Introduction: Periodontitis is a prevalent and severe dental condition characterized by the gradual degradation of the bone surrounding the teeth. Over the past two decades, numerous epidemiological investigations have suggested a potential link between periodontitis and cardiovascular disease. However, the complex mechanistic relationship between oral health issues and cardiovascular disorders remains unclear.Aim: This study aimed to explore comprehensively the cardiac function through various methods, including conventional echocardiography, intraventricular pressure gradient (IVPG) analysis, speckle tracking echocardiography (STE), and hemodynamics analysis.Methods: Ligature-induced periodontitis was established in a group of rats while the second group served as sham. The successful establishment of the periodontitis model was confirmed through staining and radiographic examination of the affected mandibles.Results: X-ray films and methylene blue staining revealed alveolar bone resorption in the affected first molar in the model rats, confirming the successful induction of periodontitis. The rats with periodontitis displayed a decrease in ejection fraction compared to the sham group, accompanied by a decrease in mid-to-apical IVPG and mid IVPG. Lower values of strain rate were recorded in the apical segment of the septum, the middle segment of the septum, and the basal segment of the lateral free wall in the periodontitis group, which was associated with histopathological examination showing some degree of myocardial tissue damage. Conversely, rats with periodontitis showed an increase in heart rate, end-systolic volume, and arterial elastance when compared to the sham rats. However, they also exhibited a decrease in stroke work, stroke volume, cardiac output, and end-systolic pressure.Conclusion: This study suggests that experimental periodontitis may lead to cardiac dysfunction especially compromised systolic function and myocardial relaxation, potentially indicating an increased risk of cardiovascular events in clinical periodontitis cases. The comprehensive assessment of cardiac function, hemodynamics, and histopathological evaluation underscores the profound impact of periodontitis on heart functions within this specific experimental model.

We examined urine excretion during primary acute sympathetic activation (PASA) in anesthetized Wistar-Kyoto rats. Since arterial pressure (AP) changes with sympathetic nerve activity (SNA) during PASA, urine excretion reflects a neurally-mediated antidiuretic effect combined with an effect of pressure diuresis. We hypothesized that preventing AP changes under PASA would enable the direct estimation of the neurally-mediated antidiuretic effect alone. We changed the isolated carotid sinus pressure stepwise from 60 to 180 mmHg and compared the relationship of normalized urine flow (nUF, urine flow normalized by body weight) versus SNA between conditions allowing and preventing baroreflex-mediated changes in the mean AP. The slope of the SNA-nUF relationship was nUF_var = 0.444 ± 0.074 μL·min⁻¹·kg⁻¹·%⁻¹ when the mean AP was variable, whereas it was nUF_fix = −0.143 ± 0.032 μL·min⁻¹·kg⁻¹·%⁻¹ when the mean AP was fixed at 100 mmHg (n = 7 rats). The slope associated with the effect of pressure diuresis alone, calculated as nUF_var − nUF_fix, was 0.586 ± 0.105 μL·min⁻¹·kg⁻¹·%⁻¹. Hence, the potency of the neurally-mediated antidiuretic effect, | nUF_fix| / ( nUF_var − nUF_fix), was 0.235 ± 0.014 relative to the effect of pressure diuresis under PASA. Our findings would aid an integrative understanding of the effects of renal hemodynamic and sympathetic modulations on urine output function.

Hypertrophic cardiomyopathy (HCM) is a common form of cardiomyopathy in cats, and heart failure occurs as diastolic dysfunction progresses. HCM in cats is broadly classified as non-obstructive and obstructive hypertrophic cardiomyopathy, depending on the presence or absence of outflow tract obstruction. Measurement of the intraventricular pressure differences (IVPD) using color M-mode (CMM) has attracted attention as a reliable diastolic index as it correlates with catheterization, the gold standard for the assessment of diastolic performance. Because IVPD is affected by the size of the heart, the intraventricular pressure gradient (IVPG) index, which is unaffected by heart size, is by calculated by dividing IVPD by LV length. In the present study, CMM IVPG was used to non-invasively assess diastolic impairment in cats with obstructive hypertrophic cardiomyopathy. This study was conducted on 10 control cats and 18 cats in the HCM group. Although no severe left atrial enlargement was observed in the HCM group, the basal IVPG was significantly increased in the HOCM group compared to the control group. Although IVPD typically suggests impaired diastolic function and reduced ventricular compliance, the significant increase observed in the HOCM group compared to controls may suggest an indirect elevation in left atrial pressure, likely secondary to left ventricular outflow tract obstruction. The increase in IVPG in HOCM, as shown in this study, is a pathological effect of left ventricular outflow tract obstruction that cannot be detected by conventional echocardiographic indices, and evaluating IVPG is useful to evaluate cardiac function from a perspective that differs from conventional methods.

