Yeeran

Yiren Hengye Science Popularization Lecture

Application of Mouse and Rat Ultrasound in Cardiovascular Disease Research (Part 1) — Basics of Mouse and Rat Cardiac Anatomy, Physiology, and Ultrasound Detection

Previous articles in this series have systematically discussed the development history, scientific research value, imaging mechanisms, functional imaging modules, standardized experimental operating procedures, and solutions to common experimental errors in small animal ultrasound. This chapter focuses on the field of cardiovascular research, systematically elaborating on the cardiac anatomy, physiological characteristics, cardiac cycle pumping mechanism, and systemic blood circulation patterns in mice and rats. It also concurrently reviews the core theoretical framework of cardiac ultrasound, thereby strengthening the foundational theoretical support for cardiovascular ultrasound research.

In the field of basic cardiovascular research, mice and rats are currently the most widely used and academically recognized model animals due to their excellent experimental suitability. For primary cardiovascular diseases such as heart failure, acute myocardial infarction, and hypertrophic cardiomyopathy, as well as secondary myocardial injury induced by hypertension and diabetes, experiments involving the investigation of pathological mechanisms, targeted drug screening, and verification of treatment efficacy all rely on precise quantitative assessment of cardiac structure and function in mice and rats.

High-resolution small animal ultrasound is currently recognized as the gold standard non-invasive, in vivo quantitative technique for assessing cardiac structure and function in mice and rats. Compared to traditional methods such as invasive catheter-based measurements and endpoint histopathological sectioning, small animal ultrasound enables dynamic, in vivo examination of experimental animals throughout the entire study period, making it an indispensable core imaging technology for cardiovascular animal research.

In cardiac ultrasound experiments involving mice and rats, issues such as high data variability, deviations in index interpretation, and non-standard imaging planes are common. The root cause lies in the researcher's lack of understanding of the cardiac anatomical structure and physiological operational mechanisms. Without mastering the cardiac pumping mechanism, blood circulation patterns, and functional derangements under pathological conditions, it is impossible to accurately interpret ultrasound images and analyze experimental data.

Therefore, this article starts from the fundamental theoretical level, systematically breaking down the cardiac anatomy, complete pumping process, blood circulation patterns, and species-specific physiological characteristics of mice and rats. It also concurrently explains the ultrasound imaging modes and core research indices, aiming to improve the theoretical framework for cardiovascular animal experiments and provide a theoretical basis for subsequent standardized experimental operations and normalized data analysis.

I. Cardiac Anatomy of Mice and Rats: Similarities and Differences Between Humans and Rodents, and Key Features for Ultrasound Imaging

The hearts of mice and rats exhibit a typical mammalian four-chamber structure. Their anatomical framework, chamber distribution, valve morphology, and vascular configuration share high homology with the human heart, which forms the core anatomical basis for their ability to model the pathological progression of human cardiovascular diseases. The heart can be divided into four core modules: the chamber structure, the valve system, the great vessels, and the coronary circulation. Pathological morphological changes in each module can be visualized through ultrasound imaging.

1. Core Chamber Structure

The heart is composed of four independent chambers: the left and right atria and the left and right ventricles. The left and right cardiac systems are completely separated, responsible for systemic and pulmonary circulation, respectively. The atrial walls are thin and highly compliant, primarily serving to receive returning blood and assist the ventricles in the filling process. The ventricular myocardium is thick and exhibits excellent contractile performance, representing the core structure for the heart's pumping function.

Among these, the left ventricle is the central observation target in cardiovascular research. It is primarily responsible for supplying blood to the systemic circulation. It possesses highly developed myocardial fibers and the greatest wall thickness. It is highly sensitive to pressure overload injury, ischemic-hypoxic injury, and metabolic injury, making it the core region for ultrasound imaging and quantitative analysis. The right ventricle is mainly involved in regulating pulmonary circulation; its wall is thinner, and its chamber volume is relatively large. It is highly susceptible to volume overload-related injury and is often studied in models of pulmonary hypertension and right heart failure.

