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

We noninvasively evaluated the effects of nicardipine on cerebral vascular responses to hypocapnia and blood flow velocity in the middle cerebral artery of 10 patients aged 17-60 (mean +/- SD 46.1 +/- 11.8) years. During fentanyl/diazepam/nitrous oxide anesthesia, mean blood flow velocity in the middle cerebral artery was measured and cerebral vascular reactivity to hypocapnia induced by hyperventilation was assessed before and during the administration of nicardipine. Mean blood flow velocity was measured using transcranial Doppler ultrasonography, and the cerebral vascular reactivity was expressed as the percentage change in mean blood flow velocity per unit change in end-tidal PCO2. During the administration of 5.1 +/- 1.3 micrograms/kg/min nicardipine, which caused a 26% reduction in mean arterial blood pressure, mean blood flow velocity increased significantly from 57.2 +/- 19.2 to 64.2 +/- 21.6 cm/sec (p less than 0.01, paired t test), whereas cerebral vascular reactivity showed no significant change (4.0 +/- 1.2% and 4.9 +/- 2.5%, respectively). In conclusion, during fentanyl/diazepam/nitrous oxide anesthesia in patients, cerebral vascular reactivity to hypocapnia was maintained and nicardipine-induced hypotension resulted in increased middle cerebral artery blood flow velocity with maintenance of carbon dioxide reactivity to hypocapnia.
Stroke 1991 Sep
PMID:Effects of nicardipine on cerebral vascular responses to hypocapnia and blood flow velocity in the middle cerebral artery. 192 59

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.
J Appl Physiol (1985) 1990 Sep
PMID:Hypoxic exposure and activation of the afterdischarge mechanism in conscious humans. 212 78

To determine whether afferents in the middle cardiac nerves (MCN) contribute to extrapulmonary PaCO2 sensitivity, we did the following: we anesthetized six cockerels with sodium pentobarbital (25-35 mg/kg), and cannulated the cutaneous ulnar vein, and the carotid and brachial arteries. The thorax was opened and each lung unidirectionally ventilated from separate gas delivery systems. A ligature, which temporarily occluded blood flow, was placed around the right pulmonary artery. Both cardiac sympathetic nerves were cut, as well as the left vagus just above the level of the recurrent branch. We exposed the non-perfused right lung to 105 Torr PCO, to silence intrapulmonary chemoreceptors (IPC). We measured blood pressure, heart rate and ventilatory movements while the denervated left lung was used to fix PaCO2 at seven levels ranging from 7-140 Torr. As arterial PCO2 increased, ventilatory amplitude increased from 0.3 mm to 3.6 mm, while frequency decreased from 140 to 24 per min. After cutting the MCN, ventilatory movements were less responsive to PaCO2 changes. Ventilatory amplitude was 3.0 mm at the lowest PaCO2 and increased to 4.0 at the highest PaCO2. We conclude that: 1) when IPC discharge is low, afferents in the MCN inhibit ventilatory movements during hypocapnia, and 2) these afferents may contribute to systemic CO2 sensitivity.
Respir Physiol 1990 Sep
PMID:Middle cardiac nerve section alters ventilatory response to PaCO2 in the cockerel. 212 69

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.
J Card Surg 1990 Sep
PMID:Myocardial protection: what the anesthesiologist does. 213 51

