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PubMed2006

Diagnostic studies in patients with acute respiratory distress syndrome.

Acute respiratory distress syndrome (ARDS) is a clinical-radiological diagnosis. Clinical diagnosis comprises severe hypoxemia assessed by arterial oxygen tension/fraction of inspired oxygen ratio of less than 200 and bilateral infiltrate on a chest radiograph in the absence of left atrial hypertension. The sensitivity and specificity of the clinical diagnosis vary based on the underlying etiology for ARDS. Except for presence of bilateral infiltrate on chest radiograph and severe hypoxemia on arterial blood gas, most diagnostic studies are used to exclude mimics of ARDS and potentially modify treatment. Computerized tomography of the chest is helpful in understanding the extent of the disease and is more sensitive in identifying pneumomediastinum and pneumothoraces seen frequently in patients with ARDS, which can be missed on a chest radiograph, especially if they are small in size. Measurements of alveolar dead space ventilation fraction can be helpful in determining the prognosis in individuals with ARDS. Bronchoalveolar lavage, transbronchial lung biopsy, and open lung biopsies can be safely performed in patients with ARDS. Bronchoalveolar lavage fluid in patients with ARDS shows neutrophil predominance with increased edema fluid to serum protein ratio. Diffuse alveolar damage, a pathognomic of ARDS, is seen on histopathology on transbronchial lung biopsy or open lung biopsy. Most common complications of these procedures include transient hypoxemia, respiratory acidosis, and pneumothorax with occasional persistent air leak. The potential risk of diagnostic studies should be balanced against the possible foreseeable benefits of the diagnostic studies.

Biopsy↗
PubMed1987

Roles of gill and red cell carbonic anhydrase in elasmobranch HCO3- and CO2 excretion.

We studied the roles of gill and erythrocyte carbonic anhydrase in normal CO2 transfer (metabolic CO2 elimination) and in HCO3- excretion during metabolic alkalosis in the resting and swimming dogfish shark, Squalus acanthias. Gill carbonic anhydrase was selectively inhibited (greater than 98.5%) by 1 mg/kg benzolamide, which caused no physiologically significant red cell carbonic anhydrase inhibition (approximately 40%). Enzyme in both tissues was inhibited by 30 mg/kg methazolamide (greater than 99%). Both drugs caused equivalent reductions in HCO3- excretion following an infusion of 9 mmol/kg NaHCO3 as measured by the rate of fall in plasma HCO3- and by transfer into seawater. Methazolamide (red cell and gill carbonic anhydrase inhibition) caused a respiratory acidosis in fish with normal acid-base status, whereas benzolamide (gill carbonic anhydrase inhibition) did not. The only effect observed with benzolamide in these fish was a small elevation in plasma HCO3-. These findings, taken together, suggest that red cell carbonic anhydrase is required for normal metabolic CO2 elimination by the gill. Although carbonic anhydrase is located in the respiratory epithelium, it appears to have no quantitative role in transfer of metabolic CO2 to the environment, a pattern similar to all terrestrial vertebrates. However, carbonic anhydrase in the gill is crucial to this organ's function in acid-base regulation, both in the excretion of H+ or HCO3- generated in normal metabolism and in various acid-base disturbances.

Acid-Base Equilibrium↗
PubMed1975

Changes in intracranial pressure and brain hydration during acute ethanolism.

Intracranial hypertension and brain hydration were scrutinized during acute ethanolism for consideration in the combined head injury setting. Intraventricular pressures and whole brain water levels rose with moderate or high ethanol dosages. The most prominent alterations were associated with respiratory acidosis and hypoxia; less marked changes were found in their absence and point to a second mechanism. Elevated central venous pressures appeared as well in some instances to constitute a third action. It is accordingly suggested that ethanol may add significantly to the combined pathology with associated acute head injury in several ways. These include: contributions to edema formation, to respiratory depression, and to alterations in local hemodyamics.

Alcoholic Intoxication↗
PubMed2000

Tromethamine buffer modifies the depressant effect of permissive hypercapnia on myocardial contractility in patients with acute respiratory distress syndrome.

