Effects of an acute, outpatient physiotherapy exercise program following pediatric heart or lung transplantation.

This prospective interventional study investigated the impact of a three-month, ambulatory HA or HB, semi-individualized, PT-prescribed exercise program following pediatric HTx or LTx. SMW distance, strength, and flexibility were assessed at start and completion of the program and one yr after enrollment. Subjects received either an HB or HA exercise program three times per week. The cohort demonstrated clinically and statistically significant improvements in SMW distances at three months (425.7 ± 109.4-500.6 ± 93.6 m, p < 0.001) and at one yr (528.5 ± 66.6 m, p = 0.001), although there was no difference between the two groups at any time. Similar improvements were also observed in strength and flexibility measures. Correlates with higher SMW distance at three months and one yr included older age, male gender, and underlying diagnosis other than CHD. Male gender and diagnosis other than CHD were associated with a slower improvement in the SMW distance. This is the first report of institutionally based, outpatient exercise rehabilitation in the recovery following pediatric thoracic transplantation. We found similar improvements to HB interventions up to one yr after surgery. Further study of the role of exercise rehabilitation and long-term fitness outcomes is needed.

Reduced baroreceptor sensitivity during hypotension in ANP-knockout mice.

We studied baroreflex gain in inactin-anesthetized mice that had been genetically modified to be depleted of atrial natriuretic peptide (ANP -/-). Wild-type mice (ANP +/+) served as controls. ANP -/- mice had a significantly higher basal arterial blood pressure (ABP) than ANP +/+ mice [112+/-7 vs. 80+/-5 mmHg (mean +/- SEM)]. Their basal heart rates were not different (491+/-13 vs. 446+/-19 bpm). A third group, composed of ANP +/+ mice only, was rendered acutely hypertensive by an intravenous infusion of arginine vasopressin acetate (0.3 pg bolus followed by 0.3 pg/h) so as to serve as a control for the elevated ABP in the ANP -/- mice. Transient changes in ABP were caused by bolus injections of oxymetazoline hydrochloride (1.5-3 ng) or sodium nitroprusside (20-100 ng). Baroreflex gain was calculated as the ratio of the peak heart rate change that followed the peak change in mean ABP resulting from injection of oxymetazoline or nitroprusside. There were no significant differences among the groups in their responses to transient hypertension. On the other hand, the ANP -/- mice showed a significantly depressed tachycardic response to transient hypotension when compared with the other two groups. We conclude that the ANP -/- mice are unable to increase efferent sympathetic nervous activity adequately above the high basal activity that is a feature of this animal model.

Atrial natriuretic peptide and mechanisms of cardiovascular control. Role of serotonergic receptors.

Atrial natriuretic peptide (ANP) inhibits renal sympathetic nerve activity (RSNA), provided the vagi are intact. Afferents from chemosensitive cardiopulmonary receptors are specifically required. Such receptors produce the Bezold-Jarisch reflex, are prominent on the ventricular epicardium, and are richly supplied with 5-hydroxytryptamine type 3 (5-HT3) receptors. We tested the hypothesis that epicardial 5-HT3-sensitive neurons mediate depressor effects of ANP. Through a special catheter, anesthetized, sinoaortically denervated rats received pericardial test injections of ANP (28-amino acid rat ANP; 100 and 1,000 ng) in the presence or absence of 5-HT3 antagonist (Ondansetron, 20 micrograms/kg; n = 9). In other groups we observed the effects of systemic ANP while blocking either epicardial or systemic 5-HT3 receptors. Arterial blood pressure (ABP), heart rate, and RSNA were recorded continuously. Intravenous ANP (100 or 200 ng) decreased ABP and RSNA significantly. In contrast, intrapericardial ANP (100 or 1,000 ng) caused no significant fall in ABP or RSNA. Both intravenous and pericardial Ondansetron reduced the effects of intravenous ANP significantly, but the intravenous antagonism was significantly greater. We conclude that epicardial chemosensitive afferents are not sensitive to ANP and that sympathoinhibitory effects of ANP arise from a 5-HT3 agonist that cannot be produced when ANP is confined to the pericardial space.