2. Valve Opening and Closing System

The mouse and rat heart contains four functional valves that maintain unidirectional blood flow through rhythmic opening and closing, preventing blood regurgitation. These are core structures ensuring hemodynamic stability.

. Mitral Valve: Located between the left atrium and left ventricle, it regulates filling and closure within the left cardiac system.

. Tricuspid Valve: Located between the right atrium and right ventricle, it regulates blood flow within the right cardiac system.

. Aortic Valve: Connects the left ventricle and the aorta, regulating the ejection process for systemic circulation.

. Pulmonary Valve: Connects the right ventricle and the pulmonary artery, regulating the ejection process for pulmonary circulation.

Pathological changes such as valve thickening, tissue adhesion, valvular insufficiency (incompetence), and valve prolapse can induce abnormal phenomena like blood regurgitation and turbulent flow. These lesions can all be accurately identified and quantitatively analyzed using Doppler ultrasound.

Figure 1 Schematic Diagram of Cardiac Structure

 

3. Great Vessels and Coronary Circulation

The aorta, pulmonary artery, superior and inferior venae cavae, and pulmonary veins together constitute the peripheral vascular circulation system of the heart, responsible for the pumping out and return of systemic blood. The coronary arteries in mice and rats are slender in diameter and densely distributed, covering the full thickness of the myocardium, making them difficult to observe directly with the naked eye. Coronary microcirculatory perfusion impairment is a core trigger for inducing myocardial ischemia, myocardial fibrosis, and cardiac dysfunction, which can be accurately assessed using contrast-enhanced ultrasound imaging.

4. Species-Specific Features for Ultrasound Imaging

While the overall cardiac anatomical framework of mice and rats is similar to that of humans, there are significant species-specific characteristics that directly define the imaging standards and experimental technical challenges of small animal ultrasound. These features serve as a core reference for conducting scientific research.

Extremely Small Body Size and High Structural Precision: The heart weight of a mouse is only 100–150 mg, approximately 1/100 to 1/1000 the volume of a human heart. Chamber inner diameters and wall thicknesses are on the order of millimeters. Conventional low-frequency clinical ultrasound lacks the resolution to image such minute structures, necessitating the use of high-frequency ultrasound probes to achieve micron-level high-precision imaging.

Thin Ventricular Wall with Clear Layering Structure: Unlike the thick muscular layer of the human heart, the mouse and rat myocardium is thin and uniform in thickness under physiological conditions. Subtle pathological changes such as myocardial hypertrophy, edema, and fibrosis can induce characteristic alterations in wall thickness and ultrasound echo intensity, making these important imaging indicators for the early detection of myocardial injury using ultrasound.

Significant Species Differences in Heart Rate: The heart rate of mice is significantly higher than that of rats, resulting in a very short cardiac cycle duration and rapid switching between systole and diastole. This imposes stringent requirements on the imaging frame rate and instantaneous capture accuracy of ultrasound equipment. Insufficient frame rates can easily lead to image blurring and systematic bias in experimental data.

High Myocardial Metabolic Activity: The metabolic rate of cardiomyocytes in mice and rats is significantly higher than in humans, making them highly sensitive to ischemia, hypoxia, pressure overload, and glucolipid metabolic disorders. Even mild external stimuli can induce structural and functional remodeling of the myocardium. The resulting pathological phenotypes are stable and highly discernible, making them suitable for dynamic tracking studies of cardiovascular disease progression.

In summary, the anatomical specificities of the mouse and rat heart dictate that conventional clinical ultrasound equipment cannot meet the demands of scientific research. Dedicated high-resolution small animal ultrasound systems are the only suitable tools for achieving precise cardiac assessment in mice and rats.

