Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nitroglycerin was administered to a group of 11 patients with chronic obstructive pulmonary disease in a dose of 0.4 mg sublingually. Arterial blood gases and blood pressure and pulse were measured at 5-min intervals for 30 min after nitroglycerin. There was a slight decrease in arterial O2 tension for the duration of the study; the maximal change was from a mean pre-nitroglycerin value of 53.5 mm Hg to 50.3 mm Hg at 20 min. In addition, there was a slight reduction in arterial CO2 tension and bicarbonate for 25 min. It is postulated that decreased O2 transport (due to increased hypoxemia and probably decreased cardiac output) plus hypocapnia were a sufficient stimulus to raise blood lactate. It is recommended that in patients receiving nitroglycerin who have obstructive airway disease, attention be directed toward the effect on arterial blood gases.
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PMID:The effect of nitroglycerin in gas exchange on chronic obstructive pulmonary disease. 23 14

We evaluated the effects of hypocapnia on arterial oxygenation during induced hypotension with nitroglycerin (TNG) or prostaglandin E1 (PGE1) in patients undergoing mastectomy. Of the 20 patients studied, 10 belonged to TNG group and 10 belonged to PGE1 group. Mean arterial pressure during induced hypotension was maintained at 70% of the values observed before hypotension. A significant decrease in PaO2 was observed during hypotension under normocapnia (PaCO2 35-40 mmHg) in both groups. In addition, small but significant reduction in PaO2 from 128.5 +/- 23.7 mmHg to 122.5 +/- 25.5 mmHg in TNG group and from 129.9 +/- 11.9 mmHG to 116.7 +/- 15.6 mmHg in PGE1 group were induced by hypocapnia (PaCO2 27-30 mmHg) during hypotension. These findings suggest that usual dose of TNG and PGE1 might not or might partially inhibit hypoxic pulmonary vasoconstriction.
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PMID:[Effect of hypocapnia on arterial oxygenation during induced hypotension]. 156 May 71

The role of the anesthesiologist in myocardial protection is to optimize myocardial oxygen balance during the perioperative period. Nonpharmacological steps that can be taken to achieve this revolve around maintaining a satisfactory hemoglobin concentration and oxyhemoglobin saturation through maximizing ventilation. In addition, alkalosis and hypothermia should be prevented since they cause a left shift of the oxyhemoglobin dissociation curve, thus interfering with tissue oxygen delivery. Hypocarbia increases coronary vascular resistance. Blood volume must be adequate with an optimal hemoglobin concentration. Pharmacological measures should also be used, and it is important to continue through the perioperative period any previously administered cardioactive drugs. Furthermore, in the prebypass period, tachycardia may not be controlled by anesthetics; unless the tachycardia is paroxysmal, beta blockers are the drugs of choice. Depending on the cause, diastolic hypotension also needs to be treated either with volume, vasoconstrictors, or inotropes. Likewise, major hypertension can produce increased demand and, again depending on the cause, either anesthetics, vasodilators, beta blockers, or calcium blockers may be useful. Finally, myocardial ischemia without obvious cause probably should be treated with nitroglycerin or calcium blockers. During surgery, the effect of the anesthetic drugs on myocardial oxygen balance is important.
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PMID:Myocardial protection: what the anesthesiologist does. 213 51

