Prior studies have shown that removal of vestibular inputs produces lability in blood pressure during orthostatic challenges (Holmes MJ, Cotter LA, Arendt HE, Cass SP, and Yates BJ. Brain Res 938: 62-72, 2002; Jian BJ, Cotter LA, Emanuel BA, Cass SP, and Yates BJ. J Appl Physiol 86: 1552-1560, 1999). Furthermore, these studies led to the prediction that the blood pressure instability results in susceptibility for orthostatic intolerance. The present experiments tested this hypothesis by recording common carotid blood flow (CCBF) in conscious cats during head-up tilts of 20, 40, and 60 degrees amplitudes, before and after the surgical elimination of labyrinthine inputs through a bilateral vestibular neurectomy. Before vestibular lesions in most animals, CCBF remained stable during head-up rotations. Unexpectedly, in five of six animals, the vestibular neurectomy resulted in a significant increase in baseline CCBF, particularly when the laboratory was illuminated; on average, basal blood flow measured when the animals were in the prone position was 41 +/- 17 (SE) % higher after the first week after the lesions. As a result, even when posturally related lability in CCBF occurred after removal of vestibular inputs, blood supply to the head was not lower than when labyrinthine inputs were present. These data suggest that vestibular influences on cardiovascular regulation are more complex than previously appreciated, because labyrinthine signals appear to participate in setting basal rates of blood flow to the head in addition to triggering dynamic changes in the circulation to compensate for orthostatic challenges.
"Subsequently, a baroreflex fall in HR and total peripheral resistance occurs and BP returns to resting levels (Galland et al., 2000a,b; Yiallourou et al., 2008a). Conversely, it is also believed that the traditional baroreflex response to HUT may be preceded by a fast-acting vestibular-mediated increase in BP in the initial phase following HUT (Doba and Reis, 1974; Wilson et al., 2006). Doba and Reis (1974) identified that denervation of baroreceptors in cats impaired cardiovascular responses to passive HUT and subsequent lesion of the cerebellar fastigial nucleus (an area thought to be triggered by the vestibular apparatus) increased this deficit. "
[Show abstract][Hide abstract] ABSTRACT: Dramatic changes in cardiovascular control occur in sleep during infancy, when sleep time is at a lifetime maximum. In infants born preterm there are significant cardiovascular complications later in life, and also an increased risk for sudden infant death syndrome (SIDS), possibly a result of inadequate compensation to a cardiorespiratory challenge in sleep. We aimed to examine the consequences of preterm birth on heart rate (HR) and blood pressure (BP) responses to head-up tilting (HUT) during sleep in infants. Preterm (n = 25) and term (n = 20) infants were studied using daytime polysomnography at 2-4 weeks', 2-3 months' and 5-6 months' term-corrected age (CA). BP was recorded using a photoplethysmographic cuff (Finometer); 15 degrees HUTs were performed during both quiet and active sleep. Preterm infants responded to HUT with increased HR and BP, followed by a bradycardia and a subsequent return of HR and BP to baseline. Overall, HUT responses were similar between term and preterm infants at matched ages. Notably, however, return of BP to baseline was considerably delayed in preterm infants ( approximately 37 beats post-tilt) compared with term infants ( approximately 23 beats post-tilt) at both 2-4 weeks' and 2-3 months' CA (P < 0.05). Our study has demonstrated that preterm infants respond to a BP perturbation with changes in HR that match those of term infants. However, delayed recovery of BP during sleep in the preterm infant may be indicative of underlying deficits or immaturity in vascular function or control, which may contribute to their vulnerability to SIDS and cardiovascular complications later in life.
Journal of Sleep Research 11/2009; 19(1 Pt 1):93-102. DOI:10.1111/j.1365-2869.2009.00793.x · 3.35 Impact Factor
"Animals underwent an aseptic surgery that employed standard techniques and incorporated anesthetic and post-surgical procedures we have employed in many previous studies (e.g., Wilson et al., 2006; Arshian et al., 2007). A fixation plate was mounted on the skull so that the head could subsequently be immobilized during recordings. "
[Show abstract][Hide abstract] ABSTRACT: The rostral fastigial nucleus (RFN) of the cerebellum is thought to play an important role in postural control, and recent studies in conscious nonhuman primates suggest that this region also participates in the sensory processing required to compute body motion in space. The goal of the present study was to examine the dynamic and spatial responses to sinusoidal rotations in vertical planes of RFN neurons in conscious cats, and determine if they are similar to responses reported for monkeys. Approximately half of the RFN neurons examined were classified as graviceptive, since their firing was synchronized with stimulus position and the gain of their responses was relatively unaffected by the frequency of the tilts. The large majority (80%) of graviceptive RFN neurons were activated by pitch rotations. Most of the remaining RFN units exhibited responses to vertical oscillations that encoded stimulus velocity, and approximately 50% of these velocity units had a response vector orientation aligned near the plane of a single vertical semicircular canal. Unlike in primates, few feline RFN neurons had responses to vertical rotations that suggested integration of graviceptive (otolith) and velocity (vertical semicircular canal) signals. These data indicate that the physiological role of the RFN may differ between primates and lower mammals. The RFN in rats and cats in known to be involved in adjusting blood pressure and breathing during postural alterations in the transverse (pitch) plane. The relatively simple responses of many RFN neurons in cats are appropriate for triggering such compensatory autonomic responses.
"These results suggest that the orthostatic intolerance induced by vestibular lesions is not the result of a decreased ability to produce compensatory heart rate responses. On the other hand, a recent animal study has demonstrated the blood supply to the head during a 60 • tilt in pitch plane to not be lower in cats with the removal of vestibular inputs in comparison to cats with normal vestibular inputs . Therefore it is still unclear whether the vestibular-sympathetic system plays a role in regulating the cerebral vascular resistance. "
[Show abstract][Hide abstract] ABSTRACT: A number of animal studies have confirmed that the otolith organs may contribute to the maintenance of blood pressure during positional change; however, the contribution of such organs remains to be elucidated in humans.
This study investigated whether acute dizzy patients (n = 11) with an abnormal deviation of the subjective visual vertical (SVV) show an abnormality in the orthostatic regulation of blood pressure in comparison to acute dizzy patients with a normal deviation of the SVV (n = 11) and control subjects (n = 11).
The average change in the systolic blood pressure (SBP) at 1 minute after active standing in comparison to that at baseline in dizzy patients with an abnormal deviation of the SVV was -6.8 +/- 3.0 mmHg. The change was significantly lower than that in the control subjects (2.1 +/- 2.6 mmHg, p < 0.05), while the change in dizzy patients with a normal deviation of the SVV (2.6 +/- 2.2 mmHg) was not significantly different from that in the control subjects (p > 0.05). Active standing significantly increased the heart rate (HR) in all participants (p < 0.01) and there was no significant difference in the change of the HR among the 3 groups (p > 0.05).
These results suggest that dizzy patients in the acute phase of recovery from vestibular dysfunction have an orthostatic dysregulation of the blood pressure, thus resulting in such patients suffering from orthostatic intolerance.
Journal of Vestibular Research 01/2008; 18(4):223-9. · 1.19 Impact Factor
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