Thrombogenic stimulus causes long-term decrease of muscle flap perfusion.

This study was designed to evaluate the effect of a continuous thrombogenic insult at the feeding artery on skeletal muscle flap perfusion over 24 hours. Twelve male Sprague-Dawley rats were divided into two experimental groups. In the control group (N = 6) and in the treatment group (N = 6) the right cremaster muscle was isolated on its neurovascular pedicle and the tubular muscle flap was preserved in the medial part of the hind limb over a 24-hour period for subsequent microcirculatory observation. In the treatment group, an inverting suture was applied over half of the circumference of the ipsilateral common iliac artery to create a continuous thrombogenic stimulus. Intravital microcirculatory measurements obtained were red blood cell velocities, vessel diameters, capillary perfusion, endothelial edema index, and leukocytic-endothelial interactions. There were no statistically significant differences seen in red blood cell velocities, vessel diameters, and leukocytic-endothelial interactions between the groups. However, the inverting suture caused a significant drop in capillary perfusion from 6.23 to 1.50 capillaries per visual field (median; p = 0.002). An arterial thrombogenic insult may result in a significant decrease in capillary perfusion in muscle flaps over 24 hours although the blood flow through the thrombogenic main feeding vessel is maintained.

Activation of nitric oxide synthase gene expression by hypoxia in central and peripheral neurons.

In the present study we examined the effects of hypobaric hypoxia on neuronal (n) and endothelial (e) nitric oxide synthase (NOS) gene expression in the central and peripheral nervous system. Adult rats were exposed either to normoxia (room air) on to hypobaric hypoxia (0.4 atm) for 4, 12 or 24 h and cerebellum and nodose ganglion representing the central and peripheral neurons, respectively, were removed. Messenger RNAs encoding n- and eNOS as well as beta-actin were analyzed by reverse transcriptase polymerase chain reaction (RT-PCR) technique. Hypoxia increased nNOS mRNA expression with maximal changes occurring after 12 h wherein mRNA levels were increased by 10.4 +/- 1.3 and 2 +/- 0.4 fold in nodose ganglion and cerebellum, respectively. Hypoxia, on the other hand, had no significant effect on eNOS and beta-actin mRNA levels. Analysis of nNOS protein and enzyme activity showed near doubling of these variables in both tissues after 24 h of hypoxia, indicating that nNOS protein levels are increased and that the protein is functionally active. These observations demonstrate that 12-24 h of hypobaric hypoxia selectively activates nNOS gene expression, which is reflected in an increase in nNOS protein in central and peripheral neurons. It is suggested that up-regulation of nNOS leads to increased generation of nitric oxide, which in turn may contribute to the readjustments of cardio-respiratory systems during the early stages of chronic hypoxia.