In patients with acute respiratory distress syndrome (ARDS), permissive hypercapnia is a strategy to decrease airway pressures to prevent ventilator-induced lung damage by lowering tidal volumes and tolerating higher arterial carbon dioxide tension. However, in experimental studies hypercapnia impairs myocardial contractility and hemodynamic function. We investigated the effect of short-term permissive hypercapnia on myocardial contractility and hemodynamics in patients with ARDS. We hypothesized that the administration of tromethamine (THAM), a buffer which does not increase carbon dioxide production, would modify these changes. In 12 patients with ARDS, permissive hypercapnia was implemented for 2 h with a target Pa(CO(2))of 80 mm Hg. Patients were randomized to have respiratory acidosis corrected by THAM (pH-corrected group), or not corrected (pH-uncorrected group). Hemodynamic responses were measured, and transesophageal echocardiography (TEE) was used to determine myocardial contractility. Permissive hypercapnia resulted in significant decreases in systemic vascular resistance (SVR) and increases in cardiac output (Q). Myocardial contractility decreased in both groups but significantly less in the pH-corrected group (approximately 10%) than in the pH-uncorrected group (approximately 18%, p < 0.05). Mean arterial pressure decreased and mean pulmonary arterial pressure increased significantly only in the pH-uncorrected group. All values returned to baseline conditions 1 h after permissive hypercapnia was terminated. Our study demonstrates a reversible depression of myocardial contractility and hemodynamic alterations during rapid permissive hypercapnia which were attenuated by buffering with THAM. This may have applicability to the clinical strategy of permissive hypercapnia and allow the benefit of decreased airway pressures to be realized while minimizing the adverse hemodynamic effects of hypercapnic acidosis.

Acid-Base Equilibrium↗
PubMed1986

Reversible depression of ventilation and cardiovascular function by ventriculocisternal perfusion with gamma-aminobutyric acid in dogs.

Gamma-aminobutyric acid (GABA) is a putative central neurotransmitter that depresses respiratory neurons and has a metabolism in the brain that is tied to CO2 fixation and H+ metabolism. Therefore, the effect of 3 concentrations of GABA (10, 30, and 50 mM) in different groups of pentobarbital-anesthetized dogs was investigated by ventriculocisternal perfusion for 15 to 45 min. During multiple perfusion sequences, tidal volume (VT) and respiratory frequency were recorded continuously, whereas heart rate (HR), mean systemic arterial pressure (Psa), cardiac output, mean pulmonary arterial pressure, and pulmonary capillary wedge pressure were monitored periodically. Minute ventilation decreased by a reduction in VT. The mean VT (+/- SEM) decreased after 15 min of GABA perfusion from 365.9 +/- 19.5 to 151.0 +/- 15.0 ml with 50 mM GABA in mock CSF, from 272.8 +/- 25.1 to 110.6 +/- 7.4 with 30 mM GABA, and from 223.6 +/- 22.3 to 155.3 +/- 21.8 with 10 mM GABA. A decrease in mean inspiratory flow was associated with the reduction in VT. The decrease in ventilation was associated with respiratory acidosis. At each GABA concentration, mean Psa decreased, whereas HR fell only with 50 mM. Other cardiovascular parameters did not change. Perfusion with mock CSF alone restored cardiorespiratory depression caused by GABA. Mean Psa fell with GABA whether ventilation was kept constant mechanically or not. These results support the hypothesis of a GABA-sensitive mechanism via a population of receptors that affect respiratory and cardiovascular function and are accessible by ventriculocisternal perfusion.

Animals↗
PubMedDate not supplied

[Respiratory form of onset of motor neuron disease].

OBJECTIVE: To present a case of respiratory failure as the form of onset of amyotrophic lateral sclerosis, to review the main clinical findings, data of the investigations done which suggest the presence of this disorder and describe its therapeutic management. CLINICAL CASE: A 68 year old man presented with a subacute illness characterized by a sleep disorder with sleep fragmentation, snoring of increasing intensity, without clear pauses of apnea, progressive diurnal hypersomnia accompanied by progressive dyspnea followed by respiratory failure with respiratory acidosis and difficulty in manipulating things with his hands. Diagnostic investigations showed a restrictive pattern without pulmonary fibrosis, due to paralysis of the diaphragm, and the presence of electromyographic signs compatible with motorneuron disease. The patient was treated with riluzole 100 mg/day and non-invasive mechanical ventilation and maintained an acceptable quality of life. CONCLUSIONS: Motorneuron disease may start with acute or progressive respiratory failure without a clear etiological cause and may appear to be similar to obstructive sleep apnea syndrome. The treatment of choice for this respiratory problem is non-invasive mechanical ventilation. Absence of symptoms of bulbar involvement is essential for a favourable prognosis.

