***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Previous studies have shown unequivocally a lack of pituitary-adrenocortical stress hormone activation during lactate-induced panic attacks despite considerable psychopathological alterations , signs of arousal and several vegetative symptoms regularly occurring during stressful conditions . To study the possible inhibitory action of atrial natriuretic hormone ( ANH ) on adrenocorticotrophic hormone ( ACTH ) and cortisol release in humans , 10 patients with panic disorder ( DSM-III-R ) received sodium lactate and placebo ( 0.9 % saline ) infusions and ten healthy comparison subjects additionally received a 2.5 % saline infusion and the response of ANH , vasopressin , ACTH , cortisol , and several biochemical and physiological cardiovascular parameters were measured . In comparison to placebo , lactate infusion led to enhanced ANH levels in both non-panicking comparison subjects and panickers . Importantly , panickers showed significantly lower baseline levels of ANH than comparison subjects followed by a faster release . No significant concomitant changes in vasopressin , ACTH , and cortisol were observed . During lactate infusion , heart rate was accelerated considerably in the two groups ; in contrast , the reduction of pCO2 indicated an enhanced ventilation only in panickers . The pattern of ANH release can not be attributed simply to either the volume load administered , the cardiac activation or an osmotic effect since neither 0.9 nor 2.5 % saline result ed in comparable effects . Additional central nervous mechanisms must be considered for the increased ANH concentrations in lactate-induced panic attacks . We propose that the release of ANH is an intrinsic mechanism contributing to the apparent unresponsiveness of the pituitary-adrenocortical system in lactate-induced panic attacks . In addition , we surmise that ANH may also play a role in the yet unknown mechanisms for termination of panic attacks , e.g. either by inhibitory actions on the locus coeruleus or by bronchiorelaxation and consecutive decatastrophization Experiments design ed to establish the effects of video games on breathing patterns have led to contradictory results . Several authors reported that video games tended to increase breathing frequency ( i.e. to reduce breath duration ) , whereas others reported the opposite . We postulated that video games contain different psychophysiological components which may have opposite effects on breathing pattern . On the one h and , arousal and emotion may tend to stimulate breathing . On the other , focusing attention on the game may prompt subject to inhibit any movement -- including breathing -- which might be a potential nuisance variable . The aim of this study was to assess the specific effects of the attentional load in an experimental environment characterized by its low emotional impact . We measured breathing variables , cardiac frequency and cortisol levels in 10 healthy children ( mean age = 9.2 + /- 1.5 years ) who were familiar with the environment , the experimenter and the video game .  Breath duration rose significantly , from 2.56 to 3.16 s , as a function of game difficulty . Cortisol levels , heart rate and the thoracic contribution to breathing displayed no significant changes . Taken together , these data suggest that focusing attention on the game tended to inhibit breathing and that previous contradictory reports in this respect were due to the confounding effects of emotion BACKGROUND Dysregulated respiratory control may play a role in the pathophysiology of panic disorder . This could be due to abnormalities in brain stem respiratory nuclei or to dysregulation at higher brain levels . Results from previous studies using the doxapram model of panic have yielded an unclear picture . A brief cognitive manipulation reduced doxapram-induced hyperventilation in patients , suggesting that higher level inputs can substantially alter their respiratory patterns . However , respiratory abnormalities persisted , including a striking irregularity in breathing patterns . METHODS To directly study respiratory irregularity , breath-by-breath records of tidal volume ( V(t ) ) and frequency ( f ) from previously studied subjects were obtained . Irregularity was quantified using von Neumann 's statistic and calculation of " sigh " frequency in 16 patients and 16 matched control subjects . Half of each group received a st and ard introduction to the study and half received a cognitive intervention design ed to reduce anxiety/distress responses to the doxapram injection . RESULTS Patients had significantly greater V(t ) irregularity relative to control subjects . Neither the cognitive intervention nor doxapram-induced hyperventilation produced significant changes in V(t ) irregularity . The V(t ) irregularity was attributable to a sighing pattern of