Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “SYMPATHECTOMY”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 613 records · Page 34Linked to original sources

Neonatal sympathectomy reduces NADPH oxidase activity and vascular resistance in spontaneously hypertensive rat kidneys.

Neonatal sympathectomy reduces arterial pressure in spontaneously hypertensive rats (SHR). In SHR transplanted with a kidney from sympathectomized SHR, arterial pressure was lower and less Na+ sensitive than in SHR transplanted with a kidney from hydralazine-treated SHR. This study was performed to identify underlying renal mechanisms. Tests for differential renal mRNA expression of nine a priori selected genes revealed robust differences for renal medullary expression of the NADPH oxidase subunit p47phox. Therefore, we investigated the effects of neonatal sympathectomy on renal mRNA expression of NADPH oxidase subunits, NADPH oxidase activity, and renal function. In 10-wk-old sympathectomized SHR fed a 0.6% NaCl diet, medullary p47phox and gp91phox expression was 40% less than in hydralazine-treated SHR. Also, after a 1.8% NaCl diet, medullary p47phox mRNA expression was lower in sympathectomized than in hydralazine-treated SHR. We found lower cortical (-30%, P<0.01) and medullary (-30%, P<0.05) NADPH oxidase activities in sympathectomized than in hydralazine-treated or untreated SHR. Glomerular filtration rate, renal blood flow, medullary blood flow, and fractional Na+ excretion in kidney grafts from sympathectomized and hydralazine-treated donors (n=8 per group) were similar at baseline and in response to a 20-mmHg rise in renal perfusion pressure. Renal vascular resistance was lower in kidneys from sympathectomized than hydralazine-treated donors (25+/-2 vs. 32+/-4 mmHg.min.ml-1, P<0.05). The results indicate that the sympathetic nervous system contributes to the level of renal NADPH oxidase activity and to perinatal programming of alterations in renal vascular function that lead to elevated renal vascular resistance in SHR.

Animals↗

Dietary obesity and neonatal sympathectomy. II. Thermoregulation and brown adipose metabolism.

Neonatal sympathectomy with guanethidine (50 mg/kg for 3 wk) in Sprague-Dawley rats was previously shown not to significantly affect body weight gain, even when rats were raised in small litters and fed a high-calorie diet from weaning to produce diet-induced obesity (15). In our study rectal temperatures of cold-stressed (24 h at 4 degrees C) sympathectomized rats (obese and lean) fell only 1.4 degrees C after 4 h and were normal by 24 h, as were plasma catecholamine, glycerol glucose, and insulin levels after 4 h at 4 degrees C. Obese rats (with or without sympathectomy) had decreased 4-h (at 4 degrees C) plasma norepinephrine (NE) and increased basal and 4-h plasma glycerol, glucose, and insulin levels. Despite greater than 95% depletion of interscapular brown adipose tissue (IBAT) NE in sympathectomized rats, there was no alteration in beta-adrenoreceptor binding and only 10 and 32% decreases in basal and maximal NE-stimulated O2 consumption, respectively. Obese rats had significant increases in IBAT beta-receptor binding (148-190%/cell, 77-155%/pad) and in basal (11-19%) but not maximal O2 consumption. These results suggest that factors other than the sympathetic nervous system can effectively control thermoregulation, IBAT metabolism, and body weight in the presence of a chronic defect in sympathetic function.

Adipose Tissue, Brown↗

Exercise and cardiac performance capacity in rats with partial sympathectomy.

This study was undertaken to examine maximal oxygen uptake (VO2 max) and heart rate (HR) during exercise, in situ derived cardiac contractile capacity, and Ca2+ regulation of cardiac myofibril ATPase in normal female rats and in rats with partial sympathectomy (SYMX) induced by chronic injections of guanethidine. Also, normal control (NC) rats were studied during exercise with and without the beta 1-blocking drug atenolol. The results show that SYMX did not have any effect on Ca2+-regulated cardiac myofibril ATPase activity. Also similar cardiac functional capacity, as reflected in left ventricular pressure development and +dP/dtmax, was observed for both groups when the heart was stressed by either exogenous norepinephrine or maximal afterload (aortic constriction). Exercise VO2 max was reduced by 15% (P less than 0.05) in the SYMX compared to the NC group. Although this reduction in VO2 max corresponded to a parallel reduction in HRmax, NC rats with cardiac beta-blockade attained normal VO2 max even though their exercise HRmax was below the SYMX group. These findings suggest that normal rats with attenuated HR and contractility have a better capacity to acutely maintain VO2 max during exercise than rats with chemical sympathectomy.