Acute Disease↗
PubMed2004

[Sivelestat sodium hydrate was effective for ARDS in a patient suffering from chronic rheumatoid arthritis with acute exacerbation after failing to respond to high dose steroid pulse therapy].

Sivelestat sodium hydrate (ELASPOL) was effective for ARDS in a fifty-year-old female patient suffering from chronic rheumatoid arthritis with acute exacerbation, after failing to respond to high dose steroid pulse therapy. In ICU, the patient had bilateral lung opacities, especially of the upper lobes, respiratory acidosis, hypercapnea (PaCO2 89 mmHg), and poor oxygenation (P/F ratio 193). High dose steroid pulse therapy had been performed, but oxygenation was not improved, and a low level of oxygenation (P/F ratio 155) persisted. Sivelestat was started two days after finishing the steroid pulse therapy. The butterfly shadow on chest X ray and impaired oxygenation were markedly improved from the third day of sivelestat administration. Respiratory support was terminated with P/F ratio 300. Plasma concentrations of SP-A and SP-D decreased after sivelestat administration, but concentration of KL-6 was still elevated. In this case, sivelestat was effective for ARDS in the patient not responding to steroid pulse therapy, and clinical finding and plasma concentrations of SP-A and SP-D were correlated well.

Antigens↗
PubMed2001

Neurophysiological changes in COPD patients with chronic respiratory insufficiency.

Chronic hypoxemia is known to cause peripheral neuropathy (PNP) in chronic obstructive pulmonary disease (COPD) patients. We aimed to know how often PNP is encountered in such patients and the changes in the central nervous system (CNS) if any. We enrolled 32 patients (30 M, 2 F; mean age +/- SD: 61.5 +/- 8.8 years) with COPD into the study. PaO2 > or = 55 mmHg was considered as the cut-off value designating tissue hypoxia. According to this cut-off value the subjects were divided into two groups: Group I, n: 19, PaO2 < 55 mmHg and Group II, n: 13, PaO2 > or = 55 mmHg. All subjects were evaluated with motor and sensory nerve conduction studies (MNCV and SNCV, respectively), electromyography, visual and brainstem evoked potentials (VER and BAER, respectively). We detected PNP in 93.8% of the study subjects. Distal latency of sural nerve correlated significantly with cigarette consumption and reduction in PEFR. SNCV of median nerve was reduced as PaCO2 was elevated and pH was lowered. BAER wave III latency showed significant inverse correlation with PEFR, FEF25 and FEF25-75. Interpeak latency (IPL) of BAER I-III was also significantly and inversely correlated with FEV1/FVC and FEF25-75. IPL of BAER III-V too showed significant correlations with PaCO2, HCO3- and pH of the arterial blood. As BAER III and IPLs of it represent the pontomedullary portion of the brain, cigarette smoking and airways obstruction may not only cause peripheral neuropathy but also a delay in evoked responses of the brain stem by inducing chronic hypercapnia and respiratory acidosis in patients with COPD.

Aged↗
PubMed1990

[Effects of lidocaine cervical epidural blockade on respiratory function].

Cervical epidural anesthesia with 2% lidocaine has been shown to reduce ventilatory capacity in patients with normal lungs by Dr. Bromage. It is important to evaluate the respiratory effect of this technique which may induce intercostal and phrenic nerve paralysis. After institutional approval and informed content had been obtained, 50 patients undergoing OR & IR of upper limbs, mean age 24 +/- 4 yrs mean weight 65 +/- 6 kg, ASA status I-II without preoperative pulmonary dysfunction were studied. C7-T1 intervertebral space was identified by the hanging-drop technique using a 16G Tuochy needle. A catheter was inserted cranially to a distance of 12 cm. Pulmonary function measurement and arterial blood gas data were obtained before and 20', 50', 105' min after injection of 12 ml 2% plain lidocaine. The anesthesia levels were between C3-T3 and obtained at 13 +/- 2 min. Mean arterial blood gas analysis showed mild respiratory acidosis at 20 min (PaCO2: 46.0 +/- 3.5 mmHg). The measured values of IVC, VC, FVC, FEV1, PEF, when compared with control values were decreased over 15.60% of control values and 20% of predicted data at 20 min. The ratio of FEV1/VC, FEV1/FVC were still within normal limit (greater than 80%). The result was significantly compatible to the criteria of mild type of pulmonary function test. No respiratory distress was complained of and only cause little change of arterial blood gas.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

[Comparative studies on premedication and general anesthesia for endoscopies of the upper airways].

