Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0231835 (tachypnea)
 2,543 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Six subjects with agoraphobia with panic attacks were pretreated with placebo and restricted use of lorazepam for 4 or 5 days. Then l-norepinephrine was infused intravenously with stepwise increases to 4 to 16 micrograms/min. All subjects developed DSM-III symptoms of a panic attack. Subjective results including idiosyncratic symptoms closely resembled the spontaneous panic attacks of these subjects. Cardiac rhythm and rate changes contradicted subjective reports of racing heart and palpitations. Tachypneic and hypertensive reactivities were benign. Both anxiety symptoms and cardiovascular changes reversed rapidly and spontaneously upon discontinuation of the infusion. To validate the possibility that norepinephrine infusion may specifically and reliably simulate spontaneous panic attacks, the authors recommend further work, particularly blinded controlled studies.
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PMID:Norepinephrine challenges in panic patients. 377 9

Four hours after having taken 10 ecstasy tablets a Grand Mal seizure occurred in a 19-year-old woman followed by coma, hyperthermia, tachycardia, tachypnea, and renal failure. After awakening she was oriented but presented with helplessness, disconcertion, hallucinations, panic attacks, and amnesic syndrome. Computed tomography and magnetic resonance imaging scans of the brain were normal. [99Tc]-hexamethylpropyleneamine oxime (HMPAO)-single photon emission computed tomography (SPECT), 20 days after intoxication, showed reduced, inhomogeneous, supratentorial tracer uptake bilaterally. Electroencephalography (EEG) disclosed diffuse slowing and occasionally generalized sharp waves. Valproic acid was begun. Except for slight amnesia, neuropsychological deficits had disappeared and [99Tc]-HMPAO-SPECT normalized, 29 days later. Decreased cortical blood flow was explained by vasoconstriction following ecstasy-induced depletion of serotonin.
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PMID:Long lasting impaired cerebral blood flow after ecstasy intoxication. 1266 70

Intravenous sodium lactate infusions or the noradrenergic agent yohimbine reliably induce panic attacks in humans with panic disorder but not in healthy controls. However, the exact mechanism of lactate eliciting a panic attack is still unknown. In rats with chronic disruption of GABA-mediated inhibition in the dorsomedial hypothalamus (DMH), achieved by chronic microinfusion of the glutamic acid decarboxylase inhibitor L-allylglycine, sodium lactate infusions or yohimbine elicits panic-like responses (i.e., anxiety, tachycardia, hypertension, and tachypnea). In the present study, previous injections of the angiotensin-II (A-II) type 1 receptor antagonist losartan and the nonspecific A-II receptor antagonist saralasin into the DMH of "panic-prone" rats blocked the anxiety-like and physiological components of lactate-induced panic-like responses. In addition, direct injections of A-II into the DMH of these panic-prone rats also elicited panic-like responses that were blocked by pretreatment with saralasin. Microinjections of saralasin into the DMH did not block the panic-like responses elicited by intravenous infusions of the noradrenergic agent yohimbine or by direct injections of NMDA into the DMH. The presence of the A-II type 1 receptors in the region of the DMH was demonstrated using immunohistochemistry. Thus, these results implicate A-II pathways and the A-II receptors in the hypothalamus as putative substrates for sodium lactate-induced panic-like responses in vulnerable subjects.
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PMID:Angiotensin-II is a putative neurotransmitter in lactate-induced panic-like responses in rats with disruption of GABAergic inhibition in the dorsomedial hypothalamus. 1695 77

PANIC DISORDER IS THE MOST COMMON TYPE OF ANXIETY DISORDER, AND ITS MOST COMMON EXPRESSION IS PANIC ATTACKS CHARACTERIZED WITH SUDDEN ATTACKS OF ANXIETY WITH NUMEROUS SYMPTOMS, INCLUDING PALPITATIONS, TACHYCARDIA, TACHYPNEA, NAUSEA, AND VERTIGO: ie, cardiovascular, gastroenterologic, respiratory, and neuro-otologic symptoms. In clinical practice, panic disorder manifests with isolated gastroenteric or cardiovascular symptoms, requiring additional clinical visits after psychiatric intervention. The first-line treatment for anxiety disorders, and in particular for panic disorder, is the selective serotonin reuptake inhibitors. However, these drugs can have adverse effects, including sexual dysfunction, increased bodyweight, and abnormal bleeding, that may be problematic for some patients. Here we report the case of a 29-year-old Caucasian woman affected by panic disorder with agoraphobia who was referred to our clinic for recurrent gastroenteric panic symptoms. The patient reported improvement in her anxiety symptoms and panic attacks while on a selective serotonin reuptake inhibitor, but not in her gastric somatic problems, so the decision was taken to start her on duloxetine, a serotonin-norepinephrine reuptake inhibitor. After 6 months of treatment, the patient achieved complete remission of her gastric and panic-related symptoms, and was able to stop triple gastric therapy. Other authors have hypothesized and confirmed that duloxetine has greater initial noradrenergic effects than venlafaxine and is effective in patients with panic disorder. This case report underscores the possibility of tailoring therapeutic strategies for the gastroenteric expression of panic disorder.
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PMID:Duloxetine in panic disorder with somatic gastric pain. 2429 1

A 67-year old female with moderate chronic obstructive pulmonary disease (COPD) and generalized anxiety disorder presents with three episodes of severe hypercapnic respiratory failure over the previous three months without a clear precipitant that were treated with invasive and non-invasive ventilation. These episodes were labelled as acute exacerbations of COPD, however she lacked any typical features or triggers and responded faster than expected to treatment and she underwent extensive investigations to identify an alternative etiology. While admitted and under observation, she became extremely anxious, began to hyperventilate and went into hypercapnic respiratory failure, which was successfully aborted with sublingual lorazepam causing resolution of tachypnea. It became clear that the patient was suffering from panic attacks as the precipitant for her respiratory failure and she was successfully treated with psychiatric medication and breakthrough anxiolytics. Anxiety and panic disorders are more prevalent in patients with COPD than the general population and effective management is important as patient's with anxiety and COPD have worse clinical outcomes than with COPD alone. Additionally, panic attacks should be considered as an etiology for hypercapnic respiratory failure in patients with COPD and anxiety when the clinical presentation is atypical.
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PMID:Recurrent episodes of hypercapnic respiratory failure triggered by panic attacks in a patient with chronic obstructive pulmonary disease. 3225 94