Cardiovascular Responses During Stimulation Of Hindlimb Skeletal Muscle Nerves In Anaesthetized Rats

Abstract

1. Cardiovascular responses during static skeletal muscle contraction in anaesthetized rats appear to be contradictory. The present study attempted to explain such variations by stimulating different peripheral nerves supplying the hindlimb skeletal muscles using anaesthetized Sprague-Dawley rats. 2. Muscle contractions were evoked by a 30 s stimulation of the sciatic, tibial, peroneal nerves or the sciatic nerve with transected peroneal branch at threefold the motor threshold, 0.1 msec duration and 40 Hz frequency. 3. Contractions during stimulation of the tibial or the sciatic nerve with severed peroneal branch evoked similar increases in arterial pressure and heart rate. Following stimulation of the tibial nerve, blood pressure, heart rate and muscle tension increased by 23 +/- 3 mmHg, 31 +/- 5 b.p.m. and 789 +/- 34 g, respectively. For the sciatic nerve with transected peroneal branch, increases the respective increases were 27 +/- 5 mmHg, 32 +/- 6 b.p.m. and 802 +/- 43 g. In contrast, peroneal nerve stimulation produced depressor and bradycardic responses of -22 +/- 5 mmHg and -40 +/- 9 b.p.m., respectively. Interestingly, intact sciatic nerve stimulation elicited pressor, depressor or no responses (average being -10 +/- 8 mmHg), along with a consistent increase in heart rate of 24 +/- 7 b.p.m. 4. The results demonstrate that static muscle contraction following stimulation of the tibial or sciatic nerve with transected peroneal branch, elicits consistent increases in blood pressure and heart rate. Furthermore, stimulation of the peroneal nerve elicits a depressor response, while stimulation of the intact sciatic nerve evokes variable cardiovascular responses. Overall, anaesthetized rats can be excellent models to study the variable cardiovascular responses during activation of group III and/or group IV muscle afferents.

Cobalt injections into the pedunculopontine nuclei attenuate the reflex diaphragmatic responses to muscle contraction in rats

“…Although the results of the present study do not support a role for the PPN in driving the cardiovascular responses to static muscle contraction in the anesthetized rat, the possibility remains that the PPN modulates reflex cardiovascular responses to muscle contraction in nonanesthetized rats or other species, which exhibit more typical pressor responses to muscle contraction (6, 7, 13, 18, 20, 26). Along similar lines, it would be interesting to test our hypothesis in rat preparations with pressor responses to muscle contraction as reported by Ishide et al (14). Although their model contrasts with our preparation on several levels, including anesthetic regimen, higher tibial nerve stimulation intensity, and markedly lower average force generation, it could shed light on a potential role for the PPN in modulation of pressor responses to muscle contraction.…”

Renal sympathetic and circulatory responses to activation of the exercise pressor reflex in rats

“…However, this species had been little used in studies of the EPR till recently. This is because of the previous conflicting data in anaesthetized rats, in which activation of the EPR has been shown to elicit both a pressor (Ishide et al 2002) and depressor response (Smith et al 2001; Hayashi, 2003; Plowey & Waldrop, 2004) or no response at all (Vissing et al 1991). These discrepancies could be due to an unknown effect of anaesthesia in this species (Smith et al 2001; Hayashi, 2003).…”

Region-Dependent Increase of Cerebral Blood Flow During Electrically Induced Contraction of the Hindlimbs in Rats

“…From these data, increased cardiac output was expected to occur during stimulation. However, the substantial mortality (50%) observed in rats anesthetized with ketamine/xylazine in combination with the suspicion of interaction between anesthesia and the effect of ISMC on BP ( Ishide et al, 2002 ) led us to conduct the same experiments in artificially ventilated rats anesthetized with choral hydrate. As observed under ketamine/xylazine anesthesia, stimulation at 5-fold motor threshold induced a time-dependent elevation of HR without associated changes in BP ( Figure 1 ) in chloral hydrate-anesthetized rats ( n = 6).…”

“…In opposition to the plethora of studies on the cardiovascular (CV) effects of physical activity, the CV effects of ISMC are poorly documented. Nevertheless, tachycardia was consistently reported during induced contraction ( Crayton et al, 1979 ; Ishide et al, 2002 ). More controversial and for still hypothetical reasons ( Ishide et al, 2002 ) is the effect of ISMC on arterial BP (an augmentation, a decrease or no effect), while BP increases during physical activity as a consequence of increased cardiac output.…”

“…CBF and c-fos levels were measured in the area representing the hindlimb and in two cognition-related brain regions (the hippocampus and the prefrontal cortex). Electrically induced bilateral hindlimb contraction was performed according to an acute stimulation protocol (stimulation for 30 min under ketamine/xylazine or chloral hydrate anesthesia) since an interaction between anesthesia and the effect of ISMC on blood pressure (BP) was previously suspected by Ishide et al (2002) or to a subchronic stimulation protocol (stimulation of 30 min a day for 7 consecutive days under isoflurane anesthesia).…”