Search PubMed⌕ Search

Biomedical subjects

H Najafi

Publications and source records attributed to H Najafi.

At least 55 records · Page 3Linked to original sources
PubMed1987

The healing characteristics of autogenous saphenous vein used in the reconstruction of previously implanted arterial saphenous vein grafts.

Aortocoronary saphenous vein grafts with early isolated stenoses pose the technical problem of how to deal with these grafts at reoperation. The advisability of using a portion of old graft when reconstructing these grafts was examined. An experimental model was devised in which the anatomical and pathological interfaces between fresh vein and previously inserted vein were studied. Superficial femoral artery from the thigh of 15 dogs was replaced by reversed autogenous saphenous vein. Four months later, the animals were divided into two groups. Group 1 consisted of 8 animals that underwent transection and reimplantation of the middle 4 cm of the vein graft in exactly the same position in which it had been. In Group 2, the 7 animals had the middle 4 cm of the graft replaced with newly harvested reversed saphenous vein. Six months after initial vein graft implantation, the animals were studied. No critical stenoses were seen in the grafts. Pathological study of Group 1 grafts revealed fibrous graft disease of uniform severity throughout the graft, thereby demonstrating that new anastomoses in an old graft do not affect graft disease. Group 2 grafts revealed that the severity of disease in the new interposed segment of the vein graft was less than in the old retained portions of the graft. No untoward reaction causing acceleration of graft disease occurred between old and new vein. Operations using undiseased portions of old vein grafts should be considered a viable option in repeat coronary revascularization for early stenoses.

Animals↗
PubMed1987

Postperfusion coronary stenosis.

A patient is described who had left main coronary artery stenosis four months after aortic valve replacement. He was seen with unstable angina, and subsequent catheterization revealed stenosis of a previously normal left main coronary artery. The diagnosis, treatment, and means of prevention are discussed.

Aortic Valve Stenosis↗
PubMed1987

Fuel-stimulated insulin secretion by clonal hamster beta-cell line HIT T-15.

Insulin secretion by monolayer cultures of HIT T-15 cells was measured in response to various fuel molecules (glucose, dihydroxyacetone, lactate, glutamine, alpha-ketoisocaproic acid, alpha-ketoisovaleric acid) and a nonmetabolized glucose analogue (3-O-methylglucose). HIT cells secreted insulin in response to fuel molecules, but 3-O-methylglucose was ineffective. Stimulation of insulin release by fuels was increased by isobutylmethylxanthine and blocked by antimycin A. Iodoacetate selectively inhibited glucose-stimulated insulin release but had little effect on alpha-ketoisocaproic acid-stimulated insulin secretion. These results indicate that HIT cells retain the capacity of normal beta-cells to act as fuel sensors. Thus, HIT cells may provide a well-defined and relatively abundant tissue source in studies of stimulus-secretion coupling in beta-cells stimulated by fuels.

3-O-Methylglucose↗
PubMed1986

Acetylcholine stimulates glucose metabolism by pancreatic islets.

Acetylcholine stimulates insulin secretion in the presence of physiological concentrations of glucose. Stimulation of insulin secretion by acetylcholine is accompanied by an increase in glucose usage by isolated rat islets. Acetylcholine increased glucose usage by 38%, 28%, and 12% at 3.5 mM, 5.5 mM, and 10 mM glucose, respectively, compared to glucose usage by isolated islets incubated with glucose alone. Data showing increased glucose usage in islets treated with acetylcholine converge with data from an earlier report (J. Biol. Chem. 254 3921-3929 [1979]) showing a crossover point for glycolytic metabolites at phosphofructokinase to indicate that activation of glycolysis by acetylcholine results from increased phosphofructokinase activity and coordinate activation of hexokinase in intact islets.

Acetylcholine↗
PubMed1986

Identification of glucokinase as an alloxan-sensitive glucose sensor of the pancreatic beta-cell.