The effects of mild hypoxia on brain oxyhemoglobin, cytochrome a,a3 redox status, and cerebral blood volume were studied using near-infrared spectroscopy in eight healthy volunteers. Incremental hypoxia reaching 70% arterial O2 saturation was produced in normocapnia [end-tidal PCO2 (PETCO2) 36.9 +/- 2.6 to 34.9 +/- 3.4 Torr] or hypocapnia (PETCO2 32.8 +/- 0.6 to 23.7 +/- 0.6 Torr) by an 8-min rebreathing technique and regulation of inspired CO2. Normocapnic hypoxia was characterized by progressive reductions in arterial PO2 (PaO2, 89.1 +/- 3.5 to 34.1 +/- 0.1 Torr) with stable PETCO2, arterial PCO2 (PaCO2), and arterial pH and resulted in increases in heart rate (35%) systolic blood pressure (14%), and minute ventilation (5-fold). Hypocapnic hypoxia resulted in progressively decreasing PaO2 (100.2 +/- 3.6 to 28.9 +/- 0.1 Torr), with progressive reduction in PaCO2 (39.0 +/- 1.6 to 27.3 +/- 1.9 Torr), and an increase in arterial pH (7.41 +/- 0.02 to 7.53 +/- 0.03), heart rate (61%), and ventilation (3-fold). In the brain, hypoxia resulted in a steady decline of cerebral oxyhemoglobin content and a decrease in oxidized cytochrome a,a3. Significantly greater loss of oxidized cytochrome a,a3 occurred for a given decrease in oxyhemoglobin during hypocapnic hypoxia relative to normocapnic hypoxia. Total blood volume response during hypoxia also was significantly attenuated by hypocapnia, because the increase in volume was only half that of normocapnic subjects. We conclude that cytochrome a,a3 oxidation level in vivo decreases at mild levels of hypoxia. PaCO is an important determinant of brain oxygenation, because it modulates ventilatory, cardiovascular, and cerebral O2 delivery responses to hypoxia.
J Appl Physiol (1985) 1990 Sep
PMID:Cerebral oxygen availability by NIR spectroscopy during transient hypoxia in humans. 217 31

The cerebral effects of sevoflurane were compared in dogs with those of enflurane and isoflurane. Initially, the minimum alveolar concentrations (MAC) of sevoflurane and enflurane were determined and the electroencephalographic (EEG) responses to increasing doses of sevoflurane (1.5, 2.0 and 2.5 MAC) or enflurane (1.5 and 2.0 MAC) in unparalysed animals were examined. Administration of sevoflurane was not associated with seizure activity at any concentration either during normocapnia (PaCO2 5.3 kPa) or hypocapnia (PaCO2 2.7 kPa), even in the presence of intense auditory stimuli. All dogs anaesthetized with enflurane demonstrated sustained EEG and motor evidence of seizure activity induced by auditory stimuli at concentrations of enflurane greater than 1 MAC, particularly during hypocapnia. In a separate group of dogs, the effects of increasing concentrations of sevoflurane and isoflurane (0.5, 1.5 and 2.15 MAC) were compared directly on arterial pressure, cardiac output and heart rate, cerebral blood flow and the cerebral metabolic rate for oxygen (CMRO2) using the venous outflow technique. Sevoflurane, in common with isoflurane, had minimal effects on cerebral blood flow at the concentrations studied, but significantly reduced the CMRO2 at end-tidal concentrations sufficient to produce a burst suppression pattern on the EEG (approximately 2.15 MAC). Both sevoflurane and isoflurane significantly decreased arterial pressure in a dose-dependent manner, but neither drug significantly altered cardiac output.
Br J Anaesth 1990 Sep
PMID:Cerebral effects of sevoflurane in the dog: comparison with isoflurane and enflurane. 222 68

Respiratory alkalosis is the consequence of primary hypocapnia of divergent etiologies. Any pathologic process that increases ventilation to levels beyond that required to excrete the CO2 byproduct of metabolism, will result in an inappropriately low systemic pCO2 and a tendency to an alkaline systemic pH. The increased drive to ventilation may be due predominantly to a primary increase in central nervous system activity, either within the respiratory center itself or from more centrally placed areas with neural projections that extend to and control the respiratory center. Alternatively, an increased drive to ventilation may result from an "appropriate" physiologic response to another more important stimulus that overrides the human's needs to protect pCO2 and pH. Hypoxia (of different causes), is the most important and most commonly encountered such stimulus.
Bol Med Hosp Infant Mex 1990 Sep
PMID:[Water-electrolyte and acid-base imbalance. IX. Respiratory alkalosis]. 227 Nov 31