Ozai Y, et al. J Vet Sci. 2022 Feb;23:e39. https://doi.org/10.4142/jvs.21314

Accentuated antagonism refers to a phenomenon in which the vagal effect on heart rate (HR) is augmented by background sympathetic tone. The dynamic aspect of accentuated antagonism remains to be elucidated during different levels of vagal nerve stimulation (VNS) intensity. We performed VNS on anesthetized rats (n = 8) according to a binary white noise signal with a switching interval of 500 ms at three different stimulation rates (low-intensity: 0-10 Hz, moderate-intensity: 0-20 Hz, and high-intensity: 0-40 Hz). The transfer function from VNS to HR was estimated with and without concomitant tonic sympathetic nerve stimulation (SNS) at 5 Hz. The asymptotic low-frequency (LF) gain (in beats·min⁻¹·Hz⁻¹) of the transfer function increased with SNS regardless of the VNS rate [low-intensity: 3.93 ± 0.70 vs. 5.82 ± 0.65 (P = 0.021), moderate-intensity: 3.87 ± 0.62 vs. 5.36 ± 0.53 (P = 0.018), high-intensity: 4.77 ± 0.85 vs. 7.39 ± 1.36 (P = 0.011)]. Moreover, SNS slightly increased the ratio of high-frequency (HF) gain to the LF gain. These effects of SNS were cancelled by the pretreatment of ivabradine, an inhibitor of hyperpolarization-activated cyclic nucleotide-gated channels, in another group of rats (n = 6). Although background sympathetic tone antagonizes the vagal effect on mean HR, it enables finer HR control by increasing the dynamic gain of the vagal HR transfer function regardless of VNS intensity. When interpreting the HF component of HR variability, the augmenting effect from background sympathetic tone needs to be considered.

Aims: To quantify in vivo the effects of the soluble guanylate cyclase (sGC) stimulator, vericiguat, on autonomic cardiovascular regulation in comparison with the nitric oxide (NO) donor, sodium nitroprusside. Methods: In anesthetized Wistar–Kyoto rats, baroreflex-mediated changes in sympathetic nerve activity (SNA), arterial pressure (AP), central venous pressure (CVP), and aortic flow (AoF) were examined before and during the intravenous continuous administration (10 μg·kg⁻¹·min⁻¹) of vericiguat or sodium nitroprusside (n = 8 each). Systemic vascular resistance (SVR) was calculated as SVR = (AP–CVP) / AoF. Results: Neither vericiguat nor sodium nitroprusside affected fitted parameters of the baroreflex-mediated SNA response. Both vericiguat and sodium nitroprusside decreased the AP mainly through their peripheral effects. Vericiguat halved the slope of the SNA–SVR relationship from 0.012 ± 0.002 to 0.006 ± 0.002 mmHg·min·mL⁻¹·%⁻¹ (P = 0.008), whereas sodium nitroprusside caused a near parallel downward shift in the SNA–SVR relationship with a reduction of the SVR intercept from 1.235 ± 0.187 to 0.851 ± 0.123 mmHg·min/mL (P = 0.008). Conclusion: Neither vericiguat nor sodium nitroprusside significantly affected the baroreflex-mediated SNA response. The vasodilative effect of vericiguat became greater toward high levels of SNA and AP, possibly reflecting the increased sGC sensitivity to endogenous NO. By contrast, the effect of sodium nitroprusside was more uniform over the range of SNA. These results help better understand cardiovascular effects of vericiguat.