Regulation of central vascular blood flow in the turtle

1994 ◽  
Vol 267 (2) ◽  
pp. R569-R578 ◽  
Author(s):  
S. G. Comeau ◽  
J. W. Hicks

The purpose of this study was to determine the effects of vagal nerve stimulation on the pulmonary and systemic circulations in the turtle Pseudemys scripta. The heart rate (HR), systemic vascular resistance (Rsys), pulmonary vascular resistance (Rpul), total pulmonary blood flow (Qpul), and total systemic blood flow (Qsys) were measured during electrical stimulation of the vagal efferent and the vagal afferent nerves. Vagal efferent nerve stimulation resulted in a bradycardia, increased Rsys and Rpul, and a 60% reduction in the Qpul and Qsys. These cardiovascular changes were eliminated after an intravenous injection of atropine. In contrast, vagal afferent nerve stimulation resulted in a tachycardia, a twofold increase in Rsys, a reduction in Rpul, and an 85% increase in Qpul. These changes were eliminated after pretreating the animals with bretylium tosylate (10 mg/kg). An intravenous infusion of epinephrine (0.1 micrograms/kg) produced cardiovascular changes similar to vagal afferent stimulation. The cardiovascular changes resulting from afferent and efferent nerve stimulation were similar to the cardiovascular adjustments often associated with intermittent lung ventilation in reptiles. The results of our study suggest that such cardiovascular changes are under cholinergic and adrenergic control.

2008 ◽  
Vol 5 (2) ◽  
pp. 145-151 ◽  
Author(s):  
Sae Uchida ◽  
Harumi Hotta

In this review, our recent studies using anesthetized animals concerning the neural mechanisms of vasodilative effect of acupuncture-like stimulation in various organs are briefly summarized. Responses of cortical cerebral blood flow and uterine blood flow are characterized as non-segmental and segmental reflexes. Among acupuncture-like stimuli delivered to five different segmental areas of the body; afferent inputs to the brain stem (face) and to the spinal cord at the cervical (forepaw), thoracic (chest or abdomen), lumbar (hindpaw) and sacral (perineum) levels, cortical cerebral blood flow was increased by stimuli to face, forepaw and hindpaw. The afferent pathway of the responses is composed of somatic groups III and IV afferent nerves and whose efferent nerve pathway includes intrinsic cholinergic vasodilators originating in the basal forebrain. Uterine blood flow was increased by cutaneous stimulation of the hindpaw and perineal area, with perineal predominance. The afferent pathway of the response is composed of somatic group II, III and IV afferent nerves and the efferent nerve pathway includes the pelvic parasympathetic cholinergic vasodilator nerves. Furthermore, we briefly summarize vasodilative regulation of skeletal muscle blood flow via a calcitonin gene-related peptide (CGRP) induced by antidromic activation of group IV somatic afferent nerves. These findings in healthy but anesthetized animals may be applicable to understanding the neural mechanisms improving blood flow in various organs following clinical acupuncture.


1988 ◽  
Vol 66 (1) ◽  
pp. 101-105 ◽  
Author(s):  
P. Kubes ◽  
C. K. Chapler ◽  
S. M. Cain

Redistribution of blood flow away from resting skeletal muscle does not occur during anemic hypoxia even when whole body oxygen uptake is not maintained. In the present study, the effects of sympathetic nerve stimulation on both skeletal muscle and hindlimb blood flow were studied prior to and during anemia in anesthetized, paralyzed, and ventilated dogs. In one series (skeletal muscle group, n = 8) paw blood flow was excluded by placing a tourniquet around the ankle; in a second series (hindlimb group, n = 8) no tourniquet was placed at the ankle. The distal end of the transected left sciatic nerve was stimulated to produce a maximal vasoconstrictor response for 4-min intervals at normal hematocrit (Hct.) and at 30 min of anemia (Hct. = 14%). Arterial blood pressure and hindlimb or muscle blood flow were measured; resistance and vascular hindrance were calculated. Nerve stimulation decreased blood flow (p < 0.05) in the hindlimb and muscle groups at normal Hct. Blood flow rose (p < 0.05) during anemia and was decreased (p < 0.05) in both groups during nerve stimulation. However, the blood flow values in both groups during nerve stimulation in anemic animals were greater (p < 0.05) than those at normal Hct. Hindlimb and muscle vascular resistance fell significantly during anemia and nerve stimulation produced a greater increase in vascular resistance at normal Hct. Vascular hindrance in muscle, but not hindlimb, was less during nerve stimulation in anemia than at normal Hct. The data indicate that (i) maximal sympathetic stimulation produced a significant decrease in both skeletal muscle and hindlimb blood flow during anemia, (ii) the reduction in blood flow in these areas was less with sympathetic stimulation during anemia than at normal Hct., and (iii) the anemic stimulus (Hct. = 14%) does not activate maximal sympathetic vasoconstrictor tone in the skeletal muscle.


