Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute postoperative hypertension (APH) has been documented in the PACU. Over half of the patients who exhibit APH have pre-existing primary hypertension. Sustained blood pressure (BP) elevation increases the risk of myocardial ischemia, infarction, surgical site bleeding, or cerebral hemorrhage in these patients. Following surgery and anesthesia, increased sympathetic stimulation caused by a high level of circulating catecholamines can lead to APH. Some direct perioperative stimulants include pain, anxiety, hypoxia, hypercapnia, hypothermia, shivering, volume overload, and bladder distension. Nursing interventions are directed toward identifying and relieving the cause of APH. Antihypertensive drug therapy with vasodilators or adrenergic inhibitors is used if initial nursing interventions are not effective. Vasodilators frequently used are hydralazine, sodium nitroprusside, and nitroglycerin. Nicardipine has recently been introduced as an intravenous calcium channel blocker. Vasodilators are effective in BP reduction but may cause reflex tachycardia when used alone. Adrenergic inhibitors, such as esmolol and labetalol, block alpha and/or beta receptors to decrease heart rate and BP. Labetalol's effectiveness, relative freedom from side effects, and ease of administration have made it a useful drug in the treatment of APH.
 ...
PMID:Acute postoperative hypertension in the hypertensive patient. 173 70

Anesthetic management during 85 STA-MCA anastomoses with or without encephalo-myosynangiosis for 64 patients with Moyamoya disease was evaluated retrospectively. Anesthetic agents included nitrous oxide-NLA (GONLA), nitrous oxide-halothane (GOF), nitrous oxide-enflurane (GOE), and their combinations. Slight hypercarbia (40 mmHg less than PaCO2 less than 50 mmHg) was essential to avoid cerebral ischemia. Several procedures to control heart rate by beta blockade or to control hypertension by nitroglycerin were required, because tachycardia and hypertension interfered with fine surgical procedure. During microsurgery HR of GONLA anesthetized patients was significantly lower. Postoperatively the patients anesthetized by GOE showed significantly lower PaCO2 compared with the GONLA anesthetized patients. So we recommend GONLA for anastomosis in patients with Moyamoya disease.
 ...
PMID:[Anesthetic management of revascularization for moyamoya disease]. 192 Jul 89

To identify central sites of potential CO2/H+-chemoreceptive neurons, and the mechanism responsible for neuronal chemosensitivity, intracellular recordings were made in rat tissue slices in two cardiopulmonary-related regions (i.e., nucleus tractus solitarii, NTS; nucleus ambiguus, AMBc) during exposure to high CO2. When the NTS was explored slices were bisected and the ventral half discarded. Utilizing such "dorsal" medullary slices removed any impinging synaptic input from putative chemoreceptors in the ventrolateral medulla. In the NTS, CO2-induced changes in firing rate were associated with membrane depolarizations ranging from 2-25 mV (n = 15). In some cases increased e.p.s.p. activity was observed during CO2 exposure. The CO2-induced depolarization occurred concomitantly with an increased input resistance ranging from 19-23 M omega (n = 5). The lower membrane conductance during hypercapnia suggests that CO2-induced depolarization is due to a decreased outward potassium conductance. Unlike neurons in the NTS, AMBc neurons were not spontaneously active and were rarely depolarized by hypercapnia. Eleven of 12 cells tested were either hyperpolarized by or insensitive to CO2. Only 1 neuron in the AMBc was depolarized and it also showed an increased input resistance during CO2 exposure. Our findings suggest that CO2/H+-related stimuli decrease potassium conductance which depolarizes the cell and increases firing rate. Although our in vitro studies cannot guarantee the specific function of these cells, we believe they may be involved with brain pH homeostasis and cardiopulmonary regulation.
 ...
PMID:CO2 decreases membrane conductance and depolarizes neurons in the nucleus tractus solitarii. 250 42

