Search PubMed⌕ Search

Biomedical subjects

H Kazemi

Publications and source records attributed to H Kazemi.

At least 109 records · Page 6Linked to original sources
PubMed1976

The CSF HCO3 increase in hypercapnia relationshp to HCO3, glutamate, glutamine and NH3 in brain.

To study the role of carbonic anhydrase in the CSF [HCO3] increase in respiratory acidosis and its effect on brain ammonia, anesthetized rats were subjected to hypercapnia (7% CO2) for 2 hours. The animals received periodic intraventricular injections of either 'mock' CSF or 'mock' CSF and acetazolamide for 45 minutes prior and during hypercapnia when: (a) plasma [HCO3-] was allowed to increase normally and (2) plasma [HCO3] increase was prevented by i.v. HC1 infusion, CSF [HCO3] increased 8.5 mM/L after 2 hours of hypercapnia (delta PCO2 40) in the rats with intraventricular 'mock' CSF injections, and only 6 mM/L in the animals with acetazolamide injections. CSF [HCO3-] increased 7 mM/L during hypercapnia and HCl infusion with intraventricular 'mock' CSF injections, but only 2 mM/L with acetazolamide injections. Changes in total brain CO2 (increase) and brain glutamic acid (decrease) in hypercapnia were not affected by intraventricular acetazolamide and i.v. HCl. The increase of brain NH4+ and glutamine in hypercapnia was reduced in these conditions. It is concluded that there are at least two sources for the CSF [HCO3-] increase in hypercapnia; one formed in the CNS and dependent on carbonic anhydrase, and the other derived from plasma [HCO3-] increase.

Acetazolamide↗
PubMed1976

Dual contribution theory of regulation of CSF HCO3 in respiratory acidosis.

Regulation of CSF HCO3-in respiratory acidosis was studied in light of the "dual contribution theory," which proposed that there were two sources for the CSF HCO3-increase: 1) HCO3-by diffusion from plasma and 2) HCO3-generated in the CNS and catalyzed by the local carbonic anhydrase (J. Appl. Physiol. 38: 504-512, 1975). In anesthetized dogs with an increase in Paco2 of 30 mmHg for 4 h the plasma HCO3 increased 2 meq/1 and CSF 6 meq/1. In combined respiratory and metabolic acidosis, plasma HCO3-did not increase but CSF HCO3-increased 6 meq/1. In combined acidosis and intraventricular injections of acetazolamide no increase in plasma or CSF HCO3-occurred. In combined respiratory acidosis and metabolic alkalosis and intraventricular acetazolamide, plasma HCO3-increased 15 meq/1 but CSF HCO3-increased 6 meq/1. Brain and CSF ammonia increased linearly and selectively with the increase in the relative contribution of CNS HCO3-increase. Therefore regulation of CSF HCO3-in respiratory acidosis depends on both components of the dual contribution theory, where each component can provide the total CSF HCO3-increase under appropriate experimental conditions. The control mechanism may be sensitive to changes in [H+] on the brain side of the blood-brain barrier.

Acid-Base Equilibrium↗
PubMed1976

Determinants of regional distribution of a bolus inhaled from residual volume.

The volume of lung at residual volume (RV) which fails to receive an inhaled tracer bolus (EXV) was quantitated in 13 normals by comparison of a scintigram of the distribution of a tracer bolus inhaled from RV (BORV) with a scintigram at RV of lung equilibrated with the tracer (EQRV). EXV was found in the dependent lung in the erect position in all subjects but also occurred to a lesser degree at the apex in 11 of 13 subjects. Basal EXV ranged from 1 to 7% of TLC, and unlike apical EXV increased with age (r= 0.91, P less than 0.01). EXV in the decubitus position shifted largely to the dependent lung with none remaining in the original erect apical and basal locations, demonstrating that gravity determined EXV location. Nitrous oxide, which is highly diffusible, failed in four subjects to carry the tracer to basal EXV even though perfusion was documented to persist to this area, implying basal EXV airways were closed, not narrowed. In one of the four subjects apical EXV was readily definable. Nitrous oxide carried tracer into this region, implying patent apical EXV airways.

Adolescent↗
PubMed1976

Presence of a bradykinin-like substance in pulmonary washings.

Pulmonary washings were studied for the presence of bradykinin-like substances and the capacity for their formation and degradation. Bronchopulmonary lavage with saline was performed in anesthetized, exsanguinated Syrian golden hamsters with a cell yield of 99 per cent alveolar macrophages. In the presence of inhibitors of both kinin formation (hexadimethrine) and destruction (1,10-phenanthroline), immunoreactive kinin was found in bronchopulmonary lavage fluid (12.5 ng per 5 x 10(6) cells lavaged), washings of pooled macrophages (5.62 ng per 5 x 10(6) cells washed), and lysates of alveolar macrophages (3.97 ng per 5 x 10(6) cells lysed). Higher kinin concentrations were obtained by selective inhibition of kinin-destroying enzymes with phenanthroline. Inhibition of kinin formation with hexadimethrine alone rendered nearly all concentrations below the limit of detectability. These findings demonstrated that the capacity for kinin formation and degradation exists in pulmonary washings. The precise origin of this kinin and its forming and destroying enzymes (whether from the pulmonary alveolar macrophage, other sites in the bronchopulmonary tree, or plasma) is not yet known.

Animals↗
PubMed1975

Role of histamine in the hypoxic vascular response of the lung.

