Biomedical subjects

A H al Dhaheri

Publications and source records attributed to A H al Dhaheri.

2 recordsLinked to original sources

PubMed1996

Lead alters structure and function of mouse flexor muscle.

To evaluate the effect of long-term exposure to heavy metals on skeletal muscle, chronic subcutaneous injections for 7 days of two level treatments (low dose, 0.1 mg/kg and high dose, 1 mg/kg) of lead acetate were investigated. Comparative analyses of in situ dorsiflexor muscle isometric contractile characteristics were studied in urethane-anesthetized (2 mg/g, i.p.) control and lead-exposed male mice. Control muscle-twitch tension reached an average of 1.81 +/- 0.06 g. Chronic lead (Pb2+) treatments did not affect muscle contractile speed, but reduced significantly the twitch tension in both high and low doses when compared to control animals. This effect was in a dose-dependent manner; 1.21 +/- 0.07 g for low dose and 0.90 +/- 0.05 g for high dose. These chronic Pb2+ treatments accelerated muscle fatigue after 250 stimuli (25 Hz for 10 sec) in both the low and high doses equally. However, marked elevation in tetanic (25 Hz) specific tension were observed in the high-dose, chronically treated animals, indicating some changes in contractile apparatus function. The high dose of chronic Pb2+ treatment induced ultrastructural changes, including reduced number of synaptic vesicles, disruption of mitochondria and increased number of smooth endoplasmic reticulum and myelin-like figures in the intramuscular axons and neuromuscular junctions. Chronic Pb2+ treatment caused extensive disruption of the sarcoplasmic mitochondria and increased the number of myelin-like figures in the muscle. These results suggest that exposure to Pb2+ at a low concentration can compromise the in situ skeletal muscle isometric contraction.

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PubMed1995

Chronic lead treatment accelerates photochemically induced platelet aggregation in cerebral microvessels of mice, in vivo.

Effects of two chronic treatment levels with lead on platelet aggregation in cerebral (pial) microcirculation of the mouse were investigated. Exposure to lead was made by subcutaneous injections for 7 days of lead acetate dissolved in 5% glucose solution, vehicle. Two doses of lead were used, a low dose of 0.1 mg/kg and a high dose of 1.0 mg/kg. Adult male mice were divided into three groups, 10 each; one group was injected with vehicle (control), another was injected with the low dose, and the third was injected with the high dose. Additional mice were used for the determination of hematological parameters and for the lead level in serum of the three groups. On the eighth day, platelet aggregation in pial microvessels of these groups of mice was carried out in vivo. Animals were anesthetized (urethane, 1-2 mg/g, ip), the trachea was intubated, and a craniotomy was performed. Platelet aggregation in pial microvessels was induced photochemically, by activation of circulating sodium fluorescein (0.1 mg/25 g, iv) with an intense mercury light. The time required for the first platelet aggregate to appear in pial arterioles was significantly shorter in the lead-treated mice than in control. This effect was in a dose-dependent manner; 113 +/- 44 sec for low dose and 71 +/- 18 sec for high dose vs 155 +/- 25 sec for control, P < 0.02 and P < 0.001, respectively. Between the two lead-treated groups, the high dose significantly (P < 0.05) shortened the time to first aggregate. These data evidenced an increased susceptibility to cerebrovascular thrombosis as a result of exposure to lead.

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