Adenosine Triphosphatases↗

Chemical sympathectomy decreases alveolar hypoxic vasoconstriction in lambs but not in sheep.

We studied the role of the sympathetic nervous system in the augmented vasoconstrictor response of the newborn lamb, compared with the adult sheep, by producing a chemical sympathectomy with 6-hydroxydopamine (6-OHDA). Seven lambs, age 4-16 days, and five sheep, age 2 yr, were anesthetized and intubated with a double-lumen endotracheal tube, allowing ventilation of one lung with O2 to maintain systemic oxygenation while the contralateral lung was ventilated with N2 as a hypoxic challenge. Distribution of perfusion to each lung was evaluated using positron scintigraphy after inferior vena caval injections of 13N, a positron-emitting isotope. In the lambs, prior to 6-OHDA, distribution of perfusion to the test lung was 43 +/- 3% of total lung perfusion during bilateral O2 ventilation and fell with hypoxia to 24 +/- 2%, a reduction of 44 +/- 3% during N2 ventilation as compared with O2 ventilation. After 6-OHDA, hypoxic challenge reduced perfusion by only 22 +/- 2% (P less than 0.01 compared with pre-6-OHDA). In the adult sheep, hypoxic vasoconstriction reduced perfusion to the test lung by 28 +/- 2% but was unaffected by 6-OHDA. Absence of rise in pulmonary vascular resistance (PVR) or femoral artery pressure (Pfa) in response to Tyramine infusions after 6-OHDA confirmed complete sympathectomy in lambs and sheep. Persistent increases in PVR and Pfa to infusions of prostaglandin F2 alpha before and after 6-OHDA showed that the loss of alveolar hypoxic vasoconstriction in the lamb was specific. Thus sympathetic innervation may contribute to the greater strength of alveolar hypoxic vasoconstriction found in lambs than in sheep.

Aging↗

Effect of vagotomy and thoracic sympathectomy on responses of the monkey to water immersion.

Cardiopulmonary stretch receptors have been implicated as part of a reflex mechanism linking changes in blood volume to changes in renal excretion. Experiments were performed to determine whether total denervation of these receptors by combined cervical vagotomy and thoracic sympathectomy affects the renal responses of the monkey to head-out water immersion, a maneuver that translocates blood to the thorax and elicits an increase in renal salt and water excretion. Macaca fascicularis monkeys first underwent chronic bilateral thoracic sympathectomy or sham denervation performed in two stages a week apart. One to two weeks later, they were anesthetized with pentobarbital sodium, and the sympathectomized animals underwent bilateral cervical vagotomy. Control renal function did not differ between the two groups. Immersion of 90-min duration increased central venous and mean arterial pressures by similar amounts in both groups, but heart rate increased only in the sham-denervated animals. Denervation did not affect the magnitudes or delay the times of onset of the increases in urine flow, absolute and fractional sodium excretion, and osmolar and free water clearances occurring with immersion. These results demonstrate that in the anesthetized monkey cardiopulmonary receptors are not necessary for eliciting the renal responses to immersion.

Animals↗

Pulmonary vascular responses to surgical chemodenervation and chemical sympathectomy in dogs.

We investigated the effects of surgical peripheral chemoreceptor denervation, chemical sympathectomy with 6-hydroxydopamine (6-OHDA), and the peripheral chemoreceptor stimulant almitrine on multipoint pulmonary arterial pressure-cardiac index (PAP/Q) plots in 30 pentobarbital sodium-anesthetized dogs ventilated alternatively in hyperoxia [fraction of inspired O2, (FIO2) = 0.4] and hypoxia (FIO2 = 0.1). A hypoxic pulmonary vasoconstriction (HPV), i.e., a hypoxia-induced increase in PAP over the entire range of Q studied, from 2 to 5 l.min-1.m-2, was elicited in all the animals. Surgical denervation of the carotid and aortic chemoreceptors in a first group of nine dogs increased PAP at the lowest Q of 2 and 3 l.min-1.min-2 in hyperoxia and increased PAP at all levels of Q in hypoxia, so that HPV was enhanced. Chemical sympathectomy in a second group of eight dogs increased PAP at all levels of Q to a comparable extent in hyperoxia and hypoxia so that HPV remained unchanged. Almitrine (8 micrograms.kg-1.min-1 iv) in a third group of eight dogs increased PAP at all levels of Q in hyperoxia but had no effect on PAP/Q plots in hypoxia, so that HPV was inhibited. Almitrine had these same pulmonary vascular effects when administered to the chemodenervated and the sympathectomized dogs. Sham operation and a 2-h delay in a final group of five dogs had no effect on hyperoxic or hypoxic PAP/Q plots. We conclude that in intact dogs 1) the sympathetic nervous system reduces both hyperoxic and hypoxic pulmonary vascular tone, 2) stimulation of the peripheral chemoreceptors inhibits HPV, and 3) almitrine has direct pulmonary vasoconstricting effects in hyperoxia but not hypoxia.