This study examined the effect of hypocapnia (PaCO2 20 mm Hg) on cerebral metabolism and the electroencephalogram (EEG) findings in 12 dogs during nitroglycerin (NTG)-induced hypotension. Previous studies suggest that NTG is a more potent cerebral vasodilator than sodium nitroprusside or trimethaphan. It was speculated that combining hypocapnia with NTG-induced hypotension would cause less disturbance of cerebral metabolism and the EEG than the disturbances previously reported when hypocapnia was combined with hypotension induced by sodium nitroprusside or trimethaphan. All 12 dogs were examined at 1) normocapnia with normotension; 2) hypocapnia with normotension; and 3) hypocapnia combined with NTG-induced hypotension to mean arterial blood pressure (MABP) levels of 60, 50, and 40 mm Hg. In six dogs the cerebral metabolic rate of oxygen was determined, and the EEG was evaluated using compressed spectral analysis. Brain tissue metabolites were calculated in the other six dogs. During normotension, hypocapnia caused no deterioration of cerebral metabolism or of the EEG. Hypocapnia combined with NTG-induced hypotension caused a decrease of the power of the alpha and beta 2 spectra of the EEG at MABP's of 60 mm Hg or less. At an MABP of 40 mm Hg, brain tissue phosphocreatine and the cerebral energy charge decreased, while the brain tissue lactate:pyruvate ratio increased. Thirty minutes after restoration of normocapnia with normotension, cerebral metabolites returned to initial values, but the power of the EEG alpha and beta 2 spectra was decreased compared to baseline values. The cerebral metabolic disturbances and EEG alterations seen here with hypocapnia plus NTG-induced hypotension were similar to those previously reported with hypocapnia plus sodium nitroprusside-induced hypotension, and less than those previously reported with hypocapnia plus trimethaphan-induced hypotension. For hyperventilated patients, administration of NTG may be a better hypotensive treatment than trimethaphan, but similar in effect to sodium nitroprusside.
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PMID:Cerebral effects of hypocapnia plus nitroglycerin-induced hypotension in dogs. 308 20

For many neurosurgical procedures, elective hypotension is used to reduce the risk of cerebral vessel rupture and hypocapnia is used to constrict cerebral vessels, thereby reducing cerebral blood volume. Although nitroglycerin (NTG) often is used to produce hypotension during neurological surgery, it is not known whether NTG-induced cerebral vasodilation interferes with the cerebral vasoconstrictor response to hypocapnia. This study examined cerebral vascular responses to hypocapnia during NTG-induced hypotension in eight dogs that were lightly anesthetized with halothane and had an open cranium. Cerebral vascular resistance (CVR) and cerebral blood flow (CBF) at PaCO2 = 40 mm Hg and at PaCO2 = 20 mm Hg were examined first at normal mean arterial pressure (MAP) and then at MAP = 50 mm Hg. CO2 responsiveness, as indicated by increased CVR and decreased CBF, was intact at normal MAP but absent during hypotension. These results suggest that the cerebral vasodilation that accompanies NTG-induced hypotension exerts a greater influence on cerebral vessels than the cerebral vasoconstricting influence of hypocapnia. It is concluded that, during NTG-induced hypotension and craniotomy, hypocapnia will not reduce cerebral blood volume or further decrease CBF to cause ischemia.
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PMID:Cerebral vascular responses to hypocapnia during nitroglycerin-induced hypotension. 392 65

Cerebrovascular reactivity during hypocapnia was tested in 20 migraineurs (8 with aura, 12 without aura) and 30 sex- and age-matched healthy subjects, and during nitroglycerin-induced headache in 12 healthy subjects. Before and during hyperventilation, mean blood-flow velocity (Vmean) in the middle cerebral artery was measured with transcranial Doppler. In each subject a pCO2 reactivity index (RI) was calculated as (delta Vmean/baseline Vmean)/delta pCO2. Interictally, patients with migraine with aura showed higher RI (p < 0.05 ANOVA and multiple range test) than controls, whereas migraineurs without aura did not differ from healthy subjects. Ictal and interictal RIs were similar in 9 patients suffering from migraine without aura. No side-to-side differences were detected in RI. During nitroglycerin-induced headache, the RIs were no different from those recorded during migraine attacks and in non-nitroglycerin-provoked healthy controls (p > 0.05, ANOVA and multiple range test). The exaggerated response in migraine with aura might predispose for the characteristic changes in rCBF seen during attacks.
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PMID:Increased cerebrovascular pCO2 reactivity in migraine with aura--a transcranial Doppler study during hyperventilation. 755 11