Differential effects of sympatholytic agents on the power spectrum of rats during the cooling-induced hemodynamic perturbations.

Cold stress-elicited hemodynamic perturbations (CEHP) its underlying mechanisms still not clear. We examined the difference of two effector arms of sympathetic outflows, the sympathoadrenal system, and postganglionic sympathetic neurons, their role in CEHP genesis by using two sympatholytic agents, fusaric acid (FA, dopamine-ß-hydroxylase inhibitor) and guanethidine (GUA, norepinephrine-depleting drug). Adult male Sprague-Dawley rats were divided into three groups (n = 6, each), an intraperitoneal injection of control vehicle saline or FA or GUA and then all rats were subjected to a 10-min CS trial. Systolic blood pressure (SBP), heart rate (HR), dicrotic notch (Dn), power spectrum of blood pressure variability and HR variability (BPV, HRV), and coherence spectrum at very-low, low, and high frequency regions (VLF: 0.02-0.2 Hz, LF: 0.2-0.6 Hz, and HF: 0.6-3.0 Hz) were monitored using telemetry throughout the experiment course. We observed both FA and GUA attenuated SBP and HR and the spectral powers of BPV at VLF, LF, and HF in both baseline (PreCS) and cold stimuli (CS) conditions, but apparently, FA exerted stronger effects than GUA did. Both FA and GUA generally attenuated the responses of CS-induced pressor and tachycardia and the CS-increased VLFBPV, LFBPV, and HFBPV, but different effects between FA and GUA, when compared with control vehicle under CS. FA reduced the CS-reduced VLFHRV and the CS-increased LFBPV and HFBPV more than GUA did. We further observed in both PreCS and CS, GUA but not FA increased HFHRV; FA reduced but apparently, GUA increased the occurrence of Dn. Finally, we observed FA weakened, but GUA strengthened the coherence between BPV and HRV at both LF and HF regions. Taken together, the different effects between FA and GUA on CEHP indicate a role of the sympathoadrenal mechanism in response to CS.

Role of vasopressin V1 antagonist in the action of vasopressin on the cooling-evoked hemodynamic perturbations of rats.

We aimed to investigate the role of arginine vasopressin (AVP) acting via the AVPV1 receptor in the autonomic cardiovascular responses to cold stress (CS). The study was conducted on adult male Sprague-Dawley rats with telemetry transmitters implanted to monitor heart rate (HR) and systolic blood pressure (SBP) throughout the experiment course. Rats were divided into four groups and were given, respectively, saline (control group), AVPV1 antagonist (V1880) alone, and V1880 following the removal of sympathetic outflows using hexamethonium (HEX+V1880) or guanethidine (GUA + V1880). Rats were subjected to the CS stimuli (rapid immersion of the rat's limbs into 4 °C water). Hemodynamic responses were recorded at baseline (PreCS), during CS, and after CS. Data analysis was performed using descriptive methods and spectral and cross-spectral analysis of blood pressure variability (BPV) and heart rate variability (HRV). Key results showed that at PreCS, inhibition of AVPV1 increases SBP and HR as well as very-low-frequency BPV and low-frequency BPV, which is attenuated by hexamethonium (effect on SBP only) and guanethidine (effect on both SBP and HR). HEX+V1880 results in increased high-frequency BPV and attenuated very-low-frequency HRV, while GUA + V1880 results in increased high-frequency HRV and attenuated very-low-frequency HRV. During CS, we observed that SBP and HR, as well as very-low-frequency BPV and low-frequency BPV, were similar in the control group and the group with AVPV1 inhibition, while AVPV1 inhibition results in attenuated high-frequency BPV. Furthermore, we observed that changes produced by AVPV1 inhibition alone were affected differently by HEX+V1880 and GUA + V1880, particularly in low-frequency HRV and very-low-frequency HRV. The results support that AVPV1 mediates autonomic cardiovascular responses at both baseline and CS stimuli conditions are associated with central mechanism engagement.

Effects of prolonged paradoxical sleep deprivation with or without acute cold stress on hemodynamic perturbations in rats.