Cardiovascular disorders during endoscopy of the upper respiratory tract have since long induced anaesthetists and laryngologists to find a suitable anaesthetic procedure. It was the purpose of the present study to determine the influence exerted by different kinds of premedication and different modes of anaesthesia on the cardiovascular system, pO2, and the acid-base status. The results obtained show that a hypertensive-tachycardiac response to direct laryngo-tracheoscopy could not be prevented in any of the groups under investigation. Lowest blood pressure and heart rate increases were seen in those groups of patients which received an analgetic drug (Fentanyl or nitrous oxide) in addition to hexobarbital. During endoscopy, respiratory acidosis occurred in five groups of patients. All patients were sufficiently oxygenated.

Acid-Base Equilibrium↗
PubMed1972

Effect of acid-base alterations on hepatic lactate utilization.

1. The effect of acid-base changes on hepatic lactate utilization was investigated in anaesthetized, mechanically ventilated dogs.2. Portal vein flow and hepatic artery flow were measured with electromagnetic flowmeters, lactate concentration of portal vein, arterial and mixed hepatic venous blood was determined by an enzymatic technique, and hepatic lactate uptake was calculated using the Fick principle.3. Respiratory alkalosis (Delta pH 0.25 +/- 0.02) in four dogs resulted in a significant fall in total hepatic blood flow (-22 +/- 4%) and a significant rise in both arterial lactate concentration (2.18 +/- 0.32 m-mole/l.) and hepatic lactate utilization (3.9 +/- 1.2 mumole/min.kg).4. 0.6 M-Tris buffer infusion (Delta pH 0.21 +/- 0.02) in four dogs produced no significant changes in liver blood flow, arterial lactate concentration or hepatic lactate uptake.5. Respiratory acidosis (Delta pH -0.20 +/- 0.03) in six dogs and metabolic acidosis (Delta pH -0.20 +/- 0.02) in four dogs produced no significant changes in liver blood flow, decreases in arterial lactate concentration of 0.38 +/- 0.09 m-mole/l. (P < 0.05) and 0.13 +/- 0.13 m-mole/l., respectively, and no significant changes in hepatic lactate uptake.6. A significant correlation (r = 0.63; P < 0.01) was found between hepatic lactate utilization and arterial lactate concentration during the hyperlactataemia associated with respiratory alkalosis.7. Hyperlactataemia induced in four dogs by infusion of buffered sodium lactate (Delta pH 0.05 +/- 0.01;% Delta liver blood flow 29 +/- 7%) was also significantly correlated with hepatic lactate utilization (r = 0.70; P < 0.01) and the slope of the regression was similar to that during respiratory alkalosis.8. These data suggest that the hyperlactataemia of alkalosis is not due to impaired hepatic utilization of lactate and that the principal determinant of hepatic lactate uptake during alkalosis or lactate infusion is blood lactate concentration, rather than liver blood flow or acid-base status.

Acid-Base Equilibrium↗
PubMed2006

Ventilatory roll off during sustained hypercapnia is gender specific in pekin ducks.

