Experimental Myocardial Infarction Elicits Time-Dependent Patterns of Vascular Hypoxia in Peripheral Organs and in the Brain

Abstract

Aims: Microvascular alterations occurring after myocardial infarction (MI) may represent a risk factor for multi-organ failure. Here we used in vivo photoacoustic (PA) imaging to track and define the changes in vascular oxygen saturation (sO2) occurring over time after experimental MI in multiple peripheral organs and in the brain.Methods and Results: Experimental MI was obtained in BALB/c mice by permanent ligation of the left anterior descending artery. PA imaging (Vevo LAZR-X) allowed tracking mouse-specific sO2 kinetics in the cardiac left ventricular (LV) anterior wall, brain, kidney, and liver at 4 h, 1 day, and 7 days post-MI. Here we reported a correlation between LV sO2 and longitudinal anterior myocardial strain after MI (r = −0.44, p < 0.0001, n = 96). Acute LV dysfunction was associated with global hypoxia, specifically a decrease in sO2 level in the brain (−5.9%), kidney (−6.4%), and liver (−7.3%) at 4 and 24 h post-MI. Concomitantly, a preliminary examination of capillary NG2DsRed pericytes indicated cell rarefication in the heart and kidney. While the cardiac tissue was persistently impacted, sO2 levels returned to pre-MI levels in the brain and in peripheral organs 7 days after MI.Conclusions: Collectively, our data indicate that experimental MI elicits precise trajectories of vascular hypoxia in peripheral organs and in the brain. PA imaging enabled the synchronous tracking of oxygenation in multiple organs and occurring post-MI, potentially enabling a translational diagnostic modality for the identification of vascular modifications in this disease setting.

Angiotensin II–Mediated Neuroinflammation in the Hippocampus Contributes to Neuronal Deficits and Cognitive Impairment in Heart Failure Rats

“…Two major pathological factors have been proposed to contribute to neurological dysfunction in HF, including end-organ hypoperfusion/hypoxia [14][15][16][17][18] a state associated also to cognitive impairment and neurodegeneration such as Alzheimer. 19 Additionally, recent studies support neuroinflammation as a common finding in numerous brain regions during HF.…”

Neurovascular hypoxia after mild traumatic brain injury in juvenile mice correlates with heart–brain dysfunctions in adulthood

“…Image acquisition required 4–5 min to obtain approximately 150 frames of PAI data. Neurovascular blood and tissue oxygenation (sO 2 ) levels (respectively, mean and total oxygen saturation) and mean hemoglobin (HbT) were analyzed offline using VevoLAB (v5.5.1, FUJIFILM VisualSonics) 14 …”

“…Although imaging modalities such as magnetic resonance imaging (MRI) can assess left ventricular function, the acquisition is often time‐consuming and costly 13 . The emergence of novel technologies based on United States allows for in vivo assessment of neurovascular and cardiac changes with high specificity 11,14,15 . Furthermore, we employed high‐frequency four‐dimensional ultrasound (4DUS), a technique comparable to cine MRI, offering high spatiotemporal resolution to assess cardiac disease progression over time 16 .…”

Optoacoustic Imaging in Inflammation

“…In the visible and NIR-spectrum, there are also multiple isosbestic points (390, 422, 452, 500, 530, 545, 570, 584, and 797 nm), where signals reflect total hemoglobin (Hb T ), regardless of the hemoglobin oxygenation level [ 31 , 102 , 103 ]. Owing to this capability, OAI has been widely used to visualize blood vessels and microcirculation, and to measure blood oxygenation levels, both experimentally in multiple organs [ 93 , 104 ] and clinically in patients [ 105 ]. Additionally, OAI has the potential to image blood flow velocity, although this has proved challenging at clinically relevant depths due to poor velocity signal-to-noise ratio [ 106 , 107 , 108 ].…”