Prolonged paradoxical sleep deprivation (PSD) and cold stress (CS) are known to cause sympathoexcitation and increase the risk of cardiovascular disease. The present study examined the effect of PSD with CS on hemodynamic perturbations by investigating blood pressure and heart rate variability (BPV and HRV) in conscious rats. Adult male Sprague-Dawley rats were divided into three groups (n = 10, each): normal sleep (NS), PSD of 72 h, and recovery sleep of 7 days after PSD. When compared with NS, PSD increased systolic blood pressure in all three conditions: before CS (PreCS), CS, and after CS (PostCS). The PSD also increased heart rate in both PreCS and PostCS. Furthermore, spectral power changes were observed throughout the experiment. The PSD increased very-low-frequency BPV in PreCS, decreased very-low-frequency HRV in CS, and increased low-frequency BPV in all three conditions. The PSD increased low-frequency HRV in PreCS, increased high-frequency BPV in both CS and PostCS, and also increased high-frequency HRV in both PreCS and CS but decreased that in PostCS. On the other hand, when compared with PSD, recovery sleep has reversed most cardiovascular changes in PSD toward the NS level. However, when compared with NS, spectral powers of very-low-frequency BPV in the recovery phase showed a lower level. These results showed that in the resting condition, PSD might evoke sympathoexcitation with a tendency to increase both very-low-frequency BPV and very-low-frequency HRV, as the intensified myogenic oscillations. However, in the CS condition, PSD evoked the sympathoexcitation yet might attenuate such myogenic oscillations.

Right Ventricle Mimics Right Atrium at First Glance: A Rare Case of Congenital Right Sided Partial Pericardial Defect.

Among heart irregularities, congenital pericardial defect is an unusual anomaly, and is typically left dominant. However, cases of right pericardial defect with heart herniation are extremely rare. This is a case of congenital right pericardial defect with herniation of the right ventricle free wall and right ventricular outflow tract. The patient is asymptomatic and refused further intervention but even indolent discomfort underscores the risks of iatrogenic injuries to the heart and sudden death caused by mechanical pathogenesis due to changes in anatomical positions of the cardiac structures.

Massive pericardial effusion with diastolic right ventricular compression secondary to hypothyroidism in a 73-year-old woman.

Pericardial effusion is commonly seen in patients with hypothyroidism, but a massive pericardial effusion with obvious diastolic right ventricular compression is uncommon. We herein report a case of 73-year-old woman seen in the ED with generalized weakness and hypotension. Echocardiography revealed a massive pericardial effusion with diastolic right ventricular compression, and thyroid function testing revealed marked hypothyroidism. The pericardial effusion resolved after the administration of thyroid replacement therapy. This case reveals the importance of including hypothyroidism in the differential diagnosis of pericardia effusion.

Silent ST segment elevation myocardial infarction with multi-segmental renal infarction: an unusual presentation.

A 36-year-old diabetic man came to our institution presenting with constant left flank pain. Left renal embolic infarction was found by abdominal computed tomography. Silent ST segment elevation myocardial infarction was noted on 12-lead electrocardiogram. Emergent coronary angiography revealed large thrombus burdens with complete occlusion at the left anterior descending artery ostium, which may be the embolic origin. Silent ST segment elevation myocardial infarction with acute flank pain and multiple segmental renal infarction is an unusual presentation. High vigilance may prevent delay of the "golden hour" to treat acute myocardial infarction.

Safe right bundle branch block pattern during permanent right ventricular pacing.

It is known that an electrocardiogram (ECG) after transvenous right ventricular (RV) pacing should yield left bundle branch block (LBBB) QRS patterns. When right bundle branch block (RBBB) pacing morphology appears in a patient with a permanent or temporary transvenous RV pacemaker, myocardial perforation or malposition of the pacing lead must be ruled out, even though the patient may be asymptomatic. We report a case of a 77-year-old man who underwent permanent transvenous VDD pacemaker implantation for symptomatic heart block. The postoperative ECG revealed a RBBB pacing configuration, but his chest X-ray and echocardiographic studies confirmed uncomplicated RV pacing. We review and discuss the literature concerning the differential diagnosis of such a safe RBBB ECG pattern.