Figure 2 Portable High-Resolution Small Animal Ultrasound System

 

II. The Complete Cardiac Pumping Process + Systemic Blood Flow Mechanism

The core prerequisite for accurately interpreting cardiac ultrasound data is mastering the cardiac systole-diastole cycle and the regulatory mechanisms of blood circulation. All core ultrasound indices—such as ejection fraction, fractional shortening, E/A ratio, and blood flow velocity—correspond to the physiological processes of cardiac pumping and blood circulation. Only by clarifying these underlying mechanisms can pathological abnormalities be precisely identified.

1. Overall Logic of the Cardiac Cycle

The working cycle of the mouse and rat heart consists of two phases: the diastolic filling phase and the systolic ejection phase. These two phases alternate and operate continuously to complete systemic blood perfusion. The higher the heart rate, the higher the frequency of cardiac cycle switching, and consequently, the greater the myocardial oxygen consumption. This is the core reason for the high metabolic rate and high oxygen demand characteristic of mice and rats.

2. Diastolic Filling Phase: Blood Return and Ventricular Storage

During cardiac diastole, the myocardium of the atria and ventricles relaxes, and intracardiac pressure decreases. Systemic venous blood returns to the heart, completing the ventricular filling process and reserving sufficient blood for the subsequent pumping process. This process can be divided into two core stages.

Rapid Filling Phase: After ventricular relaxation, intracavitary pressure drops sharply. Blood from the pulmonary veins and vena cava rapidly flows into the ventricles, representing the main stage of ventricular filling. This corresponds to the E-wave (mitral inflow) signal on ultrasound. The filling volume during this phase accounts for more than 70% of the total ventricular filling volume, making it a core basis for assessing early diastolic function.

Atrial Systole Phase: At the end of diastole, the atria contract actively, squeezing residual blood from the atria into the ventricles to complete terminal filling. This corresponds to the A-wave (mitral inflow) signal on ultrasound. In aging models and diabetic cardiomyopathy models, a characteristic pathological phenotype often occurs, featuring compensatory enhancement of atrial contraction and a reversed E/A ratio.

During this phase, the valves open and close in a regular pattern: the mitral and tricuspid valves are fully open, while the aortic and pulmonary valves are fully closed. This ensures unidirectional blood filling and prevents regurgitation. If ultrasound detection captures a valve regurgitation signal, it indicates pathological changes such as valvular insufficiency or abnormal ventricular pressure.

3. Systolic Ejection Phase: Cardiac Pumping and Systemic Blood Supply

During cardiac systole, the myocardium contracts as a whole, and intracavitary pressure rises sharply, propelling ventricular blood into the great vessels to complete blood supply for the systemic and pulmonary circulations. This process is divided into the isovolumetric contraction phase and the rapid ejection phase.

Isovolumetric Contraction Phase: After the ventricles initiate contraction, intracavitary pressure rapidly exceeds atrial pressure, causing the mitral and tricuspid valves to close quickly to prevent blood backflow. During this phase, all cardiac valves are closed, ventricular volume remains constant, and intracavitary pressure continues to rise, building up energy for the ejection process.

Rapid Ejection Phase: Ventricular pressure continues to climb and exceeds the pressure within the aorta and pulmonary artery. The aortic and pulmonary valves open, and ventricular blood is rapidly ejected into the great vessels and transported throughout the body. The ejected volume and ejection rate during this phase directly determine core cardiac function evaluation indices such as ejection fraction and stroke volume.

4. Complete Blood Flow Pathways for Systemic and Pulmonary Circulation

Systemic Circulation (Left Heart System, Systemic Blood Supply): Left ventricular contraction → Aortic valve opens → Blood ejected into the aorta → Branch arteries → Material and energy exchange in capillaries of systemic tissues → Venous blood return → Superior and inferior vena cava → Right atrium. Abnormalities in systemic circulation are directly related to pathological changes such as hypertension, myocardial hypertrophy, and heart failure.

