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Biomedical subjects

H Kazemi

Publications and source records attributed to H Kazemi.

At least 91 records · Page 5Linked to original sources
PubMed1980

CSF bicarbonate regulation in metabolic acidosis: role of HCO3- formation in CNS.

In metabolic acidosis, cerebrospinal fluid bicarbonate content (CSF [HCO3-]) falls in parallel with reductions in CSF CO2 tension (PCO2), and the fall is minimal with isocapnia. Regulation of CSF HCO3- was therefore investigated during 6 h of isocapnic metabolic acidosis in dogs. One group received intraventricular injections of acetazolamide to inhibit the centrally located carbonic anhydrase, essential in central nervous system (CNS) HCO3- formation, while the control group received intraventricular saline. Plasma [HCO3-] was reduced by 10 meq/l with iv infusion of 0.2 N HCl. CSF [HCO3-] fell in the control group from 22.8 to 17.7 meq/l at 6 h, whereas in the acetazolamide group it fell from 22.9 to 13.0 meq/l. Brain ammonia content was 1,286 +/- 153 microgram/100 g in the controls and 666.2 +/- 103 microgram/100 g in the acetazolamide-treated group at 6 h. Therefore, some reduction in CSF [HCO3-] occurred during 6 h of isocapnic metabolic acidosis along the chemical concentration gradient between CSF and blood, but further falls, in CSF [HCO3-] were minimized by de novo, carbonic anhydrase-dependent HCO3- formation within the CNS. Some of H+ formed were buffered by the increase in brain ammonia. These central mechanisms contribute to local CNS H+ homeostasis in metabolic acidosis.

Acetazolamide↗
PubMed1979

Role of PCO2 as determinant of CSF [HCO-3] in metabolic acidosis.

To study regulation of CSF [HCO-3] in metabolic acidosis and in particular the role of CSF PCO2 in establishing CSF bicarbonate level, acute metabolic acidosis was induced by the intravenous infusion of HCl in three groups of anesthetized dogs for six hours when PaCO2 was changed at different rates. Plasma [HCO-3] was lowered to 12 +/- 2 meq/L within one hour and maintained at that level thereafter in all groups. (I) Seven dogs were kept isocapnic while metabolic acidosis was induced. The cisternal CSF [HCO-3] fell by only 2.6 meq/L after six hours and was not significantly different from control. (II) In 11 dogs metabolic acidosis was induced while the dogs breathed spontaneously. There was a gradual drop in PaCO2 accompanied by a similar drop in CSF PCO2 of 14.5 torr. CSF [HCO-3] fell significantly by 6.1 meq/L at 6 hours and in parallel with the fall in CSF PCO2. (III) In order to show interdependence of the rate of fall in CSF [HCO-3] with rate of fall in cisternal PCO2 six dogs were mechanically hyperventilated and PaCO2 reduced to 21 torr rapidly and maintained there for six hours. CSF PCO2 followed PaCO. CSF bicarbonate fell rapidly and by 5 meq/L. In groups II and III the fall in cisternal [HCO-3] paralleled the drop in PCO2. Therefore, in metabolic acidosis the rate of the fall in cisternal bicarbonate appears to be a function of the rate of fall in CSF PCO2. It is speculated that the coupling of CSF [HCO-3] reduction in metabolic acidosis to CSF PCO2 fall is primarily for the benefit of CNS H+ homeostasis.

Acidosis↗
PubMed1979

Restoration of CSF [HCO3-] after its experimental lowering in normocapnic conditions.