The present study was undertaken to evaluate the short-term effects of nitroglycerin, nifedipine, and supplemental oxygen on hemodynamics and gas exchange in 11 patients in stable condition with chronic obstructive pulmonary disease and cor pulmonale. In general, both intravenous nitroglycerin and sublingual nifedipine significantly reduced the pulmonary vascular resistance index. For the group as a whole, nifedipine decreased the pulmonary vascular resistance index by significantly increasing the cardiac index, with minimal reductions in mean pulmonary arterial pressure. Conversely, nitroglycerin decreased the pulmonary vascular resistance index by markedly reducing the mean pulmonary arterial pressure but also decreased the cardiac index in some patients. Nitroglycerin also caused a significant decrease in mixed venous oxygen tension. Administration of oxygen did not cause any clinically significant improvement in resting hemodynamics following short-term administration. During the follow-up period, eight of 11 patients who were treated with pulmonary vasodilators in addition to long-term therapy with low-flow oxygen died within a mean of six months. This rate of survival was not significantly different than an age-matched and sex-matched control group with similar severity of disease who received only long-term therapy with low-flow oxygen. Based on these data, it seems unlikely that a substantial increase in survival will be obtained by combining pulmonary vasodilators with long-term oxygen therapy in patients with stable emphysema who have cor pulmonale and carbon dioxide retention.
 ...
PMID:Pulmonary vasodilator therapy for chronic obstructive pulmonary disease and cor pulmonale. Treatment with nifedipine, nitroglycerin, and oxygen. 310 14

A case is presented which describes a patient who developed hypercarbia resulting from a defective humidifier. A Puritan-Bennett Cascade I humidifier was incorporated into a circle system between the inspiratory dome one way valve and the patient. A screw which supports the thermal well to the head of the humidifier was missing, thereby allowing an intermittent leak to develop in the system. The leak was present when the system pressure dropped to ambient level; however, at positive system pressure the leak sealed. This allowed exhaled gases into the inspiratory limb of the circuit unchecked by the inspiratory valve yet when the breathing circuit was occluded at the patient end and submitted to pressures of 20 and 40 cm H2O, no leaks were detected. Intraoperatively, PaCO2 was noted to be as high as 68 mmHg just prior to removing the humidifier from the circuit and corrected to 38 mmHg within 15 minutes of removal of the humidifier.
 ...
PMID:Carbon dioxide retention associated with a humidifier defect. 366 21

A study was made of external carotid, renal, and splanchnic sympathetic nerve discharge (SND) in chloralose-anesthetized cats subjected to transection of the sixth cervical spinal segment 2-37 days earlier. Minimal activity was observed under normocapnic conditions 2 days after spinal transection, and ganglionic blockade failed to lower blood pressure. Moderate hypercapnia increased SND and led to synchronization of activity into 1-6 cycle/s slow waves. Such slow-wave activity was present under normocapnic conditions in cats 9-37 days after spinal transection. Ganglionic blockade significantly reduced blood pressure in these preparations. The interval between successive 1-6 cycle/s slow waves was variable. Thus, unlike the case in baroreceptor-denervated cats with an intact neuraxis [Barman and Gebber, Am. J. Physiol. 239 (Regulatory Integrative Comp. Physiol. 8): R42-R47, 1980], chronic spinal cats are incapable of rhythm generation in the 1-6 cycle/s frequency range. Crosscorrelation analysis revealed that the discharges of pairs of segmental (but not intersegmental) sympathetic nerves were related in the chronic spinal cat. This situation differs from that in the baroreceptor-denervated cat in which the discharges of pairs of intersegmental as well as segmental sympathetic nerves are related. Thus coordination of activity in sympathetic nerves that arise from different spinal segments requires the integrity of bulbospinal connections. Finally, no evidence was obtained for the existence of a baroreceptor-like reflex mechanism acting to control SND in the chronic spinal cat.
 ...
PMID:Sympathetic nerve discharge in chronic spinal cat. 711 77