Aortic chemoreceptor influences on vascular capacitance after changes in blood carbon dioxide and oxygen were studied in mongrel dogs anesthetized with methoxyflurane and nitrous oxide. The mean circulatory filling pressure (Pmcf), measured during transient cardiac fibrillation, provided a measure of capacitance vessel tone. Hypercapnia, hypoxia, and hypoxic hypercapnia significantly increased most variables, except that hypercapnia caused the total peripheral resistance (TPR) to decrease. Hypocapnia caused a significant decrease in mean systemic (Psa) and pulmonary (Ppa) arterial blood pressures, cardiac output (CO), and central blood volume and an increase in TPR and heart rate. The changes in Pmcf on changing blood gas tensions could be described by the equation delta Pmcf = -1.60 + 0.036 (arterial PCO2) + 50.8/arterial PO2. Thus a 10 mmHg increase in arterial PCO2 caused a 0.36 mmHg increase in Pmcf with receptors intact. Cold block (2 degrees C) of the cervical vagosympathetic trunks did not significantly influence the measured variables at control. During severe hypercapnia, vagal cooling caused a small but significant decrease in Pmcf, Psa, Ppa, and CO but not TPR. During hypoxia, vagal cooling caused the Pmcf, Psa, and TPR to decrease. We conclude that although hypercapnia or hypoxia acts reflexly to increase the capacitance vessel tone (an increase in Pmcf), the aortic and cardiopulmonary chemoreceptors with afferents in the vagi have only a small influence on the capacitance system, accounting for only approximately 25% of the total body response.
Am J Physiol 1990 Sep
PMID:Effects of hypercapnia and hypoxia on the cardiovascular system: vascular capacitance and aortic chemoreceptors. 239 98

A hyperventilation provocation test (HVPT) was performed on a group (n = 63) of consecutive patients, below the age of 40 years, attending an emergency care unit complaining of chest pain without obvious organic cause. The results were compared with those for a control group (n = 32). There was no tendency to hyperventilate in the patient group, either after discontinuing hyperventilation or during the ensuing relaxation period. PETCO2 measurements during this time thus showed no significant differences between the patient group and the control group. During the HVPT, 44% of patients reported three or more listed symptoms familiar to them from earlier occasions and regarded as typical of hyperventilation, compared to 23% of the controls (P less than 0.05). In a previously reported study, 38% of the patients were found to have similar symptoms during standardized mental stress, despite lack of hypocapnia. It is concluded that, on the basis of PETCO2 measurements, there were no signs of abnormal hyperventilation in the patient group. Moreover, the HVPT did not appear to be specific for diagnosis of hyperventilation syndrome, since mental stress itself was able to reproduce symptoms without concomitant hypocapnia, and since the provocation test was 'positive' in many control subjects.
J Intern Med 1990 Sep
PMID:Acute chest pain without obvious organic cause before the age of 40 years: response to forced hyperventilation. 205 66

We investigated cerebral blood flow and metabolism, and cerebral vascular response in 9 patients with cerebrovascular Moyamoya disease or unilateral Moyamoya phenomenon using positron emission tomography (PET). The subjects consisted of 5 men and 4 women, and were from 9 to 60 years old. Five patients had bilateral occlusion in the carotid fork with Moyamoya vessels (fulfilled the criteria of cerebrovascular Moyamoya disease), and four patients had unilateral Moyamoya phenomenon. The PET scanner used was the HEADTOME III, of which spatial resolution in clinical use was 10 mm full width at half-maximum (FWHM) in the image plane. Cerebral blood flow (CBF), cerebral metabolic rate of oxygen (CMRO2), cerebral oxygen extraction fraction (OEF), and cerebral blood volume (CBV) were measured in resting state by the 15O-labelled gases steady state method in every patient and 22 normal controls (17 men and 5 women, and from 26 to 64 years old). Consecutively cerebral vascular responses were measured by H215O autoradiographic method in resting state, hypercapnia, hypocapnia, and hypertension. Forced hypercapnia, hypocapnia, and hypertension were achieved by 7% CO2 inhalation, hyperventilation, and venous infusion of angiotensin II, respectively. CMRO2 of the whole brain was significantly lower in patients than in normal controls (p less than 0.05), and CBV of the lentiform nucleus significantly increased in patients (p less than 0.01). This reflected Moyamoya vessels in the basal ganglionic regions. In 3 of 5 patients with bilateral Moyamoya vessels, CBF and CMRO2 in the symptomatic cerebral hemisphere were lower than that in the nonsymptomatic hemisphere.(ABSTRACT TRUNCATED AT 250 WORDS)
No To Shinkei 1989 Sep
PMID:[Vascular responses in cerebrovascular "Moyamoya" disease--evaluated by positron emission tomography]. 251 9


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>