Almitrine↗

Dermofluorography as a possibility for therapeutic control following sympathectomy.

The assessment of completeness of a sympathectomy can be objectively recorded and documented by dermofluorography. This method enables measurement of increased skin perfusion which leads to an earlier appearance time and steeper initial rise in fluorescence of intravenously administered sodium fluorescein. The most significant parameters are the quotients of the average appearance time and the initial rise in fluorescence of the untreated versus treated leg. Following a successful lumbar sympathectomy, these parameters were outside 3 standard deviations of the values obtained from healthy test persons.

Adult↗

Preservation of the baroreceptor heart rate reflex by chemical sympathectomy in experimental heart failure.

BACKGROUND: The mechanisms underlying impaired baroreflex sensitivity in congestive heart failure (CHF) are incompletely understood. The purpose of the present study was to test the hypothesis that this alteration depends on the marked degree of sympathetic overactivity known to characterize the CHF syndrome. METHODS AND RESULTS: Eight-week-old rats were subjected to induction of postmyocardial infarction CHF obtained by coronary ligation (Lig), chronic chemical sympathectomy by 6-hydroxydopamine (Sx), both interventions (Sx-Lig), or neither intervention (Veh-Sham, sham surgery, and vehicle administration). Four weeks after infarction, in conscious state, baroreflex sensitivity was assessed from the bradycardic responses to graded phenylephrine-induced elevations in blood pressure (BP). Left ventricular (LV) diameter was assessed by echocardiography, and plasma catecholamines were assayed to estimate sympathetic activity. Lungs were eventually excised and weighed (LW). CHF was associated with the following: (1) no changes in BP and heart rate; (2) sympathetic overactivity (norepinephrine, 320.2+/-53.8 pg/mL for Veh-Lig versus 173.4+/-20.5 pg/mL for Veh-Sham, P<0.01), prevented by Sx (181.2+/-35.5 pg/mL for Sx-Lig versus 159.8+/-33.1 pg/mL for Sx-Sham, P=NS); (3) LV enlargement (10.3+/-0.7 mm for Veh-Lig versus 6.8+/-0.6 mm for Veh-Sham, P<0.01), irrespective of Sx (9.7+/-0.7 mm for Sx-Lig versus 6.6+/-0.5 mm for Sx-Sham, P<0.01); (4) pulmonary congestion (LW, 7.55+/-0.40 mg per gram of body weight for Veh-Lig versus 5.21+/-0.44 mg per gram of body weight for Veh-Sham, P<0.01), marginally attenuated by Sx (6.54+/-0.28 mg per gram of body weight for Sx-Lig versus 4.98+/-0.22 mg per gram of body weight for Sx-Sham, P<0.05); (5) reduction in baroreflex sensitivity (0.443+/-0.032 ms/mm Hg for Veh-Lig versus 0.860+/-0.420 ms/mm Hg for Veh-Sham, P<0.01), entirely prevented by Sx (1.217+/-0.058 ms/mm Hg for Sx-Lig versus 1.345+/-0.093 ms/mm Hg for Sx-Sham, P=NS). CONCLUSIONS: In early post-MI CHF, sympathectomy only partially attenuated LV dysfunction and entirely prevented baroreflex sensitivity impairment that arises from enhanced sympathetic activity.

Adrenergic beta-Antagonists↗

Chemical sympathectomy alters the development of hypertension in miniature swine.

To determine if the neurotoxin 6-hydroxydopamine could be used to chemically sympathectomize neonatal miniature swine, eight newborn swine were treated with 6-hydroxydopamine beginning on the first day after birth and continuing at regular intervals for the next 6 months. Six littermates served as controls and received vehicle injections. A significant reduction in the pressor response to intravenous tyramine (95%) and in the tissue norepinephrine content of the kidneys, left ventricle, and gastrocnemius muscle (more than 93%) provided evidence for an effective long-term sympathectomy in the 6-hydroxydopamine-treated animals. In addition, the blood pressure response of these young, chemically sympathectomized swine to chronic deoxycorticosterone acetate treatment was evaluated. Mean arterial pressure before deoxycorticosterone was similar in the 6-hydroxydopamine-treated (116 +/- 2 mm Hg) and control (125 +/- 5 mm Hg) groups. One week after deoxycorticosterone, mean arterial pressure had risen significantly by 20-22 mm Hg in both groups. Blood pressure continued to increase in the control group, reaching a value of 163 +/- 6 mm Hg by the third week after treatment. In contrast, mean arterial pressure in the 6-hydroxydopamine group did not increase further during weeks 2 and 3 after deoxycorticosterone. In conclusion, chronic treatment of neonatal swine with 6-hydroxydopamine produced an animal model with an effective, general, peripheral sympathectomy. The significant attenuation of the hypertensive response in these sympathectomized animals lends further support to the hypothesis that an intact sympathetic nervous system is necessary for the full expression of deoxycorticosterone hypertension in miniature swine.