Pulmonary Circulation (Right Heart System, Blood Oxygen Exchange): Right ventricular contraction → Pulmonary valve opens → Blood ejected into the pulmonary artery → Oxygen exchange in pulmonary capillaries → Oxygenated arterial blood returns via the pulmonary veins → Left atrium → Left ventricle. Disruption of pulmonary circulation function is often observed in animal models of pulmonary hypertension and right heart failure.

5. Abnormal Blood Flow Changes Under Pathological Conditions

Under physiological conditions, cardiac blood flow exhibits a uniform, unidirectional, stable laminar flow state. Under pathological conditions, characteristic hemodynamic abnormalities appear, all of which can be accurately detected using ultrasound technology.

. Myocardial Stiffness and Diastolic Dysfunction: Ventricular filling rate slows down, peak E-wave decreases, peak A-wave increases, resulting in a reversed E/A ratio.

. Reduced Ventricular Systolic Function: Ejection rate decreases, ejection fraction declines, and stroke volume is significantly reduced.

. Organic Valvular Damage: Abnormal signals such as blood regurgitation and turbulent flow appear, with disrupted blood flow rhythm and direction.

. Ventricular Remodeling Pathologies: Chamber dilation and ventricular volume overload induce disordered ventricular filling and hemodynamic imbalance.

Figure 3 Mitral Valve Flow Spectrum Showing E and A Peaks

 

III. Physiological and Functional Characteristics of the Mouse and Rat Heart

The fundamental operating mechanisms of the mouse and rat heart are highly homologous to those of the human heart. However, to adapt to their own ultra-high metabolic physiological characteristics, they have evolved species-specific physiological properties including a high heart rate, high oxygen consumption, high sensitivity, and low compensatory reserve. These properties form the core physiological basis for disease model construction and the design of ultrasound detection protocols.

1. Extremely High Heart Rate and Short Cardiac Cycle

The resting heart rate of mice is 400–600 beats per minute, and that of rats is 300–400 beats per minute, significantly higher than the normal human range of 60–100 beats per minute. This extremely rapid cardiac cycle switching demands that small animal ultrasound equipment possess an ultra-high imaging frame rate. Insufficient frame rates can lead to image discontinuity, blurred structural boundaries, and data distortion. This is also the core reason why clinical ultrasound equipment cannot be adapted for cardiac detection in mice and rats.

2. High Metabolism, High Oxygen Consumption, and High Ischemic Vulnerability

Cardiomyocytes in mice and rats have a dense distribution of mitochondria and vigorous metabolic activity, resulting in an extremely high demand for oxygen and energy. When injuries such as coronary artery stenosis, myocardial ischemia, or hypoxia occur, cardiac function can become significantly abnormal within a short period. In the early stages, this often manifests as decreased diastolic function and reduced regional wall motion amplitude. These pathological phenotypes are stable and highly reproducible, making them suitable for research on myocardial ischemia, ischemia-reperfusion injury, and related models.

3. Sensitive Blood Flow Regulation and Rapid Stress Response

The neurohumoral regulatory system of the mouse and rat heart is highly sensitive. Minor external disturbances such as abnormal anesthetic depth, temperature fluctuations, surgical pain, and handling stress can rapidly alter the heart rate, myocardial contractile performance, and hemodynamic parameters of the experimental animals. Therefore, ultrasound experiments require standardized and uniform anesthetic conditions, temperature environment, and operating procedures to avoid significant data variability.

4. Limited Cardiac Compensatory Reserve and Rapid Pathological Progression

Compared to humans, the mouse and rat heart has a weak compensatory capacity. Persistent pathological stimuli such as pressure overload and metabolic injury can rapidly drive the heart from early functional impairment to organic remodeling. Typical pathologies such as myocardial hypertrophy, ventricular dilation, and myocardial fibrosis gradually appear. This allows for the complete recapitulation of the entire evolutionary process of human cardiovascular disease, from early injury to end-stage heart failure.

