Anesthetic depression of microcirculation, central hemodynamics, and respiration in decerebrate rats

Faber, James E.; Harris, Peter; Wiegman, David L.

doi:10.1152/ajpheart.1982.243.6.h837

Cited by 27 publications

(36 citation statements)

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“…This is in general agreement with what has been found to be true for arteriolar vasomotion in both connective tissue [12] and skeletal muscle [17], One implication of this lack of clear correlation between vessel size and vasomotion might be that the mechanisms un derlying vasomotion are of a uniform type in the range of vessel diameters investigated and that force production (number of muscle elements) grows approximately in pro portion with the vessel wall tension according to Laplace's law. However, Colantuoni et al [18] found that, in the hamster skin fold preparation, the vasomotion frequency decreased from a maximum of 9-15 cpm in 8-to 15-pm A4 arterioles to 1-3 cpm in 70-to lOO-pm Ai small arter ies.…”

Section: Discussionsupporting

confidence: 89%

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Effects of Buflomedil on Spontaneous Vasomotion and Mean Arteriolar Internal Diameter in the Hamster Cheek Pouch

Cyrino¹

1994

J Vasc Res

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Intravital microscopy of the hamster cheek pouch microvasculature was used for in vivo studies on the effects of buflomedil, phentolamine (α-adrenergic receptor antagonist) and norepinephrine on the mean internal arteriolar diameter and spontaneous vasomotion. All drugs were applied topically. The vasomotor activity was studied in 125 arterioles (internal diameter range 18.0–62.0 µm) of 34 preparations. Addition of buflomedil (10^–9 to 10^–5M) did not affect the arteriolar diameter significantly (from 100.7 ± 3.5 to 106.4 ± 1.8%, values expressed in percent of the initial diameter as mean ± SE), but increased the vasomotion frequency and amplitude by approximately 20% (from 7.5 ± 0.3 to 9.2 ± 0.2 cpm) and 30% (from 7.3 ± 0.3 to 10.0 ± 0.5 µm), respectively. Phentolamine (10^–9 to 10^–5M) dose-dependently increased the microvascular diameter (from 102.3 ± 1.2 to 139.1 ± 4.3%) and reduced the vasomotion frequency and amplitude (from 8.0 ± 0.3 to 1.9 ± 0.5 cpm and from 9.0 ± 2.1 to 3.1 ± 0.2 µm, respectively). Addition of buflomedil (10^–7M) reduced the vasodilation evoked by phentolamine (from 103.3 ± 0.7 to 127.0 ± 1.5%) and potentiated its depressive effect on vasomotion frequency and amplitude (from 7.6 ± 0.1 to 1.0 ± 0.3 cpm and from 9.0 ± 0.3 to 1.9 ± 0.6 µm, respectively). Norepinephrine (10^–9 to 10^–5M) dose-dependently decreased to arteriolar diameter (from 102.3 ± 0.7 to 69.6 ± 1.6%) and the vasomotion frequency and amplitude (from 8.4 ± 0.2 to 0.4 ± 0.3 emp and from 8.7 ± 0.2 to 0.5 ± 0.4 µm, respectively). Addition of buflomedil (10^–7 M) reduced the vasoconstriction elicited by norepinephrine (from 103.2 ± 0.9 to 82.9 ± 3.9%) and restored the vasomotion frequency and amplitude (from 8.4 ± 0.3 to 7.8 ± 0.4 cpm and from 8.6 ± 0.2 to 7.8 ± 0.3 µm, respectively). The effects observed with buflomedil on the hamster cheek pouch microcirculation suggest a direct action on the smooth muscle excitability and further support its properties as a competitive inhibitor of α-adrenergic receptors and as a weak calcium antagonist.

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Section: Discussionsupporting

confidence: 89%

“…However, it appears to have a lower frequency than the vasomotor activity seen in skeletal muscle, such as the rabbit tenuissimus muscle (5-32 cpm) [14,15], bat coracocutaneous muscle (24-75 cpm) [16] and the rat cremaster muscle (25-35 cpm) [17].…”

Section: Discussionmentioning

confidence: 99%

Effects of Buflomedil on Spontaneous Vasomotion and Mean Arteriolar Internal Diameter in the Hamster Cheek Pouch

Cyrino¹

1994

J Vasc Res

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“…18 > 19 The frequency of vasomotion we observed was between 5 and 8 cycles/min, which agrees with previous observations in small arterioles in the hamster skinfold preparation. 20 Higher frequencies of vasomotion were reported in the skeletal muscle of decerebrated 21 or pentobarbital-anesthetized rat, 22 whereas much lower frequencies were reported in the cerebral microcirculation of awake rabbits. 23 Apart from an influence of anesthetics, the pattern of vasomotion may vary for different arterioles.…”

Section: Discussionmentioning

confidence: 98%

Microvascular alterations in adult conscious spontaneously hypertensive rats.

