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Biomedical subjects

D A Maclean

Publications and source records attributed to D A Maclean.

5 recordsLinked to original sources
PubMed2005

Oxidative stress and nitric oxide synthase in skeletal muscles of rats with post-infarction, compensated chronic heart failure.

AIM: Involvement of oxidative stress and nitric oxide synthase (NOS) isoforms in skeletal muscle cellular adaptations to chronic heart failure (CHF) is controversial, and possible muscle fibre-type heterogeneity in the oxidative stress and NOS responses to CHF have not been examined. Consequently, we hypothesized that the changes in determinants of elevated oxidative and nitrosylative stress associated with CHF would occur in skeletal muscle and would be similar in predominantly type I slow twitch muscle (soleus) and type II fast twitch muscle (plantaris) of rats. METHODS: The purpose of this study was to measure NOS isoforms (endothelial, inducible and neuronal NOS) and antioxidant enzymes (SOD-1, SOD-2, catalase) by protein immunoblot as well as markers of oxidative stress by biochemical assays in soleus and plantaris muscle sections of the rat hind limb. This was performed for control and post-infarction, compensated CHF rats. RESULTS: Twelve weeks after coronary artery ligation-induced moderate CHF, soleus exhibited decreased SOD-1, SOD-2 and eNOS, but increased iNOS and nNOS isoforms assessed by immunoblot. This was associated with elevated lipid and DNA oxidative damage assessed by biochemical assays. In contrast, plantaris muscle exhibited no changes in antioxidant enzymes or NOS isoforms, and had lower lipid and DNA oxidative damage. CONCLUSION: These observations suggest a heretofore unreported muscle fibre-type-specific response of oxidative stress and NOS isoforms to CHF is of importance in understanding the cellular mechanisms of skeletal muscle dysfunction in CHF.

Adaptation, Physiological↗
PubMed1997

Femoral arterial injection of adenosine in humans elevates MSNA via central but not peripheral mechanisms.

The purpose of the present study was to examine the effects of femoral arterial injections of adenosine on muscle sympathetic nerve activity (MSNA) under three different conditions. These conditions were adenosine injection alone, adenosine injection after phenylephrine infusion, and adenosine injection distal to a thigh cuff inflated to arrest the circulation. The arterial injection of adenosine alone resulted in a fourfold (255 +/- 18 U/min) increase above baseline (73 +/- 12 U/min; P < 0.05) in MSNA with an onset latency of 15.8 +/- 0.8 s from the time of injection. The systemic infusion of phenylephrine resulted in an increase (P < 0.05) in mean arterial pressure of approximately 10 mmHg and a decrease (P < 0.05) in heart rate of 8-10 beats/min compared with baseline values before phenylephrine infusion. After adenosine injection, the onset latency for the increase in MSNA was delayed to 19.2 +/- 2.1 s and the magnitude of increase was attenuated by approximately 50% (123 +/- 20 U/min) compared with adenosine injection alone (P < 0.05). When a cuff was inflated to 220 mmHg to arrest the circulation and adenosine was injected into the leg distal to the inflated cuff, there were no significant changes in MSNA or any of the other measured variables. However, on deflation of the cuff, there was a rapid increase (P < 0.05) in MSNA, with an onset latency of 9.1 +/- 0.9 s, and the magnitude of increase (276 +/- 28 U/min) was similar to that observed for adenosine alone. These data suggest that approximately 50% of the effects of exogenously administered adenosine are a result of baroreceptor unloading due to a drop in blood pressure. Furthermore, the finding that adenosine did not directly result in an increase in MSNA while it was trapped in the leg but that it needed to be released into the circulation suggests that adenosine does not directly stimulate thin fiber muscle afferents in the leg of humans. In contrast, it would appear that adenosine exerts its effects via some other chemically sensitive pool of afferents.

Adenosine↗
PubMed1980

Pure fetal blood from the umbilical cord obtained at fetoscopy: experience with 125 consecutive cases.

With experience, and with the use of a 30-degree forward-oblique viewing telescope, sampling from one of the vessels of the umbilical cord produced at least 0.5 ml of pure fetal blood in 97% of the cases between 14 and 24 weeks' gestation; by aspiration through a short-tipped, 27-gauge, specially constructed needle, adequate samples were ensured. The technique used overcomes the problems previously encountered with sampling from an anteriorly situated placenta, and offers considerable potential for investigating intrauterine physiologic and pharmacologic features, as well as providing excellent specimens for diagnostic purposes. With this method, the calculated optimum time for fetoscopy and sampling of fetal blood is 16 to 18 weeks' gestation.

Blood Specimen Collection↗
PubMed1980

Acute haematogenous osteitis.

During a 10-year period 217 cases of acute haematogenous osteitis were treated. In 131 patients the diagnosis was confirmed either radiologically or bacteriologically, but in the other 86 the diagnosis was based on clinical examination. Either cloxacillin or lincomycin proved to be effective if given before bacteriological diagnosis. Frequent clinical examination, assessing both local signs and the child's general state, will decide which child requires surgery (which should be reserved for the toxic child, the child with concomitant medical disorders lowering host resistance, and the child who does not respond to, or has a lesion which flares up after, initial conservative treatment). Constant vigilance is required by clinicians looking after children with this disease in order to reduce the disabling long-term sequelae.

Acute Disease↗