1. The aims of this study were to compare in the rat isolated perfused lung preparation, the dilator actions of nicorandil, pinacidil and nitroglycerin on the hypoxic pulmonary pressure response with or without hypercapnic acidosis and to investigate the possible involvement of K channels and EDRF in these effects. 2. Isolated lungs from male Wistar rats (260-320 g) were ventilated with 21%O2 + 5%CO2 + 74%N2 (normoxia) or 5%CO2 + 95%N2 (hypoxia) and perfused with a salt solution supplemented with ficoll and gassed with 40%CO2 + 60%N2 to produce hypercapnic acidosis. Glibenclamide (1 microM), charybdotoxin (0.1 microM), NG-nitro-L-arginine methyl ester (L-NAME, 100 microM) and methylene blue (30 microM) were used to block KATP channels, KCa channels, EDRF synthesis and guanylate cyclase, respectively. 3. Hypoxic pressure response was significantly increased by hypercapnic acidosis (+115%, P < 0.001), L-NAME (+111%, P < 0.001), methylene blue (+100%, P < 0.05) but not by glibenclamide or charybdotoxin. In contrast none of these inhibitors affected the hypoxic hypercapnic acidosis response. 4. Nicorandil, pinacidil and nitroglycerin caused relaxation during the hypoxic pressure response and hypoxic hypercapnic acidosis response. Nicorandil was more potent in the latter. Glibenclamide inhibited the relaxant effects of nicorandil and pinacidil but not those of nitroglycerin during hypoxia alone. In contrast, glibenclamide inhibited the relaxant effects of the three drugs during hypoxia + hypercapnia. Charybdotoxin inhibited the relaxant effect of pinacidil during normocapnia and hypoxia but not those of nicorandil or nitroglycerin. Methylene blue inhibited partially the dilator response to pinacidil but did not modify the effects of nitroglycerin or nicorandil. 5. It is concluded that in the rat isolated lung preparation, EDRF limits hypoxic pulmonary vasoconstriction but not hypoxic vasoconstriction potentiated by hypercapnic acidosis, whereas KATP or KCa channels are not involved in either case. Nicorandil and pinacidil dilate pulmonary vessels mainly through KATP channels but the effects of pinacidil may also involve an additional mechanism of action through KCa channels. Finally it is suggested that nitroglycerin may partly exert its relaxant effects through KATP channels.
 ...
PMID:Comparison of the effects of nicorandil, pinacidil and nitroglycerin on hypoxic and hypercapnic pulmonary vasoconstriction in the isolated perfused lung of rat. 864 7

Since the nitric oxide (NO) and cyclooxygenase pathways have been suggested to have important roles in most vasodilations, our aim was to study the influence of cyclooxygenase inhibitors and nitrovasodilators on cerebrovascular reserve capacity. Corticocerebral blood flow was measured by hydrogen polarography during hypercapnia and acetazolamide stimuli in conscious rabbits. The measurements were repeated in the presence of N(omega)-nitro-L-arginine methyl ester (L-NAME) and indomethacin as nitric oxide synthase (NOS) and cyclooxygenase inhibitors. The effects of nitroglycerin and isosorbide-5-nitrate were also tested. L-NAME completely, while indomethacin markedly inhibited the hypercapnic corticocerebral blood flow response. Nitroglycerin and isosorbide-5-nitrate significantly attenuated hypercapnia elicited corticocerebral blood flow increase. The different treatments reduced only moderately the acetazolamide-induced corticocerebral blood flow response. These results lend support to the hypothesis that antithrombotic and antiinflammatory medication (cyclooxygenase inhibitors) and nitrovasodilator treatments could interfere with the measurement of cerebrovascular reactivity resulting in underestimation of the cerebrovascular reserve capacity in patients taking these drugs.
 ...
PMID:Influence of nitrovasodilators and cyclooxygenase inhibitors on cerebral vasoreactivity in conscious rabbits. 1116 94

