PubMed · 13916912
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C R STEPHEN. Postoperative temperature changes.. https://doi.org/10.1097/00000542-196109000-00013
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Mouse models mimicking human diseases are important tools in trying to understand the underlying mechanisms of many disease states. Several surgical models have been described that mimic human myocardial infarction (MI) and pressure-overload-induced cardiac hypertrophy. However, there are very few detailed descriptions for performing these surgical techniques in mice. Consequently, the number of laboratories that are proficient in performing cardiac surgical procedures in mice has been limited. Microarray technologies measure the expression of thousands of genes simultaneously, allowing for the identification of genes and pathways that may potentially be involved in the disease process. The statistical analysis of microarray experiments is highly influenced by the amount of variability in the experiment. To keep the number of required independent biological replicates and the associated costs of the study to a minimum, it is critical to minimize experimental variability by optimizing the surgical procedures. The aim of this publication was to provide a detailed description of techniques required to perform mouse cardiac surgery, such that these models can be utilized for genomic studies. A description of three major surgical procedures has been provided: 1) aortic constriction, 2) pulmonary artery banding, 3) MI (including ischemia-reperfusion). Emphasis has been placed on technical procedures with the inclusion of thorough descriptions of all equipment and devices employed in surgery, as well as the application of such techniques for expression profiling studies. The cardiac surgical techniques described have been, and will continue to be, important for elucidating the molecular mechanisms of cardiac hypertrophy and failure with high-throughput technology.
To examine acute hemodynamic responses to microgravity (microG) in the head, we measured carotid artery pressure (CAP) and jugular vein pressure (JVP) to calculate cephalic perfusion pressure (CPP = CAP - JVP) and recorded images of microvessels in the iris to evaluate capillary blood flow velocity (CBFV) and capillary diameter (CD) in anesthetized rats during 4.5 s of microG induced by free drop. Rats were placed in 30 degrees head-up whole body-tilted (HU, n = 7) or horizontal (flat, n = 6) position. In the flat group, none of the measured variables was significantly affected by microG, whereas in the HU group, CAP, JVP, and CPP increased, respectively, by 23.4 +/- 2.6, 1.3 +/- 0.2, and 22.9 +/- 3.1 mmHg, and CBFV and CD increased, respectively, by 33 +/- 8 and 9 +/- 3%, showing an increase in capillary blood flow. To further examine the mechanisms underlying these CAP and JVP increases, another experiment was performed in which CAP and JVP were measured in anesthetized rats (n = 6) during a postural change from HU to flat. In these animals, the change in JVP was similar to that observed during actual microG, but no change in CAP was seen, indicating that the JVP increase during actual microG is caused by disappearance of the gravitational pressure gradient in the head-to-foot axis, whereas the CAP increase is not. In conclusion, actual microG elicits an increase in CPP due to a greater increase in CAP than JVP, resulting in increased capillary blood flow. Although the increase in JVP is explained by the disappearance of gravitational pressure gradient in the head-to-foot axis as a result of microG, the larger increase in CAP is not.
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