2001 ◽  
Vol 81 (6) ◽  
pp. 1183-1191 ◽  
Author(s):  
Julie E Sherry ◽  
Kristin M Oehrlein ◽  
Kristin S Hegge ◽  
Barbara J Morgan

Abstract Background and Purpose. Based on changes in skin temperature alone, some authors have proposed that postganglionic sympathetic vasoconstrictor fibers can be stimulated transcutaneously. Our goal was to determine the effects of low-frequency (2 bursts per second), burst-mode transcutaneous electrical nerve stimulation (TENS) on calf vascular resistance, a more direct marker of sympathetic vasoconstrictor outflow than skin temperature, in subjects with no known pathology. Subjects. Fourteen women and 6 men (mean age=31 years, SD=13, range=18–58) participated in this study. Methods. Calf blood flow, arterial pressure, and skin temperature were measured while TENS was applied over the common peroneal and tibial nerves. Results. Blood flow immediately following stimulation was not affected by TENS applied just under or just above the threshold for muscle contraction. Transcutaneous electrical nerve stimulation applied at 25% above the motor threshold caused a transient increase in calf blood flow. Regardless of stimulation intensity, TENS had no effect on arterial pressure; therefore, calf vascular resistance decreased only during the trial that was 25% above the motor threshold. Regardless of stimulation intensity, TENS failed to alter dorsal or plantar skin temperature. Discussion and Conclusion. These results demonstrate that the effects of TENS on circulation depend on stimulation intensity. When the intensity was sufficient to cause a moderate muscle contraction, a transient, local increase in blood flow occurred. Cooling of the dorsal and plantar skin occurred in both the stimulated and control legs, most likely because skin temperature acclimatized to ambient room temperature, rather than because of any effect of TENS on circulation. The data, therefore, call into question the idea that postganglionic sympathetic efferent fibers are stimulated when TENS is applied at clinically relevant intensities to people without symptoms of cardiovascular or neuromuscular pathology.


1983 ◽  
Vol 102 (1) ◽  
pp. 327-335
Author(s):  
KNUT PETTERSSON

A perfused and ventilated gill preparation is described in which the pO2 of the perfusion medium and the irrigating water is controlled. Dorsal aorta effluent pO2 and flow were measured together with the branchial vascular resistance. Decreasing pO2 in the perfusion fluid caused increased branchial vascular resistance, probably by constriction of efferent lamellar arterioles. α-adrenoceptor stimulation caused constriction of arteriovenous connections and of efferent lamellar arterioles, and enhanced oxygenation of the perfusion fluid. β-adrenoceptor stimulation also increased O2 transfer, but to a lesser extent. It is suggested that both hypoxia and α-adrenoceptor stimulation improved O2 transfer via constriction of efferent lamellar arterioles. Both stimuli may also increase systemic blood flow by constriction of the arterio-venous connections, although such an effect of hypoxia has not been clearly shown. β-stimulation probably increased O2 transfer by dilation of afferent lamellar arterioles, thereby causing recruitment of unperfused lamellae.


1983 ◽  
Vol 245 (4) ◽  
pp. H662-H666
Author(s):  
P. C. Wong ◽  
B. G. Zimmerman

The objective of this study was to examine the effect of sodium depletion on basal sympathetic adrenergic vascular tone and vasoconstrictor responses to adrenergic nerve stimulation and norepinephrine in pentobarbital-anesthetized dogs. Mean arterial pressure, tibial blood flow, and tibial vascular resistance were not significantly different between sodium-replete and sodium-deplete dogs. However, plasma renin activity (PRA) was 11-fold higher in sodium-deplete dogs (P less than 0.01). Sympathetic denervation in sodium-replete and -deplete dogs resulted in a similar decrease in tibial vascular resistance. Nerve stimulation at 0.25 and 0.5 Hz caused 40 +/- 5 and 48 +/- 5% decreases, respectively, in tibial blood flow in sodium-replete dogs and 71 +/- 3 and 77 +/- 3% decreases, respectively, in sodium-deplete dogs (P less than 0.01). Responses to norepinephrine administered intra-arterially were similar in both groups. Neither captopril nor saralasin reduced the potentiated responses to nerve stimulation in sodium-deplete dogs. Bilateral nephrectomy 24 h prior to the experiment reduced PRA to an undetectable level in both sodium-replete and -deplete dogs and equalized the responses to nerve stimulation and norepinephrine in both groups. Because bilateral nephrectomy, but neither captopril nor saralasin, abolished the potentiated responses in sodium depletion, a renal hormone other than renin or vascular angiotensin II may be responsible for this prejunctional adrenergic potentiation.