It is accepted that in hypercapnia the rise in cerebrospinal fluid bicarbonate concentration (CSF [HCO3-]) occurs because of local HCO3--generating mechanisms, dependent on carbonic anhydrase, as well as on diffusion of HCO3- from plasma. To investigate further the regulation of CSF [HCO3-], CSF HCO3- formation was studied under conditions of pure isocapnic CSF "metabolic" acidosis. In anesthetized normocapnic dogs CSF [HCO3-] was lowered to approximately 15 mmol/l by perfusing the brain ventricles with a low HCO3- solution for 45 min. In dogs with normal plasma [HCO3-], CSF [HCO3-] rose by approximately 7 mmol/l in 2 h after the end of the perfusion. Lowering plasma [HCO3-] to 10 mmol/l by infusing HCl, limited the CSF [HCO3-] rise to 2 mmol/l, indicating the importance of plasma HCO3- for the restoration of CSF [HCO3-]. The small and persistent rise of CSF [HCO3-] at low plasma [HCO3-] occurred against a concentration gradient with blood. Intraventricular injection of acetazolamide had no further effect on this small rise. It is concluded that under the conditions of our experiments the CSF [HCO3-] rise is significantly dependent on plasma [HCO3-] and the caronic anhydrase-dependent HCO3- generation in the CNS is less important.

Acetazolamide↗
PubMed1979

Mixed pneumoconiosis: silicosis, asbestosis, talcosis, and berylliosis.

Mixed pneumoconiosis is pulmonary disease due to two or more inhaled mineral irritants. Chronic disease due to beryllium has not been a component of any described mixed pneumoconiosis. A man with occupational exposure to a combination of dusts developed severe pulmonary disease. Silicosis, talcosis, asbestosis, and berylliosis were all documented by an open biopsy of the lung. The varieties of mixed pneumoconiosis are summarized.

Asbestosis↗
PubMed1978

Interaction between PCO2 and plasma [HCO-3] in regulation of CSF [HCO-3] in respiratory alkalosis and metabolic acidosis.

The results of studies presented may be interpreted in light of the dual contribution theory of regulation of CSF acid-base balance, indicating significant interaction between systemic and local CNS mechanisms in H+ homeostasis in the brain and CSF. Both systemic and local mechanisms are at work in H+ homeostasis in the brain and CSF and depending on the specific acid-base disorder or the duration of the imbalance one or the other of the two factors may be the dominant one in maintaining H+ levels in the "normal" range. These factors come into play only when there has been a change in central pH with the primary aim of bringing the CNS [H+] towards normal.

Acidosis↗
PubMed1978

Asbestos exposure and related neoplasia. The 28 year experience of a major urban hospital.

In a retrospective study of 49 cases of asbestosis, a steady increase in the frequency of diagnosis of asbestosis and asbestos-related neoplasia is documented from a major urban hospital since 1960. Although in the majority of cases the subjects were exposed to asbestos in a neighboring shipyard, in 20 per cent of the cases, asbestos exposure was in industries not related to shipbuilding, reflecting its widespread use. This selective population of patients with asbestosis more often than not had an associated neoplasm. The most likely accompanying tumor was pleural mesothelioma, and among cell types of lung cancer, adenocarcinoma was notably frequent.

Adenocarcinoma↗
PubMed1978

Selected brain amino acids and ammonium during chronic hypercapnia in conscious rats.

Glutamic, aspartic, and gamma-aminobutyric acid (GABA), glutamine, and ammonium were measured in the brains of unanesthetized normocapnic and hypercapnic (10% CO2; 5 min to 3 wk) rats. Hypercapnia increased glutamine and GABA and decreased glutamic and aspartic acids. Changes occurred within 1 h and were maintained during the observation period of 3 wk. On return to normocapnia amino acid concentrations were almost normal after 1 h. Based on the time course it is concluded that intracerebral hypercapnia is more likely the stimulus for change than acidosis. Ammonium content was unchanged for at least 1 h after the onset of hypercapnia but increased thereafter. Experiments in which glutamine synthesis by brain was impeded by inhibiting the enzyme glutamine synthetase favor the hypothesis that the rise of ammonium content in hypercapnia is initially not seen because of increased glutamine synthesis. The changes observed may have a role in metabolic pH homeostasis of brain tissue and may also be relevant to the modified brain excitability in hypercapnia.

Acid-Base Equilibrium↗
PubMed1978

Reversible respiratory disease in beryllium workers.