The objective of the present study was to examine the relative roles of peripheral versus central mechanisms in producing ventilatory adjustments in pekin ducks during prolonged (5 h) hypercapnia (5% inspired CO2), and to determine whether these adjustments differed between male and female ducks. After 20 min of CO2 exposure, intact ducks increased total ventilation (VE) 2.5-3-fold above control values, due to large increases (approximately 200%) in tidal volume (VT) and slightly smaller increases (approximately 140%) in breathing frequency (fR). This response was accompanied by respiratory acidosis (pHa fell from approximately 7.46 to approximately 7.41) and hypercapnia (PaCO2 increased from approximately 35 to approximately 40 Torr). In males, VE fell progressively thereafter due exclusively to a fall in fR, in parallel with a rapid partial recovery of pH (to 7.44) while PaCO2 continued to climb (to approximately 42 Torr). In females, VE remained elevated during hypercapnia, and no pH recovery occurred. This suggests that a respiratory decline resulting from acid-base compensation (probably due to HCO3- mobilization) occurred in males but not in females. Bicarbonate mobilization, and thus pH compensation, may have been reduced in females due to the CaCO3 requirements of eggshell formation. In males, the acute ventilatory response was reduced slightly by denervation of the carotid bodies or intrapulmonary chemoreceptors, but there was no effect of denervation of either receptor group on the responses to prolonged CO2. We conclude that pH compensation triggered by constant or increasing PaCO2, acting at central chemoreceptors, likely mediates the respiratory adjustments seen in male pekin ducks during hypercapnia. Furthermore, we suggest that this ventilatory response be considered a gender-specific hypercapnic ventilatory roll off, in the context of the various time domains of the hypercapnic ventilatory response.

Adaptation, Physiological↗
PubMed2002

Pathogenesis of CO(2) pneumoperitoneum-induced metabolic hypoxemia in a rabbit model.

STUDY OBJECTIVE: To investigate the effects of carbon dioxide (CO(2)) pneumoperitoneum-induced changes in blood gases, acid-base balance, and oxygen homeostasis in rabbits. DESIGN: Prospective, randomized, controlled study (Canadian Task Force classification I). SETTING: University training and teaching center. SUBJECTS: Twenty-six adult female New Zealand white rabbits. INTERVENTION: Anesthesia and pneumoperitoneum. MEASUREMENTS AND MAIN RESULTS: In anesthetized rabbits arterial blood gases, acid-base balance, oxygenation values, and lactate concentrations were assayed during 2 hours. Spontaneous breathing, superficial and optimal ventilation without pneumoperitoneum, and with pneumoperitoneum at low (6 mm Hg) and higher (10 mm Hg) insufflation pressures were compared. The CO(2) pneumoperitoneum profoundly affected blood gases, acid-base balance, and oxygen homeostasis. Carboxemia with increasing end-tidal CO(2) and partial pressure of CO(2) (p <0.001), acidosis with decreasing pH (p <0.001), and base deficiency with decreasing actual base excess (p <0.001), standard base excess and standard bicarbonate and acid excess with increasing hydrogen bicarbonate (p <0.05 and <0.01) were found. Desaturation (p <0.01) with decreasing oxyhemoglobin p <0.05) and hemoglobin oxygen affinity (p <0.01) were also found. Carboxemia with acidosis was more pronounced with higher (p <0.01) than with lower (p >0.05) intraperitoneal pressures, and also with spontaneous breathing (p <0.05) and superficial ventilation (p <0.001) than with optimal ventilation, resulting in metabolic hypoxemia. CONCLUSION: In superficially ventilated and spontaneously breathing rabbits, CO(2) pneumoperitoneum profoundly affected blood gases, acid-base balance, and oxygen homeostasis, resulting in metabolic hypoxemia. With optimal ventilation and low intraperitoneal pressure carboxemia, respiratory acidosis, and changes in oxygen metabolism were minimal.

Acid-Base Equilibrium↗
PubMed1985

Selective acidosis in venous blood during human cardiopulmonary resuscitation: a preliminary report.

During experimental CPR, a marked venoarterial gradient in PCO2 has been reported. This is accompanied by a disproportionate decrease in venous pH and a simultaneous increase in arterial pH. This study includes a case report of human CPR in which simultaneous arterial and mixed venous blood gases were obtained before and after cardiac arrest. Similar venoarterial PCO2 gradients were observed subsequently in six additional patients during arrest. These clinical data indicate that arterial blood gases fail to reflect striking increases in venous PCO2 and decreases in pH due to respiratory acidosis on the venous side of the circulation.

Acidosis↗
PubMed1999

Endothelial cell changes are associated with pulmonary edema and respiratory distress in mice infected with the WA1 human Babesia parasite.

