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

The ventilatory control system was evaluated in a group of 40 diabetic patients (20 with autonomic neuropathy (AN), and 20 without autonomic neuropathy) and 20 controls. The ventilatory increase in response to transient hypoxia was less in diabetics without AN than in controls, but even weaker in diabetics with AN. This pattern was repeated in the ventilatory response to hypercapnia. There was no correlation between the presence of abnormal respiratory responses and the duration of diabetes.
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PMID:Ventilatory control in diabetes mellitus. 405 61

An unusual patient with hypoxemia, hypercapnia, and right ventricular failure is presented. Minimal skeletal muscle weakness, although present, cannot explain hypercapnia. Muscle biopsy revealed diabetic microangiopathy. Carbon dioxide stimulation demonstrated a diminished hypercapnic ventilatory response. The patient benefited from progesterone therapy. In this unusual patient, mild muscular weakness, caused by diabetes, and central alveolar hypoventilation have acted in synergism to cause abnormal ventilation and right ventricular failure.
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PMID:Right ventricular failure in a patient with diabetic neuropathy (myopathy) and central alveolar hypoventilation. 664 56

To investigate one suggested cause of unexplained deaths of diabetic patients with autonomic neuropathy, ventilatory responses to progressive hypoxemia and to progressive hypercarbia were compared among two groups of diabetic patients, with and without autonomic neuropathy, and a group of normal control subjects. Hypoxemia was induced gradually under isocapnic conditions and the arterial oxygen saturation was reduced to below 75%. In a separate test the end tidal CO2 was increased gradually to 55 mm Hg in subjects who could tolerate this degree of hypercarbia. The ventilatory responses to hypoxemia and to hypercarbia did not differ among groups nor did age, duration of diabetes, or presence of proliferative retinopathy and nephropathy have a significant effect on the ventilatory responses of diabetics. The authors conclude that defective ventilatory responses to hypoxemia or hypercarbia are not associated with the sudden unexplained deaths in diabetics with autonomic neuropathy.
Diabetes 1982 Jul
PMID:Autonomic neuropathy and the ventilatory responses of diabetics to progressive hypoxemia and hypercarbia. 716 May 39

Thick, 0.34 mm, 38% water hydrogel lenses were fitted, under a pressure patch, to one eye of 18 type I diabetic patients (aged 18-40 years) to assess the acute response to hypoxia and hypercapnia; the response was compared with that in 18 healthy, aged-matched non-diabetic subjects; the closed-eye lens wear was started mid-morning. Pre-lens wear assessments were made of acuity, intraocular pressure (IOP), central corneal thickness (CCT) and corneal appearance by biomicroscopy. The mean duration of the diabetes was 13 +/- 7 years and the average fasting blood glucose was 8.7 +/- 3.3 mMl-1. Baseline CCT values were marginally greater in diabetic patients (600 +/- 33 microns) compared with a group of non-diabetic control subjects (584 +/- 26 microns; P > 0.5). A 7.7 +/- 2.1% increase in CCT was measured after 3 h lens wear in the diabetic patients while an average 10.6 +/- 2.4% increase in CCT was measured in the control subjects (P < 0.05). The recovery of corneal thickness to baseline values in diabetic patients was slower (at 44.8 +/- 2.0% per hour) than the control subjects (53.9 +/- 2.1 per hour; P < 0.05) although recovery of corneal thickness occurred in both groups within 2.5-3h. IOP values (non-contact tonometry) were higher in the diabetic patients than in the controls (14.5 +/- 2.9 vs 12.4 +/- 1.7 mmHg; P < 0.01). Overall, those corneas with greater baseline CCT values tended to swell less than those with lower baseline CCT values (r = 0.582). Positive correlations were also found between corneal thickness and IOP and blood glucose. The diabetic patients thus tended to have slightly thicker corneas (but this could be related to blood glucose or IOP rather than true corneal disease) and also had corneas that tended to swell less with a contact lens stress test (but this could be constitutively due to the slight oedema already present). The different corneal response in diabetic patients may thus be the result of physical determinants such as initial oedema and IOP and not the result of a disease of the cornea itself.
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PMID:Corneal swelling and recovery following wear of thick hydrogel contact lenses in insulin-dependent diabetics. 766 21

The purposes of this study were (i) to determine if ventilatory control is altered in streptozotocin (STZ)-induced diabetic rats and (ii) to determine whether insulin treatment of diabetic rats could prevent ventilatory abnormalities. Male Sprague-Dawley rats were randomly assigned to three groups: control (n = 10), diabetic (n = 9), and diabetic treated with insulin (n = 9). The diabetic group exhibited a progressive reduction of tidal volume, minute ventilation, and CO2 production compared with the control and diabetic treated with insulin groups over the 4 week period. Furthermore, the ventilatory responses to the hypercapnic (3%, 6%, 9% CO2) and hypoxic (10% O2) gas challenges were significantly less in the diabetic rats than those of the control and diabetic and insulin treated groups by the third and fourth week. Ventilation and ventilatory responses to hypercapnia and hypoxia were similar in the control group and the diabetic treated with insulin group at the end of the study. In conclusion, uncontrolled diabetes induced in rats by STZ treatment resulted in altered control of ventilation that could be prevented by insulin therapy.
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PMID:Altered control of ventilation in streptozotocin-induced diabetic rats. 793 52