IV. Five Core Scientific Research Values of Mice and Rats as Primary Cardiovascular Models

Among various laboratory animals, the ability of mice and rats to serve as models for basic cardiovascular research, coupled with their unique anatomical and physiological anthropomorphism, experimental suitability, and scientific controllability, offers advantages that other laboratory animals cannot replace. This provides an important theoretical basis for conducting cardiac ultrasound-related scientific research.

1. Highly Stable Genetic Background and Excellent Experimental Reproducibility: Commonly used inbred strains of mice and rats have high genetic homozygosity and minimal inter-individual genetic differences. This effectively avoids interference from genetic factors in experimental results, ensures the stability of animal model construction and ultrasound data, and meets the core requirement of reproducible verification in scientific research.

2. Mature Gene Editing Technology and Comprehensive Disease Model Coverage: Well-established gene knockout, knock-in, overexpression, and conditional gene editing systems in mice and rats allow for the precise construction of genetic disease models such as hypertrophic cardiomyopathy, arrhythmias, heart failure, and metabolic cardiomyopathy. Concurrently, acquired cardiovascular disease models can be constructed through surgical intervention or drug induction, covering the vast majority of human cardiovascular disease types.

3. Low Rearing Cost, Short Model Induction Period, and Suitability for Large-Sample Studies: Mice and rats are easy to manage, have high reproductive efficiency, and have short life cycles. This allows for the rapid construction of large-sample models, long-term experimental interventions, and dynamic follow-up observations, effectively reducing research costs and suiting large-scale experimental studies such as batch drug screening and in-depth mechanism validation.

4. Pathological Phenotypes Highly Consistent with Clinical Disease: In models such as pressure overload-induced myocardial hypertrophy, coronary ligation-induced myocardial infarction and heart failure, and high glucose/high fat-induced diabetic cardiomyopathy, the processes of structural remodeling, functional impairment, and hemodynamic disruption in the mouse and rat heart are highly consistent with the characteristics of human clinical lesions, lending high clinical translational value to the research outcomes.

5. Supports In Vivo Longitudinal Follow-up, Ensuring Rigorous Experimental Data: Leveraging the non-invasive nature of small animal ultrasound, dynamic assessments can be performed on the same experimental animal at multiple time points (pre-surgery, post-surgery, post-drug intervention). This allows for the complete recording of the individual animal's disease progression trajectory, avoiding the issue of inter-individual variation inherent in terminal endpoint sacrifice methods, enhancing the objectivity and persuasiveness of experimental data, and meeting the research standards of high-impact journals.

V. Cardiac Ultrasound: An Essential Detection System for Cardiovascular Animal Experiments

The development of cardiovascular diseases generally follows the trajectory of "functional abnormality → structural remodeling → irreversible organic injury." In the early stages of disease, only subtle functional abnormalities in myocardial motion, blood flow filling, and diastolic function are present. Typical organic pathological changes such as ventricular dilation, myocardial hypertrophy, and pump failure appear only in the late stages of the disease.

Traditional methods like histopathological sectioning and serological testing can only reflect the injury status at the experimental endpoint and the overall level of injury, failing to capture the dynamic, subtle functional myocardial injuries in the early stages of the disease. Small animal ultrasound effectively compensates for this technical shortcoming, enabling comprehensive, dynamic, quantitative assessment of cardiac structure, pumping function, and hemodynamics.

This technology allows for precise determination of model establishment success, quantification of myocardial injury severity, monitoring of disease progression, evaluation of drug intervention efficacy, and assessment of myocardial remodeling status and perfusion abnormalities. It is a key supporting technology for generating core data in cardiovascular animal experiments.

VI. Small Animal Cardiovascular Ultrasound: Imaging Principles and Core Research Advantages

1. Core Imaging Principle

Small animal ultrasound is based on the piezoelectric effect of high-frequency piezoelectric transducers to transmit and receive ultrasound waves. It leverages the differences in acoustic impedance among different tissues (myocardium, blood vessels, blood, etc.) to generate grayscale anatomical images. Unlike clinical low-frequency ultrasound equipment operating at 3–5 MHz, small animal cardiac ultrasound utilizes ultra-high frequency transducers (10–40 MHz). It trades off some penetration depth for ultra-high spatial resolution, precisely adapting to the superficial, small, and rapidly moving structural characteristics of the mouse and rat heart, enabling clear differentiation of myocardial layers, fine blood flow signals, and subtle myocardial motion changes.