A C3H/HeN mouse model was established to study the pathogenesis of the human babesial parasites, WA1 and Babesia microti. To evaluate the course of parasitemia and the associated lesions, mice were inoculated intraperitoneally with either WA1-infected, B. microti-infected, or uninfected hamster red blood cells. WA1-infected mice developed dyspnea and moderate parasitemias, after which death occurred. Babesia microti-infected mice experienced low parasitemias with no apparent morbidity or mortality. WA1-infected mice were thrombocytopenic but not anemic. Hemograms for B. microti-infected mice were similar to controls. Postmortem examination of WA1-infected mice revealed prominent lesions in the lungs, including pulmonary edema and intravascular margination of leukocytes. No pulmonary changes were detected in B. microti-infected mice. Blood gas measurements of WA1-infected mice showed reduced oxygen saturation and pH, and increased carbonic acid compared to controls, indicating hypoxia and respiratory acidosis. Ultrastructure studies of WA1-infected lungs showed hypertrophied endothelial cells containing transcellular channels associated with protein-rich intra-alveolar fluid. Endothelial cell activation was demonstrated by an upregulation of intercellular adhesion molecule-1 in the lungs of WA1-infected mice. The results suggest that recruitment of inflammatory cells to the lungs in WA1-infected mice induces endothelial cell alterations, leading to pulmonary edema and acute respiratory failure.

Animals↗
PubMedDate not supplied

Opiate receptors and cardiovascular control in conscious SHR and WKY rats.

This study examined the cardiovascular, respiratory, and sympathetic effects of selective mu and delta opioid agonists microinjected into the hypothalamic nucleus preopticus medialis (POM) of conscious SHR and WKY rats. The mu receptor agonist D-Ala2-MePhe4-Gly5-ol-enkephalin (DAGO) at a dose of 0.6 or 6.0 nanomoles (Nmol) increased the blood pressure and heart rate in WKY rats. In SHR rats, the lower dose of DAGO similarly had a pressor effect whereas the higher dose was depressor; heart rat was increased only by the 6.0 nmol dose in these animals. In both SHR and WKY rats, this opioid caused respiratory acidosis and elevation of plasma norepinephrine (NE) and epinephrine (E); plasma vasopressin was reduced by the higher dose of DAGO. All of these effects of the mu agonist were reversed by the opiate receptor antagonist naloxone (0.5 mg/kg, i.a.). The delta opiate-receptor agonist D-Ala2-D-leu5-eukephalin at a dose of 6.0 or 20.0 nmol increased blood pressure and heart rate in both SHR and WKY rats without affecting respiratory variables. Plasma NE and EPI were elevated at the peak of the pressor period. These studies suggest that the anteroventral hypothalamic region may be an important site in central autonomic regulation by opioid peptides. The mu-receptor agonist was more potent than the delta agonist in eliciting cardiovascular and respiratory effects and associated sympatho-adrenomedullary activation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

[Severe hypophosphatemia in intensive care].

Phosphorus plays an essential role in cellular metabolism, especially in the oxidative phosphorylation process and in the synthesis of 2-3 DPG and membrane phospholipids. Moreover phosphorus is necessary as a buffer, mainly when the organism's principal buffer, the H2CO3/HCO3- system, is working at maximal rate. The authors describe a case of severe hypophosphatemia in a ICU patient with a mixed disorder of the acid-base balance. C.P., a woman, aged 71, obese (IBW 145%), at admission in ICU showed increasing dyspnea, hypoxemia and acidosis. Besides alkaline drugs a Venturi mask with FiO2 = 0.3 alternated to CPAP cycles (7 cm H2O) with facial mask applied. Bading on CVP, MAP and ABG results, a pharmacologic therapy with enoximone, furosemide, bronchodilators, mucolytics, antacids, antibiotics and inotropics was performed. TPN with only essential amino acids was performed, in order to activate lipolysis and ketogenesis; but the ABG showed over again mixed disorder of acid-base balance (metabolic and chronic respiratory acidosis), only partially leading to ketogenesis. The reduction of the hematic HCO3-, without changes of PaCO2, was justified by the blood lactic acid of 6.2 mmol/L. And what about blood lactic acid increase? During patient hospitalization, the hematic phosphorus had decreased to, 0.8 mg/dl. Diuretic therapy together with acidosis tamponage, and reduced phosphorus feed had been responsible of severe hypo-phosphatemia. Therapy adjustments brought the phosphatemia to normal values and to a substantial improvement of clinical conditions.

Aged↗