Analysis of the first year's experience of 94 patients in a tertiary referral center showed that 21% had had previous surgery. Fifty-seven percent had medical problems: 17.8% hypertension, 16% cardiac problems, 8.9% diabetes mellitus, and 6.2% chronic renal insufficiency. Four patients had hypercarbia and were acidotic. The conversion rate to open cholecystectomy was 8.7%. Only one patient required reoperation for a bile leak. Fifty-five percent of our procedures took < or = 2 h, but 45% took > or = 3 h. Just over 50% of our patients stayed 48 h postoperatively. In this complex group of patients, it appears possible to achieve results similar to those previously published, but more time was required for surgery, and length of stay was increased.
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PMID:Laparoscopic cholecystectomy in a tertiary referral center. 811 58

The medical hazards of obesity are discussed. Risks include insulin resistance, diabetes mellitus, hypertriglyceridemia, decreased levels of high-density lipoprotein cholesterol, and increased levels of low-density lipoprotein cholesterol. Obesity is also associated with gallbladder disease and some forms of cancer as well as sleep apnea, chronic hypoxia and hypercapnia, and degenerative joint disease. Obesity is an independent risk factor for death from coronary heart disease. A central distribution of body fat enhances the risk for most of these conditions.
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PMID:Medical hazards of obesity. 836 92

Weight loss reduces many of the health hazards associated with obesity including insulin resistance, diabetes mellitus, hypertension, dyslipidemia, sleep apnea, hypoxemia and hypercarbia, and osteoarthritis. Potential adverse effects of weight loss include a greater risk for gallstone formation and cholecystitis, excessive loss of lean body mass, water and electrolyte problems, mild liver dysfunction, and elevated uric acid levels. Less consequential problems such as diarrhea, constipation, hair loss, and cold intolerance may also occur. The short-term adverse effects are not severe enough to contraindicate weight loss, nor do they outweigh its short-term benefits.
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PMID:Short-term medical benefits and adverse effects of weight loss. 836 5

The ventilatory response to hyperoxic progressive hypercapnia was examined by comparing 3 test groups: 7 diabetic patients with AN, 8 diabetic patients without AN, and 8 normal control subjects. In each group, a significant linear correlation was found between PaCO2 and VE. The slopes of the regression curves relating PaCO2 to VE were significantly steeper in the healthy control subjects and diabetic patients without AN than in those with AN (P < 0.01). We conclude that the ventilatory response to progressive hypercapnia is reduced in diabetic patients with AN. By analyzing the power spectrum and the amplitude behavior of the diaphragmatic EMG (calculated from the fc and RMS, respectively), we could exclude a disturbance of neural descending pathways and respiratory muscle dysfunction as possible causal mechanisms for the impaired ventilatory response to increasing CO2. By using lung function analysis, causal factors such as alterations in respiratory system mechanics also could be excluded. As diabetes is known to affect the endogenous opioid system, which, in turn, affects the ventilatory response to CO2, naloxone, as a specific opioid antagonist, was administered in all 3 test groups. Naloxone produced a significant increase of ventilatory response to hypercapnia in the healthy control subjects (P < 0.01), but produced no effect in either of the diabetic groups.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1993 Feb
PMID:No effect of naloxone on ventilatory response to progressive hypercapnia in IDDM patients. 842 64

The effect of diabetes mellitus on the cerebrovascular response to CO2 is unclear. We examined the effects of diabetes on cerebral blood flow (CBF) and cerebral oxygen uptake (CMRO2) during CO2 alterations. Four groups of dogs were studied: nondiabetic, normoglycemic controls; non-diabetic acute hyperglycemia; diabetic (pancreatectomy) with high-dose insulin treatment to maintain blood glucose between 4.0 and 6.0 mM; and diabetic with low-dose insulin treatment to maintain blood glucose at 13.2 +/- 0.4 mM. Six weeks after either sham surgery or pancreatectomy, dogs were anesthetized with fentanyl (50 micrograms/kg) plus pentobarbital (10 mg/kg), and microsphere determinations of CBF were made during normo-, hypo-, and hypercapnia. On the day of the study, arterial glucose levels in the control, acute hyperglycemia, and high- and low-dose insulin diabetic groups were 4.0 +/- 0.3, 14.9 +/- 2.5, 3.3 +/- 0.8, and 13.3 +/- 0.7 mM, respectively, at control. The corresponding baseline CMRO2 levels were 2.8 +/- 0.2, 3.0 +/- 0.2, 4.1 +/- 0.4, and 4.0 +/- 0.3 ml O2.100 g-1 x min,1, and the values in both diabetic groups were higher than control. Normocapnic CBF in the acute hyperglycemia, high-dose insulin, and low-dose insulin groups was elevated from control (54 +/- 3, 50 +/- 3, 51 +/- 3 vs. 36 +/- 1 ml x 100 g-1 x min-1) and cerebrovascular resistance was lower (2.24 +/- 0.15, 2.51 +/- 0.14, 2.38 +/- 0.21 vs. 3.35 +/- 0.18 mmHg.ml-1 x 100 g.min). CBF responses to both hypercapnia and hypocapnia were similar among groups. Thus both acute hyperglycemia and diabetes decrease cerebrovascular resistance and increase CBF.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cerebral blood flow responsivity to CO2 in anesthetized chronically diabetic dogs. 847 84


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