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)

The human pharmacology of anxiety disorders, including panic disorder, is detailed. The major theories center around the role of benzodiazepine receptor, noradrenergic and serotonergic dysfunction. The contribution that challenge tests with lactate, hyper- and hypocapnia, beta- and alpha-2-adrenoceptor agonists, peptides, pentylenetetrazol, and caffeine make to our understanding of the biological basis of anxiety and these major theories are described and discussed.
 ...
PMID:The pharmacology of human anxiety. 197 44

Nineteen patients with panic disorder received sodium D,L-lactate (racemic) and pure sodium D-lactate infusions in a pilot study. Sodium D-lactate, which is less metabolically active than L-lactate, produced panic attacks in half the patients. D-Lactate also produced hypocapnia and alkalosis, indicating hyperventilation. These findings suggest that metabolism of lactate is not necessary for the induction of panic in susceptible patients. D-Lactate appears similar to other agents that cause panic in its capacity to stimulate respiration in the preliminary study.
 ...
PMID:Sodium D-lactate infusion of panic disorder patients. 211 19

Infusion of sodium lactate has been shown by a number of investigators to induce panic in patients with panic disorder, but the pathophysiology underlying this phenomenon is unknown. One theory to explain lactate's anxiety-producing effects involves its ability to induce alkalosis because of metabolic conversion to bicarbonate. To test this hypothesis, we administered both sodium lactate and sodium bicarbonate infusions in counterbalanced order to patients with panic disorder. Thirteen of 22 subjects panicked in response to lactate and nine of 20 subjects panicked in response to bicarbonate. Although the rate of panic between the two infusion responses was not significantly different, several aspects of response to the two infusions indicated that lactate may be a more potent producer of anxiety than bicarbonate. An unexpected finding was that bicarbonate panickers had a reduction in arterial carbon dioxide pressure during the infusion, while bicarbonate nonpanickers had an increase in arterial carbon dioxide pressure during the infusion. Induction of hyperventilation and subsequent hypocapnia appears to be a common denominator between lactate- and bicarbonate-induced panic.
 ...
PMID:A comparison of sodium bicarbonate and sodium lactate infusion in the induction of panic attacks. 253 38

Alkalosis is prominent among the many physiologic and biochemical effects of sodium lactate infusion. Though this is partially due to the conversion of lactate to bicarbonate, the metabolic component, it may also be secondary to hyperventilation before and during the infusion, the respiratory component. We analyzed pH, carbon dioxide pressure, bicarbonate, and inorganic phosphate from patients with panic disorder and agoraphobia with panic attacks and from normal controls both before and during lactate infusion. Our findings extend earlier work demonstrating that many such patients are chronic hyperventilators. Both metabolic and respiratory alkalosis develop in all subjects during lactate infusion, but only hyperventilation-induced hypocapnia differentiates patients at the point of lactate-induced panic from nonpanicking patients and normal controls. Finally, low inorganic phosphate levels at baseline appear associated with patients who will panic during the subsequent lactate infusion. This last unexpected finding may reflect hyperventilation or an abnormality in intracellular glycolysis.
 ...
PMID:Blood gas changes and hypophosphatemia in lactate-induced panic. 309 75

This study compares the hemodynamic response to panic disorder subjects with that of normal controls during respiratory challenges. Panic patients meeting DSM-IIIR criteria for panic disorder and normal controls were challenged with room air hyperventilation, 5% CO2 breathing, and 7% CO2 breathing. Measurements of pulse and blood pressure were taken at resting baseline and before and at the end of each respiratory challenge. Panic attack to each challenge was determined by using raters blinded to subject diagnosis and each subject's self-rating of panic. Significantly larger systolic and diastolic blood pressure increases were found in patients who panicked with room air hyperventilation than nonpanicking patients or normal controls. No significant blood pressure differences were found with 7% or 5% CO2 challenges, but higher pulse rates were found in the patient group. It may be possible that panic with room air hyperventilation causes a significant increase in systolic and diastolic blood pressure, or that a subgroup of panic disorder patients has a hyperactive vascular response to hypocapnia. These patients panic with room air hyperventilation and develop greater vasoconstriction and/or increased blood pressure response.
 ...
PMID:Hemodynamic response to respiratory challenges in panic disorder. 948 71

In this article, we review how the knowledge of the pathophysiology of panic disorder has expanded, with special emphasis on laboratory models using lactate and carbon dioxide challenges. Experiments in the late 1960s revealed that lactate infusion can induce panic attacks. A prominent feature of these attacks is hyperventilation. Because lactate infusion induces a metabolic alkalosis, one would rather expect a compensatory hypoventilation. For years hyperventilation was thought to be causally linked to panic, but it has since been proven to be a symptom rather than a cause of panic attacks. Similarly, it is not hypocapnia but hypercapnia that has proven to be capable of provoking panic attacks. Carbon dioxide challenges are comparable to lactate infusion in the degree to which they meet the criteria for an ideal model of panic disorder. Experiments with carbon dioxide in first-degree relatives of panic disorder patients and in monozygotic twins support the idea of a constitutional predisposition to panic disorder. Of the various other agents that have been used to trigger panic attacks, cholecystokinin seems particularly promising as a valid laboratory model of panic disorder and may provide valuable data regarding the mechanism of panic attacks. The false suffocation alarm theory, proposed by Klein, is an integrative hypothesis that may account for a large number of the laboratory as well as clinical observations.
 ...
PMID:Experimental pathophysiology of panic. 985 52