2. Research Advantages

. Completely Non-invasive, Supporting Repeated Follow-up: Requires no surgical procedures and involves no ionizing radiation, causing no damage to the experimental animal's heart or blood vessels. Allows for repeated examinations of the same animal, suitable for long-term dynamic tracking studies.

. Real-time Dynamic Imaging, Capturing Transient Abnormalities: Utilizes ultra-high frame rate imaging technology to completely reconstruct the entire process of contraction, relaxation, filling, and ejection within a single cardiac cycle, capturing transient functional injuries that static detection methods cannot identify.

. Precise Quantitative Indices, Suitable for Academic Publication: All indices related to cardiac structure, function, and blood flow can be precisely quantified and statistically analyzed. The data are objective and reproducible, meeting the publication requirements of various SCI-indexed academic journals.

. Efficient and Cost-effective, Suitable for Batch Experiments: Compared to advanced imaging technologies like MRI, CT, and PET, small animal ultrasound offers higher detection efficiency and lower equipment and consumable costs, making it suitable for rapid screening and detection of large batches of experimental samples in daily research.

. Strong Clinical Homology, Outstanding Translational Value: Its imaging modes, measurement indices, and functional evaluation logic are completely consistent with those of clinical cardiac ultrasound. The results of experimental research closely align with clinical pathological features, possessing high value for clinical translation and application.

VII. Application of Ultrasound Imaging Modes in the Cardiovascular Field

Small animal cardiac ultrasound is not a single detection technique but rather a complete scientific research system comprising multi-modal, complementary, and layer-by-layer precise assessment. Different imaging modes correspond to different detection dimensions. Their rational combination can comprehensively cover the assessment of cardiac structure, global function, hemodynamics, and subtle myocardial injury.

1. Core Imaging Modes and Applicable Scenarios

. 2D B-mode (Anatomical Foundation Imaging): As the foundational imaging mode for cardiac ultrasound, it is primarily used to observe the overall cardiac morphology, chamber dimensions, wall thickness, myocardial echo intensity, and structural integrity. It allows for rapid screening of organic lesions such as myocardial hypertrophy, ventricular dilation, wall defects, structural malformations, and pericardial effusion. It is a fundamental prerequisite for all cardiac functional assessments.

. M-mode (Gold Standard for Cardiac Function Assessment): Performs linear dynamic scanning based on a 2D section, offering ultra-high temporal resolution. It can precisely track the dynamic changes of the interventricular septum, left ventricular posterior wall, and ventricular chamber diameter during the cardiac cycle. It is the core mode for calculating ejection fraction, fractional shortening, and wall motion amplitude, and is the most commonly used functional detection technique in cardiovascular research.

. Color Doppler (Qualitative Blood Flow Screening): Uses color differences to distinguish blood flow direction and velocity (red typically indicates flow towards the transducer, blue indicates flow away). It allows for intuitive observation of atrioventricular filling blood flow and aortic ejection flow status, enabling rapid screening of hemodynamic issues such as valvular regurgitation, turbulent flow, filling abnormalities, and ejection disorders.

. Pulsed-wave Doppler (Quantitative Blood Flow Analysis): Samples target blood flow signals at specific sites to quantify core parameters such as peak flow velocity, acceleration time, deceleration time, and diastolic time intervals. It is primarily used to assess diastolic function, great vessel hemodynamics, and coronary flow reserve, serving as a core technique for detecting early functional myocardial injury.