Animals↗

Sympathectomy and cardiovascular spectral components in conscious normotensive rats.

We examined the extent to which sympathetic influences are reflected by spectral powers of blood pressure and pulse interval in specific frequency bands in spontaneously behaving Wistar-Kyoto rats subjected to continuous intraarterial blood pressure recording. The rats were pretreated with 6-hydroxydopamine (150 mg/kg twice in 1 week, n = 19) to produce chemical sympathectomy or received vehicle (n = 15). In the sympathectomized group, additional monitoring sessions were performed with rats under alpha-adrenergic receptor blockade with phenoxybenzamine (n = 8), beta-receptor blockade with propranolol (n = 7), or cholinergic receptor blockade with atropine (n = 8). Blood pressure signals were analyzed by a computer to calculate spectral powers (fast Fourier transform) in the low-frequency (0.025 to 0.1 Hz), mid-frequency (0.1 to 0.6 Hz), and high-frequency (0.8 to 3.0 Hz) bands. In sympathectomized rats, low-frequency power of blood pressure was 70% greater than in intact rats, whereas mid-frequency power was 60% smaller (P < .05 for both) and high-frequency power was unchanged. High-frequency power of pulse interval was also unchanged in sympathectomized rats, whereas low- and mid-frequency powers were reduced by approximately 50% (P < .05). No further alterations in spectral powers were observed by adding alpha- or beta-adrenergic blockade to sympathectomy, whereas adding cholinergic blockade caused a striking reduction in all pulse interval powers. Thus, mid-frequency blood pressure power depends on sympathetic but also to a substantial extent on nonsympathetic influences. Sympathetic influences do not contribute to low-frequency blood pressure power, having instead a restraining effect. The low- and mid-frequency pulse interval powers depend on both sympathetic and vagal influences. Thus, no blood pressure or pulse interval power in the mid- and low-frequency ranges can be regarded as a specific marker of sympathetic activity.

Adrenergic alpha-Antagonists↗

Sympathetic innervation of cerebral arteries: prejunctional supersensitivity to norepinephrine after sympathectomy or cocaine treatment.

The inactivation of the norepinephrine transmitter in the region of the adrenergic receptor is one important function of the sympathetic nerve terminals innervating blood vessels. This capacity was tested on isolated cat's middle cerebral artery (MCA) by recordings of the contractile response induced by norepinephrine at various stages after sympathectomy (excision of the superior cervical ganglion). Within three days after denervation, when fluorescence microscopy revealed a disappearance of neuronal norepinephrine in the vessel wall, there was a threefold increase in sensitivity of the test system which was not further enhanced at two weeks. This, and the finding of a similar amount of sensitization (of non-denervated vessels) to norepinephrine or tyramine after cocaine treatment, showed that a prejunctional type of sensitivity had developed. The sympathetic denervation did not influence the dose-response curve obtained with acetylcholine, supporting the specific nature of the supersensitivity reaction only to the sympathetic transmitter. Half a year after sympathectomy the sensitivity of the pial arteries to norepinephrine returned to control levels despite the absence of reinnervation, indicating that postjunctional changes also occurred. The findings offer further evidence for a functional role of the sympathetic nerves supplying intracranial arteries and show that the mode of innervation resembles that found in peripheral vessels.

Acetylcholine↗

Fetal cardiovascular and catecholamine responses to hypoxemia after chemical sympathectomy.