A medical and environmental survey was carried out in a beryllium extraction and processing plant in 1971, and a follow-up study was done in 1974. Peak air concentrations of beryllium of as much as 50 times the accepted peak limit value were found in the plant in 1971. Radiographic changes of interstitial disease were found in 31 workers, hypoxemia was found in 20, and in 11 workers a combination of hypoxemia and radiographic changes of interstitial disease was seen. Follow-up in 1974 showed that air concentrations had all decreased significantly, mainly because of improvements in engineering and ventilation in the plant. Improvement in hypoxemia and decreased alveolar-arterial O2 tension difference at rest ([A-a]DO2) were noted in 13 of the 20 men who had hypoxemia in 1971 and were available for follow-up. In addition, radiographic abnormalities of interstitial disease were reversed in some workers. Our results suggest that improvement in gas exchange and radiographic findings of interstitial disease occurs when peak air concentrations of beryllium are decreased. Our approach in combining environmental and medical screening in workers exposed to beryllium enabled us to identify persons with early changes, to detect reversible abnormalities, and to correlate air concentrations with the medical status of workers.

Adult↗
PubMed1978

N13-N2(1).

13N when coupled with a positron camera allows excellent quantification and imaging of regional lung function. The studies can be readily repeated since the half-life of the 13N is uncer 10 min and the radiation dose to the patient with each study is low. The very low solubility of 13N not only enhances lung imaging but reduces total body radiation by remaining confined to the lung.

Adolescent↗
PubMed1977

Role of prostaglandins in alveolar hypoxic vasoconstriction.

The role of prostaglandins as mediators of alveolar hypoxic vasoconstriction was investigated in dogs with the use of the prostaglandin synthesis inhibitors, aspirin and indomethacin. Alveolar hypoxia was induced by inserting double-lumened endotracheal tube into the carina and ventilating one lung with nigrogen while maintaining normal systemic oxygenation with 100% O(2) ventilation to the other lung. Relative perfusion to each lung was determined with 133Xenon and external counters. Infusions up to 25 mg/kg of indomethacin and up to 250 mg/kg of aspirin did not block the shift in perfusion from the alveolar hypoxic lung. In fact, the shift in perfusion from the alveolar hypoxic lung was slightly augmented by aspirin (P = 0.03). Thus, no positive role was demonstrated in the dog for prostaglandins in producing the vasoconstriction of alveolar hypoxia.

Animals↗
PubMed1977

Failure of saralasin acetate, a competitive inhibitor of angiotensin II, to diminish alveolar hypoxic vasoconstriction in the dog.

The role of angiotensin II in the pulmonary vasoconstriction induced by alveolar hypoxia was investigated with the competitive inhibitor of angiotensin, saralasin acetate. Unilateral alveolar hypoxia was induced in dogs by ventilation of one lung with 100% N2 through a double lumened endotracheal cannula while maintaining adequate systemic oxygenation by ventilating the other lung with 1oo% O2. Pulmonary perfusion was monitored with 133Xe and external detectors. In 8 dogs perfusion to the test lung on room air before N2 ventilation was 49.2% (SEM +/- 3.8) of total lung perfusion. After 7 min of nitrogen ventilation, perfusion to that lung was 35.6% (SEM +/- 2.9) of cardiac output (P less than 0.001), a reduction of 27.5% (SEM +/- 2.4). After infusion of 6--24 microgram.kg-1/min of saralasin acetate, beginning 2 min before the alveolar hypoxic challenge and continuing through it, unilateral alveolar hypoxia continued to reduce perfusion to that lung by 28.8% (P = 0.6 from control). In 2 dogs a higher infusion of 60 microgram.kg-1/min failed to reduce the alveolar hypoxic vasoconstriction and in 2 dogs a 15 min infusion of 6 microgram.kg-1 of saralasin acetate before alveolar hypoxia and continuing through it, still failed to inhibit alveolar hypoxic vasoconstriction. Thus, no role was demonstrated for angiotensin II in acute alveolar hypoxic vasoconstriction of the dog.