breathing that was characteristic of panic patients but not control subjects . Patients also had somewhat elevated f irregularity relative to control subjects . CONCLUSIONS The irregular breathing patterns in panic patients appear to be intrinsic and stable , uninfluenced by induced hyperventilation or cognitive manipulation . Further study of V(t ) irregularity and sighs are warranted in efforts to localize dysregulated neural circuits in panic to brain stem or midbrain levels RATIONALE Psychologic factors are increasingly recognized to influence the onset and course of asthma . Previous cross-sectional community-based studies have provided evidence for a relatively specific association between asthma and panic . OBJECTIVES To examine concurrent and longitudinal associations between asthma and panic in young adults . MEASUREMENTS AND MAIN RESULTS Prospect i ve  community-based cohort study of young adults ( n = 591 ) followed between ages 19 and 40 . Information was derived from six subsequent semistructured diagnostic interviews conducted by professionals . Cross-sectionally ( over the whole study period ) , asthma was more strongly associated with panic disorder ( odds ratio [ OR ] = 4.0 ; 95 % confidence interval [ CI ] , 1.7 , 9.3 ) than with any panic , which included panic disorder and panic attacks ( OR = 2.1 ; 95 % CI , 1.1 , 4.5 ) . Longitudinally , after adjusting for potentially confounding variables , active asthma predicted subsequent panic disorder ( OR = 4.5 ; 95 % CI , 1.1 , 20.1 ) , and the presence of panic disorder predicted subsequent asthma activity ( OR = 6.3 ; 95 % CI , 2.8 , 14.0 ) . Asthma predicted any panic ( OR = 2.7 ; 95 % CI , 1.1 , 7.1 ) , whereas any panic did not predict subsequent asthma activity . Associations were stronger in smokers than in nonsmokers , and stronger in women than in men . Smoking , early-childhood anxiety , and a family history of allergy were important confounders of the asthma-panic association . CONCLUSIONS This is the first long-term follow-up study on asthma and panic . It showed dose-response-type relationships between panic and asthma , and bidirectional longitudinal associations between the two conditions . It provided evidence for familial factors and smoking as possible shared etiologic explanations Progesterone administration increase VE in man , but its effects on ventilatory response to hypercapnia and hypoxia have not been well documented . Accordingly , VE , HVR , and HCVR were measured during placebo and MPA administration in 11 normal men . The effect of MPA ( 20 mg orally q 8 hr for 32 hr ) on T degrees , metabolic rate ( VO2 and VCO2 ) was also determined . With MPA , T degrees , rose 0.4 degrees C + /- 0.0008 ( S.E.M. ) p less than 0.0001 ) , VE increased 0.46 + /- 0.16 L/min ( p less than 0.01 ) , and VO2 and VCO2 did not change significantly . HCVR ( measured under hyperoxic conditions during rebreathing ) increased significantly ( P less than 0.01 ) from 2.9 + /- 0.33 L/min/mm Hg ( placebo ) to 4.0 + /- 0.29 ( MPA ) . HVR was measured as the shape parameter A , so that when A increased , HVR was augmented . During MPA , HVR increased from A = 132 + /- 19.1 to 179 + /- 20.5 ( P less than 0.02 ) . We conclude that 60 mg of MPA daily in normal men increases VE and chemosensitivity as measured by the ventilatory response to hypercapnia and hypoxia The goals of this study were to a ) confirm prior evidence that the respiratory stimulant doxapram induces panic attacks and produces excessive hyperventilation in patients with panic disorder and b ) explore the impact of cognitive mediators on symptom and respiratory responses . Method : Thirty-two subjects ( 16 patients and 16 controls ) received doxapram ( 0.5 mg/kg ) and placebo infusions while symptom , respiratory , and heart rate responses were monitored . Subjects were r and omly assigned to receive either a st and ard introduction or a cognitive intervention design ed to reduce the panic responses of panic patients to laboratory challenges . Results : Doxapram was a potent and specific panicogenic agent , inducing panic in 75 % of patients and 12.5 % of controls . Compared with controls , patients also showed a greater decrease in end tidal carbon dioxide ( CO2 ) and greater increases in minute ventilation , respiratory frequency , and heart rate . The cognitive intervention substantially attenuated the excessive hyperventilatory response of patients but did not fully normalize their breathing patterns . Tidal volume was the only respiratory measure not significantly altered by the cognitive intervention . Conclusions : In patients with panic disorder , doxagram ( 0.5 mg/kg ) triggers panic attacks about as potently as 7 % CO2 and more potently than 5 % CO2 or lactate . Psychological factors can modulate the appearance of ventilatory abnormalities in panic patients , but persistent respiratory disturbances