34 kPa 1(-1)s, P less than 0.001, mean +/- SD). The lowest PaCO2 (mean +/- SD) was observed at the end of the infusion (5.7 +/- 0.5 kPa, P less than 0.001). 4. These results confirm the benefit of almitrine in lowering PaCO2 in patients with chronic airflow obstruction who have chronic hypercapnia but also demonstrate significant pulmonary vasoconstriction.
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PMID:The pulmonary haemodynamic effects of almitrine infusion in men with chronic hypercapnia. 612 33

In a previous report, the authors demonstrated the effectiveness of mild hypercapnia in enhancing decreased perfusion flow in ischemic, non-infarcted brain tissues. However, the previous work lacked in verification of improvement of suppressed brain function. Therefore, this report was attempted to evaluate the effect of hypercapnia on somatosensory evoked potential (SEP), using the similar ischemic model as previously. The results showed that mild hypercapnia of 43 to 55 mm Hg range was beneficial not only for enhancing decreased perfusion flow but also for restoring suppressed SEP. This report seems to be the first publication which verifies a presence of correlation between local cortical blood flow (LCBF) and SEP under mild hypercapnia in mildly to moderately ischemic brain tissues.
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PMID:Effects of mild hypercapnia on somatosensory evoked potentials in experimental cerebral ischemia. 642 87

The relative effect of the temperature on respiratory rhythm generation was studied in muscle-relaxed, artificially ventilated and bilaterally vagotomized rabbits under general anaesthesia (urethane and chloralose). Hypercapnia was produced during normothermia (38.8 +/- 0.6 degrees C) and hyperthermia (40.5 +/- 0.3 degrees C). The basic physiological parameters, efferent phrenic nerve activity and gasometric determinations in arterial blood were recorded. In the animals ventilated with a classic respirator hyperthermia produced a 118% increase of Veq value with a simultaneous 28% rise of the partial pressure of CO2. An increase of the stroke volume of the respirator during hyperthermia (in a degree sufficient for achieving PaCO2 value equal to the control value during normothermia) produced a 2% fall of Veq value due to an 8% fall in amplitude of the respiratory movements without changes of respiratory rate. Breathing in of a hypercapnic mixture caused a 131% rise of Veq above the control value in normothermia. This rise was due both to the increased respiratory rate and respiratory amplitude. During ventilation by means of a respirator controlled by phrenic nerve activity hyperthermia increased the electrophysiological equivalent of minute ventilation by 34%, with a 109% rise in the respiratory rate and with no change in PaCO2. Breathing of a hypercapnic mixture increased Veq without inducing any statistically significant changes in the respiratory rate and amplitude. The analysis of the results suggests that the effect of raised temperature on respiratory rhythm generation is manifested mainly as an impairment of the respiratory amplitude. Maintaining of minute ventilation proportional to the magnitude of respiratory drive is decisive in this phenomenon.
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PMID:Changes of minute ventilation in rabbits in experimental hyperthermia. 644 72

The effect of profound hypercapnia on acute hypoxic respiratory failure is evaluated. Eight dogs were subjected to oleic acid-induced acute respiratory failure. Four dogs were ventilated normally, and four dogs were made hypercapneic by rebreathing exhaled CO2. In the hypercapneic animals, heart rate and alveolar-arterial oxygen difference were significantly lower than in normocapneic animals, while mixed venous O2 cardiac index, oxygen delivery index, stroke volume index, and left ventricular stroke work were significantly higher. Mean arterial pressure was maintained at preinjury levels. Pulmonary and systemic vascular resistance increased in both experimental groups. There was no significant difference between groups for gravimetric determination of lung water. Cardiopulmonary performance in acute respiratory failure is improved with hypercapnia. This may be related to CO2-induced catecholamine release.
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PMID:The hemodynamic effect of profound hypercapnia on acute hypoxic respiratory failure. 665 77


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