Alloxan inactivated glucokinase in intact, isolated pancreatic islets incubated in vitro. Inactivation of glucokinase was antagonized by 30 mM glucose present during incubation of islets with alloxan. Glucokinase partially purified from transplantable insulinomas or rat liver was inactivated by alloxan with a half-maximal effect at 2-4 microM alloxan. Inactivation of purified glucokinase was antagonized by glucose, mannose, and 2-deoxyglucose in order of decreasing potency but not by 3-O-methylglucose. Glucose anomers at 6 and 14 mM were discriminated as protecting agents, with the alpha-anomer more effective than the beta-anomer. Glucokinase was not protected from alloxan inactivation by N-acetylglucosamine, indicating that the reactive site for alloxan is not the active site; therefore, glucose may protect glucokinase by inducing a conformational change. Glucokinase is thought to be the glucose sensor of the pancreatic beta-cell. The finding that glucokinase is inactivated by alloxan and protected by glucose with discrimination of its anomers similar to inhibition of glucose-stimulated insulin secretion by alloxan supports this hypothesis and appears to explain the mechanism for inhibition of hexose-stimulated insulin secretion by this agent and the unique role of glucose and mannose as protecting agents.

Alloxan↗
PubMed1986

Glucose transport by radiation-induced insulinoma and clonal pancreatic beta-cells.

Sugar uptake was measured in dispersed cells prepared from radiation-induced insulinomas transplantable in NEDH rats and in three clonal beta-cell lines maintained in continuous culture (RIN m5F, RIN 1046, HIT). Uptake of D-glucose and 3-O-methyl-D-glucose by insulinoma cells was rapid so that the intracellular concentration of D-hexoses approximated the concentration in the incubation medium by 15-30 s. L-Glucose was taken up only slowly. 3-O-methyl-D-glucose uptake by RIN m5F, RIN 1046, and HIT cells was slow; with 1 mM 3-O-methylglucose in the medium, equilibrium was attained at 20 min, but with 10 mM 3-O-methylglucose, equilibrium was not attained even at 20 min. In HIT cells incubated with D-glucose for 30 min, the intracellular concentration of glucose was less than the medium glucose concentration, indicating glucose transport is a nonequilibrium reaction in this cell line. These data indicate that radiation-induced insulinoma cells retain the capacity of normal beta-cells to transport sugar at high rates. RIN m5F, RIN 1046, and HIT cells transport sugar slowly, however, and thus differ from normal beta-cells. In RIN m5F, RIN 1046, and HIT cells, unlike in normal beta-cells, glucose transport may be the site regulating glucose metabolism.

3-O-Methylglucose↗
PubMed1985

Regulatory role of fructose-2,6-bisphosphate in pancreatic islet glucose metabolism remains unsettled.

Fructose-2,6-P2 was measured in perifused, isolated rat pancreatic islets. Fructose-2,6-P2 was present in pancreatic islets at low levels approximately equal to fructose-2,6-P2 content of liver from fasted rats. In islets perifused with glucose at physiologic concentrations, fructose-2,6-P2 was increased from 0.8 microM in the presence of 5.5 mM glucose to 1.0 microM at 10 mM glucose and 1.3 microM at 16.7 mM glucose, but did not increase further at higher glucose concentration. Therefore, only modest increases in the phosphofructokinase-1 activator, fructose-2,6-P2, occur at glucose concentrations stimulating insulin secretion.

Animals↗
PubMed1983

Neurological complications of coronary revascularization.

In a series of 3,206 consecutive coronary artery bypass procedures performed between 1976 and 1981, 89 patients died (2.8% mortality) and 32 patients (1%) suffered major neurological syndromes. Among the latter patients, four distinct groups were identified. Group 1 consisted of 10 patients who remained unresponsive after operation. In Group 2 were 10 patients who awakened after operation but had clinical evidence of focal cerebral infarction. Group 3 included 6 patients who were initially intact neurologically but in whom neurological deficits later developed. In Group 4 were 6 patients who had severe mental aberration but no focal neurological deficits. The incidence of coma or focal deficit occurring without a lucid interval (Groups 1 and 2) was 0.62%, and these patients had a 30% mortality. Causative factors were suspected in 70% of the patients in Groups 1 and 2, and included atheromatous embolism, perioperative hypotension, carotid artery occlusive disease and air embolism. The outcome was poor for unresponsive patients, with 70% dying or remaining comatose, but nearly all of the patients with focal deficits or severe mental aberration demonstrated notable improvement.