. Tissue Doppler Imaging (Assessment of Myocardial Microfunction): Eliminates interference from blood flow signals to specifically capture the motion velocity of myocardial tissue itself. It can precisely identify regional abnormalities in systolic and diastolic function, detecting subclinical myocardial injury at an early stage before overall cardiac function shows a significant decline. It is a commonly used early injury assessment technique in high-level scientific research papers.

2. Ultrasound Measurement Indices

. Structural Remodeling Indices (Assessment of Organic Lesions): Core indices include left ventricular end-diastolic diameter, left ventricular end-systolic diameter, interventricular septal thickness (diastolic/systolic), left ventricular posterior wall thickness (diastolic/systolic), left atrial diameter, aortic root diameter, and right ventricular diameter. Primarily used to determine organic pathological changes such as myocardial hypertrophy, ventricular dilation, chamber remodeling, and great vessel structural abnormalities. This forms the basis for evaluating structural cardiac injury.

. Global Cardiac Function Indices (Assessment of Pumping Capacity):

Systolic Function Indices: Include ejection fraction, left ventricular fractional shortening, stroke volume, cardiac output, and mean wall thickening rate. They directly reflect the overall pumping efficiency of the heart and are the core criteria for determining the severity of heart failure.

Diastolic Function Indices: Include mitral E-wave velocity, A-wave velocity, E/A ratio, E/e' ratio, isovolumetric relaxation time, and deceleration time. Primarily used to assess diastolic filling capacity. Among these, the E/e' ratio effectively minimizes interference from factors like heart rate and ventricular load, serving as a key advanced indicator for evaluating myocardial relaxation function and identifying pseudonormal filling patterns. It holds significant diagnostic value for early, subtle diastolic dysfunction. Conditions such as diabetic cardiomyopathy, age-related myocardial injury, and heart failure with preserved ejection fraction (HFpEF) often present with diastolic dysfunction as the primary pathological phenotype.

. Hemodynamic Indices (Assessment of Circulatory Homeostasis): Encompass parameters such as aortic peak flow velocity, pulmonary artery flow parameters, valvular regurgitation velocity and area, and coronary flow reserve. Used to evaluate great vessel elasticity, valvular function, and systemic blood circulation homeostasis, suitable for animal model studies of hypertension, pulmonary hypertension, and valvular heart disease.

. Advanced Microfunctional Indices (Assessment of Early Injury): Based on speckle tracking imaging technology, these indices provide advanced parameters such as global longitudinal strain, circumferential strain, radial strain, and corresponding strain rates. They can capture subclinical myocardial subtle injury, regional myocardial dyssynchrony, early myocardial fibrosis, and other pathological changes that conventional indices cannot identify. This is currently the mainstream advanced analysis technique in high-level scientific research papers in the cardiovascular field.

Figure 4 Myocardial Strain

 

VIII. Conclusion

In summary, the unique anatomical structure and high-dynamic circulation physiological characteristics of the mouse and rat heart establish their irreplaceable position in basic cardiovascular research. The mechanisms of cardiac pumping and blood circulation form the core theoretical foundation for interpreting ultrasound images, quantifying scientific indices, and identifying pathological damage.

High-frequency small animal ultrasound, with its multiple advantages including non-invasiveness, real-time dynamic imaging, quantitative precision, and long-term follow-up capability, has become the core gold standard technology for observing cardiac structure, quantifying function, and assessing hemodynamics in mice and rats. Mastering the cardiac anatomy and physiology, blood flow pumping mechanisms, ultrasound imaging modes, and the complete set of research indices can effectively avoid experimental operational errors, improve data accuracy, and build a solid theoretical and technical foundation for research on various cardiovascular disease models, drug efficacy evaluation, and exploration of pathological mechanisms.

The next installment will focus on practical application scenarios, systematically explaining the implementation methods of mouse and rat ultrasound in various cardiovascular disease models, key points for standardized experimental quality control, and advanced cutting-edge detection techniques. We will continue to update core theories and practical knowledge for cardiovascular research as a reference and learning resource for interested researchers.