2002 ◽  
Vol 205 (21) ◽  
pp. 3335-3345 ◽  
Author(s):  
Johannes Overgaard ◽  
Jonathan A. W. Stecyk ◽  
Anthony P. Farrell ◽  
Tobias Wang

SUMMARYFreshwater turtles, Trachemys scripta, like all non-crocodilian reptiles, are able to shunt blood between the pulmonary and systemic circulations owing to their undivided ventricle. The prevailing hypothesis is that the ratio of pulmonary and systemic resistances is the primary determinant of cardiac shunting in turtles. In the present study, we have examined the adrenergic influences on vascular resistances in the pulmonary and systemic circulations and the associated effects on cardiac shunts in turtles. To achieve this objective, systemic blood flow and pressures and pulmonary blood flow and pressures were measured simultaneously in anaesthetised turtles during bolus injections of α- andβ-adrenergic agonists and antagonists. Total cardiac output, systemic vascular resistance, pulmonary vascular resistance, heart rate and cardiac stroke volume were derived from these measurements. Anaesthetised turtles showed cardiovascular characteristics that were similar to those of non-apnoeic non-anaesthetised turtles, because anaesthesia blocked the cholinergically mediated constriction of the pulmonary artery that is normally associated with apnoea. As a result, the anaesthetised turtles exhibited a large net left-to-right shunt, and the adrenergic responses could be observed without confounding changes resulting from apnoea. Potent α-adrenergic vasoconstriction and weaker β-adrenergic vasodilation were discovered in the systemic circulation. Modest β-adrenergic vasodilation and possible weak α-adrenergic vasodilation were discovered in the pulmonary circulation. This adrenergically mediated vasoactivity produced the largest range of cardiac shunts observed so far in turtles. Regression analysis revealed that 97% of the variability in the cardiac shunts could be accounted for by the ratio of the pulmonary and systemic resistances. Thus, we conclude that, independent of whether the pulmonary vascular resistance is modulated(as during apnoea) or the systemic resistance is modulated with adrenergic mechanisms (as shown here), the consequences on the cardiac shunt patterns are the same because they are determined primarily by the ratios of the pulmonary and systemic resistance.


1990 ◽  
Vol 68 (5) ◽  
pp. 2177-2181 ◽  
Author(s):  
M. Manohar

Regional distribution of diaphragmatic blood flow (Q; 15-microns-diam radionuclide-labeled microspheres) was studied in normal (n = 7) and laryngeal hemiplegic (LH; n = 7) ponies to determine whether the added stress of inspiratory resistive breathing during maximal exercise may cause 1) redistribution of diaphragmatic Q and 2) crural diaphragmatic Q to exceed that in maximally exercising normal ponies. LH-induced augmentation of already high exertional work of breathing resulted in diminished locomotor exercise capacity so that maximal exercise in LH ponies occurred at 25 km/h compared with 32 km/h for normal ponies. The costal and crural regions received similar Q in both groups at rest. However, exercise-induced increments in perfusion were significantly greater in the costal region of the diaphragm. At 25 km/h, costal diaphragmatic perfusion was 154 and 143% of the crural diaphragmatic Q in normal and LH ponies. At 32 km/h, Q in costal diaphragm of normal ponies was 136% of that in the crural region. Costal and crural diaphragmatic Q in LH ponies exercised at 25 km/h exceeded that for normal ponies but was similar to the latter during exercise at 32 km/h. Perfusion pressure for the three conditions was also similar. It is concluded that diaphragmatic perfusion heterogeneity in exercising ponies was preserved during the added stress of inspiratory resistive breathing. It was also demonstrated that vascular resistance in the crural and costal regions of the diaphragm in maximally exercised LH ponies remained similar to that in maximally exercising normal ponies.


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