Arteriosclerosis↗
PubMed1983

Chromatographic resolution and kinetic characterization of glucokinase from islets of Langerhans.

Glucokinase (ATP:D-glucose 6-phosphotransferase, EC 2.7.1.2) from rat islets of Langerhans was partially purified by chromatography on DEAE-Cibacron blue F3GA agarose. The enzyme eluted in two separate peaks. Sigmoidal rate dependence was found with respect to glucose (Hill coefficient = 1.5) for both enzyme fractions. Km values for glucose were 5.7 mM for the major fraction and 4.5 mM for the minor fraction. Neither fraction phosphorylated GlcNAc. A GlcNAc kinase (ATP:2-acetamido-2-deoxy-D-glucose 6-phosphotransferase, EC 2.7.1.59)-enriched fraction, prepared by affinity chromatography on Sepharose-N-(6-aminohexanoyl)-GlcNAc, had a Km of 25 microM for GlcNAc. Islet tissue also contained hexokinase (ATP:D-hexose 6-phosphotransferase, EC 2.7.1.1) eluting in multiple peaks. The results are consistent with the concept that glucokinase serves as the glucose sensor of pancreatic beta cells.

Animals↗
PubMed1983

Coronary revascularization in septuagenarians.

Despite a 15 year experience with the aorta-coronary bypass operation, indications for its use remain unsettled, especially in the elderly. Between January, 1974, and June, 1980, 2,667 patients underwent coronary artery revascularization with an overall mortality of 3.8% (101/2,667). During the last 12 months the mortality has decreased to 1%. There were 2,562 patients below the age of 70, with a mortality of 3.5% (90/2,562), in contrast to 105 patients over the age of 70, with a mortality of 10.5% (11/105) (p = 0.002). In patients less than 70 years of age there was a significant difference between the mortality of men, 3.12% (67/2,146), and that of women, 5.53% (23/416) (p = 0.015). This disparity of operative risk was far more pronounced in patients over 70 years of age: men 6% (5/84) and women 28.6% (6/21) (p = 0.002). The overall operative mortality of women, 6.6% (29/437), was significantly different from the overall mortality of men, 3.2% (72/2,230) (p = 0.001). An in depth analysis of past medical history, risk factors, and catheterization data is presented in those patients over the age of 70. The average number of vessels bypassed was 2.40: men 2.47 and women 2.09 (p = NS). The ages varied from 70 to 81 years with a mean of 72.5. Smoking (p = 0.012) and diabetes (p = 0.0078) were significant risk factors for coronary disease. Smoking (p = 0.032) and abnormal pulmonary artery pressures (p = 0.0429) were significant variables affecting mortality. A 97.1% follow-up was obtained up to 78 months. Coronary artery revascularization can be performed in men below the age of 70 with acceptable mortality, but there is a twofold increase above the age of 70. Women can undergo revascularization below the age of 70 with a significantly higher risk than males. Those above the age of 70 are at severe risk and should undergo revascularization only after careful selection.

Age Factors↗
PubMed1982

Diaphragmatic left ventricular aneurysm. Clinical features, surgical treatment, and long-term follow-up in 22 patients.

Although the formation of a left ventricular aneurysm (LVA) is a common and well-recognized complication of myocardial infarction (MI), diaphragmatic LVA is a rare clinical entity. Of 354 consecutive patients who underwent LVA resection, we describe the clinical features and surgical results of 22 patients (6%) with diaphragmatic LVA. All patients had a history of MI. The principal clinical indication for surgery was heart failure in nine patients, angina pectoris in ten patients, and recurrent ventricular tachycardia unresponsive to medical therapy in three patients. A ventricular septal defect was present in two patients, and moderate to severe mitral regurgitation was present in four patients. Three of the four surgical deaths (operative mortality, 18%) occurred in patients with mitral regurgitation or with ventricular septal defect. Eleven patients are alive at a mean follow-up of 40 months. Six of them are asymptomatic and two have angina at a higher level of physical activity than before surgery. Notable differences exist in the clinical presentation and surgical findings between patients with diaphragmatic and anterior LVA.

Adult↗