The rat retrotrapezoid nucleus (RTN) contains pH-sensitive neurons that are putative central chemoreceptors. Here, we examined whether these neurons respond to peripheral chemoreceptor stimulation and whether the input is direct from the solitary tract nucleus (NTS) or indirect via the respiratory network. A dense neuronal projection from commissural NTS (commNTS) to RTN was revealed using the anterograde tracer biotinylated dextran amine (BDA). Within RTN, 51% of BDA-labelled axonal varicosities contained detectable levels of vesicular glutamate transporter-2 (VGLUT2) but only 5% contained glutamic acid decarboxylase-67 (GAD67). Awake rats were exposed to hypoxia (n = 6) or normoxia (n = 5) 1 week after injection of the retrograde tracer cholera toxin B (CTB) into RTN. Hypoxia-activated neurons were identified by the presence of Fos-immunoreactive nuclei. CommNTS neurons immunoreactive for both Fos and CTB were found only in hypoxia-treated rats. VGLUT2 mRNA was detected in 92 +/- 13% of these neurons whereas only 12 +/- 9% contained GAD67 mRNA. In urethane-chloralose-anaesthetized rats, bilateral inhibition of the RTN with muscimol eliminated the phrenic nerve discharge (PND) at rest, during hyperoxic hypercapnia (10% CO(2)), and during peripheral chemoreceptor stimulation (hypoxia and/or i.v. sodium cyanide, NaCN). RTN CO(2)-activated neurons were recorded extracellularly in anaesthetized intact or vagotomized rats. These neurons were strongly activated by hypoxia (10-15% O(2); 30 s) or by NaCN. Hypoxia and NaCN were ineffective in rats with carotid chemoreceptor denervation. Bilateral injection of muscimol into the ventral respiratory column 1.5 mm caudal to RTN eliminated PND and the respiratory modulation of RTN neurons. Muscimol did not change the threshold and sensitivity of RTN neurons to hyperoxic hypercapnia nor their activation by peripheral chemoreceptor stimulation. In conclusion, RTN neurons respond to brain P(CO(2)) presumably via their intrinsic chemosensitivity and to carotid chemoreceptor activation via a direct glutamatergic pathway from commNTS that bypasses the respiratory network. RTN neurons probably contribute a portion of the chemical drive to breathe.
 ...
PMID:Peripheral chemoreceptor inputs to retrotrapezoid nucleus (RTN) CO2-sensitive neurons in rats. 1648 93

The vasodilatory response of arteries can be measured by ultrasound, and it was previously shown that brachial artery (BA) vasodilatation can be tested by postischemic hyperemia. In the current study, the primary objective was to determine if hypercapnia can be used to assess common carotid artery (CCA) flow-mediated vasodilatation (FMVD) in healthy subjects. Secondary objectives were to investigate CCA-FMVD in lacunar patients and whether BA-FMVD parallels CCA-FMVD. We used ultrasound to measure flow-mediated and nitroglycerin (NTG)-mediated vasodilatation in the CCA and BA in 20 healthy subjects and in 17 lacunar patients. BA-FMVD was induced by a postischemic maneuver. For the CCA, FMVD was induced by hypercapnia from CO(2)-enriched inhalation. BA and CCA vasodilatation were measured after sublingual NTG administration. BA dilated significantly in healthy (6.7%) and stroke subjects (4.2%) under postischemic conditions. The CCA dilated significantly after CO(2) inhalation (11.4% in healthy subjects and 4% in lacunar patients) and NTG administration (18% in healthy subjects and 10.6% in lacunar patients). Surprisingly, there was a strong negative correlation between CCA- and BA-FMVD in healthy subjects. CCA vasodilatation induced by CO(2) inhalation and NTG administration can be measured. The strong negative correlation between CCA- and BA-FMVD suggests that there could be different mechanisms of vasodilatation.
 ...
PMID:Flow-mediated vasodilatation of carotid and brachial arteries in healthy subjects and in lacunar stroke patients. 1687 51


1 2 Next >>