Angiotensin II↗
PubMed1977

H+ transport from CNS in hypercapnia and regulation of CSF [HCO3-].

CSF HCO3- increases more than plasma HCO3- in hypercapnia, and there are at least two sources for the CSF HCO3- increase--one derived from the simultaneous increase in plasma HCO3-, and the other, HCO3-formed from hydration of CO2 in the choroid plexus and glia and susceptible to inhibition by acetazolamide (J. Appl. Physiol. 38: 504-512, 1975). It was proposed that the H+ formed in the CNS in CO2 hydration is actively exchanged for plasma Na+ utilizing the Na-K ATPase pump. H+ transport from the CNS was therefore studied in four groups of dogs breathing 5% CO2 at constant VA for 4 h with repeated injections of saline, acetazolamide 5 mg/ml, ouabain 0.1 mg/ml, and acetazolamide and ouabain together into lateral cerebral ventricles. Arterial HCO3-increased 2.5 meq/l at 4 h of hypercapnia in all groups. CSF HCO3-increased 5.8 meq/l in the saline-injected animals, but it increased only about 2 meq/l and equaled plasma HCO3- rise in the other three groups. Therefore CNS HCO3- formation in hypercapnia can be blocked by inhibiting the CO2 hydration reaction with acetazolamide or by blocking H+ removal by inhibiting Na-K ATPase with ouabain. The data support the thesis of active H+ removal from the CNS in exchange for plasma Na+ in hypercapnia.

Acetazolamide↗
PubMed1977

The significance of asbestos exposure in the diagnosis of mesothelioma: a 28-year experience from a major urban hospital.

A continued increase in the incidence of diffuse mesothelioma has been attributed to greater industrial use of asbestos but is also due in part to wider acceptance of this tumor by pathologists. In this retrospective study, the epidemiology, clinical presentation, and pathology of asbestos and non-asbestos-related mesothelioma from a major urban hospital were reviewed. Of the 36 cases of mesothelioma on file, 19 were not associated with exposure to asbestos. Although a retrospective study raises the possibility of inadequate occupational histories, the lack of history of asbestos exposure correlated with postmortem histology by light microscopy. When postmortem material was reviewed, evidence of asbestos exposure was present in all cases of mesothelioma with history of exposure to asbestos, and in no cases in which the patient denied history of asbestos exposure. Using strict histologic and histochemical criteria, the diagnosis of mesothelioma was confirmed in 8 of 9 patients with asbestos-related mesothelioma but in only 4 of 13 cases of non-asbestos-related mesothelioma. The diagnosis of diffuse methelioma is often difficult to make even wtih complete autopsy examinations. It should be entertained only with adherence to strict clinical and pathologic criteria, especially in women with no history to exposure to asbestos dust.

Adult↗
PubMed1977

Clinical significance of pulmonary function tests. Pulmonary function after uncomplicated myocardial infarction.

Derangement of pulmonary function following myocardial infarction is related to the severity of hemodynamic dysfunction. Abnormalities of pulmonary function appear even in patients without clinical or radiologic evidence of congestive failure. There is a reduction in vital capacity and rates of air flow. There is evidence for dysfunction of "small airways" and diminished ventilation to dependent parts of the lung. Total lung capacity may be normal or reduced, and residual volume may be increased slightly in uncomplicated myocardial infarction. Residual volume falls with more pronounced pulmonary congestion and edema. Distribution of pulmonary perfusion is altered after myocardial infarction, with a shift of perfusion away from the dependent parts of the lung (bases) towards the apices. Pulmonary gas exchange is impaired, with hypoxemia (due to both ventilation-perfusion inequality and increased shunting); and the diffusing capacity for carbon monoxide is diminished. Dead space is increased. The basic pathophysiologic mechanism responsible for abnormalities of pulmonary function is increased pulmonary water, which may be very minimal with uncomplicated myocardial infarction and stay primarily in the pulmonary interstitial space, but becomes progressively more severe with eventual alveolar flooding and marked impairment of pulmonary function.

Humans↗