Cardiac neuromodulation with acute intermittent hypoxia in rats with spinal cord injury

Figures

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  Figure 1. Cardiovascular response to sympathetic blockade with esmolol in animals with (n = 9) and without (n = 9) spinal cord injury (SCI) A, neuroanatomical overview. B, raw traces of left ventricular pressure (LVP), heart rate (HR) and the maximal rate of rise of left ventricular pressure (dP/dt max) during baseline and sympathetic blockade with esmolol. Group data for dP/dt max (Ca), HR (Da) and DBP (Ea) during baseline and sympathetic blockade with esmolol. Cb–Eb, the magnitude of changes from baseline to blockade condition. Note that, although there was a reduction in the pressure‐generating of the heart and systemic arterial pressure in both Naive and SCI animals, the magnitude of the drop in dP/dt max was greater in SCI animals. Statistical analysis was performed using a two‐way (group × time) mixed analysis of variance, with Bonferroni correction for multiple‐comparison testing. PNS, parasympathetic nervous system; SNS, sympathetic nervous system. SNSB, SNS blockade. [Colour figure can be viewed at wileyonlinelibrary.com]

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  Figure 2. Cardiovascular response to parasympathetic blockade with atropine in animals with (n = 9) and without (n = 9) spinal cord injury (SCI) A, neuroanatomical overview. B, raw traces of left ventricular pressure (LVP), heart rate (HR) and the maximal rate of rise of left ventricular pressure (dP/dt max) during baseline and parasympathetic blockade with atropine. Group data for dP/dt max (Ca), HR (Da) and DBP (Ea) during baseline and parasympathetic blockade with atropine. Cb–Eb, the magnitude of changes from baseline to blockade condition. Note that the reduced cardiovascular function in SCI vs. Naive animals is still detectable under this blockade condition. Statistical analysis was performed using a two‐way (group × time) mixed analysis of variance, with Bonferroni correction for multiple‐comparison testing. Note that, although there was a reduction in the pressure‐generating of the heart and systemic arterial pressure in both Naive and SCI animals, the magnitude of the drop in dP/dt max was greater in SCI animals. PNS, parasympathetic nervous system; SNS, sympathetic nervous system. PNSB, PNS blockade. [Colour figure can be viewed at wileyonlinelibrary.com]

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  Figure 3. Cardiovascular response to double cardiac autonomic blockade (esmolol and atropine) in animals with (n = 9) and without (n = 9) spinal cord injury (SCI) A, neuroanatomical overview. B, raw traces of left ventricular pressure (LVP), heart rate (HR), and the maximal rate of rise of left ventricular pressure (dP/dtmax) during baseline and double blockade (DB) with esmolol and atropine. Group data for dP/dt max (Ca), HR (Da) and DBP (Ea) during baseline and DB. Cb–Eb, the magnitude of changes from baseline to blockade condition. Note the greater drop in the pressure‐generating of the heart and systemic arterial pressure in Naive vs. SCI animals, as well as equalization of cardiovascular function between these animals under DB condition. Statistical analysis was performed using a two‐way (group × time) mixed analysis of variance, with Bonferroni correction for multiple‐comparison testing. PNS, parasympathetic nervous system; SNS, sympathetic nervous system. [Colour figure can be viewed at wileyonlinelibrary.com]

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  Figure 4. Vascular influences on cardiac function in animals with (n = 9) and without (n = 9) spinal cord injury (SCI) A, neuroanatomical overview. B, raw traces of left ventricular pressure (LVP), heart rate (HR) and the maximal rate of rise of left ventricular pressure (dP/dt max) during double (DB; esmolol and atropine) and complete (CB; esmolol, atropine, and hexamethonium) blockade. Group data for dP/dt max (Ca) and DBP (Da) during DB and CB. Cb–Db, the magnitude of changes from DB to CB condition. E, association between the drops in systemic arterial pressure (i.e. DBP) and heart function (i.e. dP/dt max) in Naive and SCI rats. Note that, unlike Naive rats, the greater drops in systemic arterial pressure did not occur in concert with drops in the pressure‐generating capacity of the heart in SCI rats when transitioning from DB to CB, with SCI rats also showing a weaker association between the drops in systemic arterial pressure and heart function. Statistical analysis was performed using a two‐way (group × time) mixed analysis of variance, with Bonferroni correction for multiple‐comparison testing. The association between the drops in systemic arterial pressure and heart function was…

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  Figure 5. Cardiovascular responses to acute intermittent hypoxia (AIH) and time‐control following spinal cord injury (SCI) A, terminal preparation and B, experimental design used. Note that the maximal rate of rise of LV pressure (Ca, dP/dt max), rate pressure product (Da, RPP), diastolic blood pressure (Ea, DBP), and coronary perfusion pressure (Fa, CPP) were augmented immediately after and up to 90 min post‐AIH (10 × 1 min episodes; FIO2 = 0.1, interspersed with 2 min of FIO2 = 1.0) in AIH‐exposed animals (AIH, n = 11) vs. time control animals (TC, n = 8) without hypoxia. Cb–Fb, showing changes in metrics between each time point and baseline. Statistical analysis was performed using a two‐way (group × time) mixed analysis of variance, with Bonferroni correction for multiple‐comparison testing. For other metrics examined, see Tables 3 and 4. Estimated CPP is calculated as the difference between DBP and ventricular end‐diastolic pressure (Nguyen et al., 2018). RPP is calculated as the product of heart rate and systolic blood pressure(Ansari et al., 2012). [Colour figure can be viewed at wileyonlinelibrary.com]