were still seen . Psychological factors and respiratory physiology both appear to be important phenomena in laboratory panic OBJECTIVE The authors assessed the substance and diagnostic specificity of carbon-dioxide-induced panic since , in addition to the specific biochemical effects of inhaled carbon dioxide ( CO2 ) , simple physiologic distress is also frequently implicated as a panicogenic factor during respiratory challenge studies with CO2 in patients with anxiety disorders . METHOD Eighteen patients with panic disorder , 20 with social phobia , and 23 psychiatrically normal subjects  inhaled a mixture of 35 % CO2 and 65 % O2 for 30 seconds through a face mask . They also breathed for 30 seconds through a valve reducing the diameter of the airway . A double-blind , counterbalanced , r and omized design was used . RESULTS In spite of important similarities between the two interventions , including the induction of equal amounts of subjective respiratory distress , carbon dioxide inhalation was significantly more potent than increased airway resistance in provoking panic in the anxiety disorder patients . The patients with panic disorder were significantly more sensitive to CO2  than were the patients with social phobia or the normal subjects . CONCLUSIONS Carbon dioxide inhalation appears to have a specific panicogenic effect in panic patients that goes beyond simple breathlessness BACKGROUND Disordered breathing among patients with panic disorder , including hyperventilation during attacks and increased anxiogenic response to carbon dioxide ( CO2 ) inhalation , is well established . We wished to assess whether there is a change in the physiological response to CO2 after patients have undergone antipanic therapy with either tricyclic antidepressants or cognitive behavioral therapy ( CBT ) . METHODS Twenty-nine patients with panic disorder underwent baseline CO2 sensitivity testing using the traditional Read rebreathing method and then received either antidepressant treatment ( n = 21 ) or CBT ( n = 8) . After completing treatment , CO2 testing was repeated . A comparison sample of 14 normal volunteers also had two CO2 sensitivity tests , separated by an average of 21.6 ( SD = 8.8 ) weeks . RESULTS Using a liberal st and ard , in which all CO2 sensitivity tests whose correlations between minute ventilation and end-tidal CO2 were at least .75 were used , patients , but not controls , demonstrated a significant reduction in CO2 sensitivity between the first and second test . Using a more conservative .90 correlation st and ard reduced the sample size available and result ed in trend reduction in patients but no significant change in controls . There was a suggestion that the change was most pronounced in treatment responders , although the number of patient nonresponders is extremely small in this sample . CONCLUSIONS These data indicate that treatment reduces CO2 sensitivity in patients with panic disorder . We speculate that manipulation of the serotonergic and noradrenergic neurotransmission systems , both known to play a role in the control of respiration , may have a specific effect in reducing respiratory hyperactivity in panic disorder Panic disorder ( PD ) and asthma share many common characteristics and have been found in epidemiological studies to be significantly comorbid . To investigate possible reasons for this overlapping , the authors evaluated 51 patients with asthma , assessing the prevalence of PD and sporadic panic attacks , the temporal relationship between these two disorders , and the familial risk for PD in the families of asthmatics . The results showed significantly higher prevalences of PD , sporadic panic attacks , and social phobia in asthmatics than those reported for the general population . In 9 ( 90 % ) of the asthmatics with PD , asthma appeared first . Finally , the morbidity risk for PD in families of asthmatics with PD ( 13.5 % ) was significantly higher than in families of asthmatics without evidence of panic ( 2 % ) . Our results suggest that the high prevalence of PD in asthmatics might be related to a facilitating effect of asthma on the development of PD in subjects with familial pre 
    Output:
    
RESULTS Lower pCO(2 ) levels in PD subjects are a consistent finding during the baseline/resting condition , the challenge , and recovery phases .
Tidal volume and minute volume are increased in PD subjects relative to controls during the baseline/resting condition .
However , the most robust finding is a higher than normal respiratory variability , which appears to be a promising factor for the identification of respiratory etiopathological pathways in PD .
Respiratory variability might be a c and i date for a biological marker of PD : an abnormal breathing pattern as found in panic disorder ( PD ) patients compared with controls might indicate instability of the respiratory homeostasis