et al. 1990

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The dorsal skin flap technique was used to study skeletal muscle microcirculation in conscious 10-12-week-old spontaneously hypertensive rats and normotensive Wistar-Kyoto control rats. Videorecordings were made for off-line analysis of consecutive segments of the vascular bed. Resting diameters were significantly smaller in spontaneously hypertensive rats than in Wistar-Kyoto rats at the first-order (-28%) and second-order arteriolar (-21%) levels. Precapillary third-order and fourth-order arterioles of spontaneously hypertensive rats had normal diameters, whereas postcapillary small venule diameters were slightly larger in spontaneously hypertensive rats. Thirty percent and 41% of the spontaneously hypertensive rat and Wistar-Kyoto rat third-order arteriolar vessels and 63 and 45% of the fourth-order arteriolar vessels exhibited vasomotion. Vasomotion amplitude, but not frequency, was significantly higher in spontaneously hypertensive rats than in Wistar-Kyoto rats. It is concluded that, in the established phase of spontaneous hypertension in the rat, a decreased diameter of large arterioles is the major mechanism underlying the increased vascular resistance in cutaneous skeletal muscle. {Hypertension 1990;15:415-419) M icrovascular alterations of resistance vessels contribute to a considerable degree to the increased peripheral resistance in spontaneous hypertension.1 Skeletal muscle vascular resistance in particular is responsible for the bulk of increased peripheral resistance.2 The primary mechanism for increasing the resistance in a microvessel is the decrease of its diameter. There is growing evidence, on the basis of indirect observations, that larger arterioles of spontaneously hypertensive rats (SHR) exhibit smaller diameters and are the major contributors to the increased vascular resistance. -3However, direct microvascular observations of various skeletal muscles in situ do not consistently demonstrate a reduced diameter of arteriolar resistance vessels. -6 These studies suggest microvascular rarefaction as an alternate mechanism for increased vascular resistance.The information concerning changes of the microvasculature of the SHR as compared with

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“…We developed the DPP as an alternative to, rather than a replacement of, previous preparations because it 1) allows the study of respiratory chemosensitivity independent of heart rate and systemic blood pressure, 2) allows the use of rats, which are being used increasingly as an experimental model for studies of the control of breathing, and 3) increases the feasibility of addressing a greater range of questions, owing to the fact that the DPP requires less sophisticated surgery and can be prepared rapidly. Being decerebrate, the DPP avoids the nonspecific, depressive effects of anesthetics and paralytic agents on respiratory chemoreceptors (28,72). Although most of the other preparations used for these kinds of studies are perfused with blood, the DPP is distinct in that the brain stem and the carotid body are artificially perfused with defined media.…”

Section: Critique Of the Dppmentioning

confidence: 99%

Specific carotid body chemostimulation is sufficient to elicit phrenic poststimulus frequency decline in a novel in situ dual-perfused rat preparation

Day

Wilson

2005

American Journal of Physiology-Regulatory, Integrative and Comp

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Time-dependent ventilatory responses to hypoxic and hypercapnic challenges, such as posthypoxic frequency decline (PHxFD) and posthypercapnic frequency decline (PHcFD), could profoundly affect breathing stability. However, little is known about the mechanisms that mediate these phenomena. To determine the contribution of specific carotid body chemostimuli to PHxFD and PHcFD, we developed a novel in situ arterially perfused, vagotomized, decerebrate rat preparation in which central and peripheral chemoreceptors are perfused separately (i.e., a nonanesthetized in situ dual perfused preparation). We confirmed that 1) the perfusion of central and peripheral chemoreceptor compartments was independent by applying specific carotid body hypoxia and hypercapnia before and after carotid sinus nerve transection, 2) the PCO(2) chemoresponse of the dual perfused preparation was similar to other decerebrate preparations, and 3) the phrenic output was stable enough to allow investigation of time-dependent phenomena. We then applied four 5-min bouts (separated by 5 min) of specific carotid body hypoxia (40 Torr PO(2) and 40 Torr PCO(2)) or hypercapnia (100 Torr PO(2) and 60 Torr PCO(2)) while holding the brain stem PO(2) and PCO(2) constant. We report the novel finding that specific carotid body chemostimuli were sufficient to elicit several phrenic time-dependent phenomena in the rat. Hypoxic challenges elicited PHxFD that increased with bout, leading to progressive augmentation of the phrenic response. Conversely, hypercapnia elicited short-term depression and PHcFD, neither of which was bout dependent. These results, placed in the context of previous findings, suggest multiple physiological mechanisms are responsible for PHxFD and PHcFD, a redundancy that may illustrate that these phenomena have significant adaptive advantages.

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Anesthetic depression of microcirculation, central hemodynamics, and respiration in decerebrate rats

Cited by 27 publications

References 0 publications

Effects of Buflomedil on Spontaneous Vasomotion and Mean Arteriolar Internal Diameter in the Hamster Cheek Pouch

Effects of Buflomedil on Spontaneous Vasomotion and Mean Arteriolar Internal Diameter in the Hamster Cheek Pouch

Microvascular alterations in adult conscious spontaneously hypertensive rats.

Specific carotid body chemostimulation is sufficient to elicit phrenic poststimulus frequency decline in a novel in situ dual-perfused rat preparation

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