The lung vasculature responds to alveolar hypoxia by constriction and when the hypoxia is localized to one region of the lung, vasoconstriction is also localized to that region. Histamine has been alleged to have a role in the vasoconstrictor response with generalized alveolar and thus systemic hypoxia, but the role for histamine is not clear in localized alveolar hypoxia. Studies were, therefore, undertaken to determine the contribution of histamine to the localized pulmonary vasoconstrictor response to hypoxia. A divided tracheal cannula was used in anesthetized dogs which allowed for ventilation of one lung with oxygen to maintain normal systemic oxygenation (mean PaO2 =73 mm Hg) while the other lung was ventilated with nitrogen as an alveolar hypoxic stimulus. Perfusion to each lung was determined with the 133Xe technique utilizing external counters over the chest. Perfusion (Q) was decreased by 32% (P = 0.002) to the hypoxic lung after 10 minutes of unilateral nitrogen breathing. After intravenous infusion of 20 mg of chlorpheniramine maleate, a potent antihistamine, the decrease in Q to the hypoxic lung was unchanged at 30%. After 40-100 mg chlorpheniramine the decrease in perfusion was again unchanged at 34%. Therefore a significant role was not demonstrated for histamine in the regional pulmonary vasoconstrictor response to alveolar hypoxia in the absence of systemic hypoxemia.

Animals↗
PubMed1975

CSF bicarbonate regulation in respiratory acidosis and alkalosis.

CSF bicarbonate regulation was studied in respiratory acidosis and alkalosis of 4h duration in antsthetized dogs. PCO2, pH, HCO3, ammonia, and lactate in CSF and arterial and safittal sinus bloof were measured when equal volumes of saline or acetazolamide (8 mg) were injected into lateral cerebral ventricles. The brain CO2 dissociation curve was determined at the end of all experiments. CSF and arterial bicarbonate increased 11.8 and 5.9 meg/l, respectively, in acidosis. Acetazolamide limited the rise in CSF bicarbonate to 4.2 meg/l, and prevented the CSF bicarbonate increase associated with hyperammonemia. During alkalosis CSF bicarbonate fell 6.5 meg/l and CSF lactate increased almost 2 meg/l while arterial bicarbonate fell 5.7 meg/l and lactate remained unchanged. Thus plasma bicarbonate changes account for some of the CSF unchanged. Thus plasma bicarbonate changes account for some of the CSF bicarbonate alterations in respiratory acid-base-disturbances. In acidosis additional CSF bicarbonate is formed by the choroid plexus and glial cells on the inner and outer surfaces of the brain--a reaction catalyzed by the locally present carbonic anhydrase. In alkalosis the greater fall in CSF bicarbonate than blood is due to selective brain and CSF lactic acidosis.

Acetazolamide↗
PubMed1975

Strength of pulmonary vascular response to regional alveolar hypoxia.

Regional alveolar hypoxia in the lung induces regional pulmonary vasoconstriction which diverts blood flow from the hypoxic area. However, the predominant determinant of the distribution of perfusion in the normal erect lung is gravity so that more perfusion occurs at the base than at the apex. To determine the strength of the regional alveolar hypoxic response in diverting flow with or against the gravity gradient a divided tracheal cannula was placed in anesthetized dogs and unilateral alveolar hypoxia created by venilating one lung with nitrogen while ventilating the other lung with oxygen to preserve normal systemic oxygentation. Scintigrams of the distribution of perfusion obtained with intravenous 13-N and the MGH positron camera revealed a 34 and 32 per cent decrease in perfusion to the hypoxic lung in the supine and erect positions and a 26 per cent decrease in the decubitus position with the hypoxic lung dependent (P equal to 0.94 from supine shift), indicating nearly equal vasoconstriction with shift of perfusion away from the hypoxic lung in all positions. Analysis of regional shifts in perfusion revealed an equal vasoconstrictor response from apex to base in the supine position but a greater response in the lower lung zones in the erect position where perfusion was also greatest.

Animals↗
PubMed1975

Response to exercise in upper airway obstruction.

Mild excerice in 7 patients with upper airway obstruction but without diffuse lung disease caused a mean decrease in arterial oxygen tension of 11 mm Hg. Exercise hypoxemia disappeared after surgical removal of obstruction in 3 patients tested. Exercise hypoxemia due to relative alveolar hypoventilation was observed in 4 normal subjects with external combined inspiratory and expiratory resistance. Analysis of mechanics of air flow through an orifice suggests that exertional dyspnea is caused by manifold increase of airway resistance during exercise; acute respiratory failure might be precipitated by further minimal reduction in airway lumen once it has reached a diameter of 8 mm. Clinicians should be alert to the possibility of upper airway obstruction in any symptomatic patient who has had tracheal intubation or in patients with obscure wheezing, especially on exercise.

Adult↗
PubMed1975

Interstitial lung disease resistant to corticosteroid therapy. Report of three cases treated with azathioprine or cyclophosphamide.

Three patients with severe progressive interstitial lung disease refractory to steroid therapy were treated with immunosuppressive drugs. Biopsy material of one showed mainly fibrosis, while that of the second showed interstitial pneumonitis as well; both patients received azathioprine. Cyclophosphamide was employed in the third patient with systemic vasculitis and massive hemoptysis. All patients had reduced lung volumes and abnormal gas exchange, which continued to worsen on high doses of steroids. In patients 1 and 2, there was long-term stabilization of lung function, while pulmonary physiologic abnormalities in the patient with vasculitis reverted to normal on five months of cyclophosphamide. Although the etiology of most forms of interstitial lung disease is unknown, several reports suggest at least a partial immunologic basis. Abatement in progression of disease in this small series would suggest that a trial of immunosuppressive drugs be considered in interstitial lung disease when steroid therapy fails.

Adult↗