Panic patients consistently show exaggerated lactic acid response to alkalosis, whether produced by hyperventilation or by sodium lactate infusion. Understanding why this occurs may provide important clues to the pathogenesis of panic disorder. Although brain hypoxia from excessive hypocapnia-induced cerebral vasoconstriction is often cited as the mechanism of elevated brain lactic acid in panic disorder, studies of brain metabolism show that hypocapnia rarely leads to brain hypoxia. Increased lactic acid production is a normal response to intracellular alkalosis and to intracellular cyclic AMP. Thus, other possible mechanisms of the exaggerated lactic acid response in panic disorder include a disturbance of mechanisms regulating intracellular pH and factors increasing intracellular cyclic AMP. Both mechanisms are consistent with the suffocation false alarm theory of panic disorder. This review suggests a theoretical framework for future magnetic resonance spectroscopy studies that can test some of the predictions of these competing models.
 ...
PMID:The lactic acid response to alkalosis in panic disorder : an integrative review. 1120 26

Respiration is a complex physiological system affecting a variety of physical processes that can act as a critical link between mind and body. This review discusses the evidence for dysregulated breathing playing a role in three clinical syndromes: panic disorder, functional cardiac disorder, and chronic pain. Recent technological advances allowing the ambulatory assessment of endtidal partial pressure of CO2 (PCO2) and respiratory patterns have opened up new avenues for investigation and treatment of these disorders. The latest evidence from laboratories indicates that subtle disturbances of breathing, such as tidal volume instability and sighing, contribute to the chronic hypocapnia often found in panic patients. Hypocapnia is also common in functional cardiac and chronic pain disorders, and studies indicate that it mediates some of their symptomatology. Consistent with the role of respiratory dysregulation in these disorders, initial evidence indicates efficacy of respiration-focused treatment.
 ...
PMID:Respiratory dysregulation in anxiety, functional cardiac, and pain disorders. Assessment, phenomenology, and treatment. 1153 Jul 14

The authors describe a new methodologically improved behavioral treatment for panic patients using respiratory biofeedback from a handheld capnometry device. The treatment rationale is based on the assumption that sustained hypocapnia resulting from hyperventilation is a key mechanism in the production and maintenance of panic. The brief 4-week biofeedback therapy is aimed at voluntarily increasing self-monitored end-tidal partial pressure of carbon dioxide (PCO2) and reducing respiratory rate and instability through breathing exercises in patients' environment. Preliminary results from 4 patients indicate that the therapy was successful in reducing panic symptoms and other psychological characteristics associated with panic disorder. Physiological data obtained from home training, 24-hour ambulatory monitoring pretherapy and posttherapy, and laboratory assessment at follow-up indicate that patients started out with low resting PCO2 levels, increased those levels during therapy, and maintained those levels at posttherapy and/or follow-up. Partial dissociation between PCO2 and respiratory rate questions whether respiratory rate should be the main focus of breathing training in panic disorder.
 ...
PMID:Respiratory biofeedback-assisted therapy in panic disorder. 1153 Jul 17

Our aim was to determine whether panic disorder (PD) patients, major depressive patients without panic attacks (MD) and major depressive patients with panic attacks (MDP) respond similarly to hyperventilation challenge tests. We randomly selected 35 PD patients, 33 MDP patients, 27 MD patients and 30 normal volunteers with no family history of anxiety or mood disorder. The patients had not been treated with psychotropic drugs for at least 1 week. They were induced to hyperventilate (30 breaths/min) for 4 min, and anxiety was assessed before and after the test. A total of 16 (45.7%) PD patients, 12 (36.4%) MDP patients, four (11.1%) MD patients, and two (6.7%) normal volunteers had a panic attack after hyperventilating. The PD and MDP patients were significantly more responsive to hyperventilation than the MD patients and the normal volunteers. The MD patients had a significantly lower heart-rate response to the test than all the other groups. There is growing evidence that PD patients are more sensitive to the vasoconstrictive effects on basilar arterial blood flow caused by hyperventilation-induced hypocapnia than are comparison subjects. Our data suggest that there is an association between panic attacks and hyperreactivity to an acute hyperventilation challenge test.
 ...
PMID:Hyperventilation challenge test in panic disorder and depression with panic attacks. 1174 Sep 75


1 2 Next >>