Chemical sympathectomy was performed in fetal lambs in utero by daily intravenous administration of 6-hydroxydopamine (6HD) until a total dose of 60-70 mg/kg was reached. The completeness of adrenergic denervation was confirmed by the absence of any cardiovascular response to tryamine infusion. Baseline plasma catecholamine concentrations in normoxemic, sympathectomized fetuses were slightly higher than controls but the differences were not statistically significant. The concentration of norepinephrine (NE) was 313 +/- 73 pg/ml after 6HD administration compared with 259 +/- 25 pg/ml in control animals. Similarly, the concentration of epinephrine (E) was 39 +/- 15 pg/ml (6HD) versus 21 +/- 4 pg/ml (control). These mildly elevated catecholamine levels were accompanied by a small but significant increase in resting blood pressure (BP) (P less than 0.05). Heart rate (HR), however, was no different from control. Hypoxemia induced a marked increase in plasma catecholamines in control animals (NE, 2416 +/- 419 pg/ml and E, 2017 +/- 749 pg/ml) along with hypertension and bradycardia. Sympathectomized fetuses maintained a profound NE response to hypoxemia (NE, 1550 +/- 261 pg/ml) but a significant reduction in peak E response was observed (E, 244 +/- 42 pg/ml, P less than 0.05). HR and BP responses to hypoxemia were generally similar to control animals though there appeared to be a brief 1-3 min lag period between the nadir of the bradycardia and the peak of the BP response. We conclude that the generalized chemical sympathectomy after 6HD administration in the fetal lamb in utero is useful in evaluating the interaction of the autonomic nervous system and adrenal medullary function on the regulation of the fetal cardiovascular system.

Animals↗

The effect of chemical sympathectomy on catecholamine release at birth.

The precise source of circulating catecholamine (CA) at birth and their role in circulatory adaptation is unclear. In order to determine the contribution of increased postganglionic sympathetic nerve activity to the CA surge at birth, we induced complete sympathectomy in near term fetal lambs prior to delivery by giving 6-hydroxydopamine. Chronically catheterized fetal sheep received either 6-hydroxydopamine (n = 5) or control infusion (n = 6). Chemical sympathectomy was verified by tyramine infusion. Lambs were delivered at 142 +/- 1 days of gestation and serial plasma CA, heart rate, blood pressure, cardiac output, blood gases, blood glucose, and free fatty acids, were measured before and for 4 h after delivery. Myocardial beta-adrenergic receptors and tissue CA concentration were determined following sacrifice. Baseline circulating norepinephrine (NE) values were lower in sympathectomized animals (183 +/- 45 versus 373 +/- 125 pg/ml, p less than 0.05) and epinephrine values were slightly higher (118 +/- 89 versus 48 +/- 1 pg/ml, NS). There was only a 2-fold increase in NE after cord cutting in sympathectomized animals while control animals had a 4-fold increase (peak NE values 354 +/- 121 versus 1305 +/- 363 pg/ml respectively, p less than 0.001). Epinephrine increased significantly in both groups and there were no significant differences between sympathectomized and control animals. Heart rate and blood pressure rose abruptly in both groups after cord cutting and there were no significant differences.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Basal and adrenocorticotropin-stimulated corticosterone in the neonatal rat exposed to hypoxia from birth: modulation by chemical sympathectomy.

We previously demonstrated that 7-d-old rat pups exposed to hypoxia from birth exhibit ACTH-independent increases in corticosterone associated with an increase in steroidogenic acute regulatory (StAR) and peripheral-type benzodiazepine receptor (PBR) proteins. The purpose of the present study was to determine whether this increase in corticosterone could be attenuated by chemical sympathectomy induced with guanethidine treatment. Rat pups were exposed to normoxia or hypoxia from birth and treated with vehicle or guanethidine and studied at 7 d of age. Hypoxia per se resulted in an increase in plasma corticosterone without a change in plasma ACTH. Guanethidine treatment attenuated the increase in basal corticosterone in hypoxic pups but did not attenuate ACTH-stimulated corticosterone production. This effect was specific as basal and ACTH-stimulated aldosterone was not affected. Guanethidine also attenuated the increase in StAR protein induced by hypoxia. Neither the effect of hypoxia nor that of guanethidine could be explained by changes in the levels of adrenal tyrosine hydroxylase, StAR, or P450scc mRNA, adrenal tyrosine hydroxylase immunohistochemistry, or adrenal catecholamine content. We conclude that chemical sympathectomy normalizes basal corticosterone levels but has no effect on ACTH-stimulated corticosterone levels in 7-d-old rats exposed to hypoxia from birth. The mechanism of the effect of guanethidine to normalize hypoxia-stimulated basal corticosterone remains to be identified, although StAR protein may be an important mediator. This ACTH-independent increase in corticosterone may be a mechanism by which the neonate can increase circulating glucocorticoids necessary for survival while bypassing the hyporesponsiveness of the neonatal hypothalamic-pituitary-adrenal axis.

Adrenal Glands↗

Use of the pulse-wave monitor as a measurement of diagnostic sympathetic block and of surgical sympathectomy.

Changes in skin blood flow in a digit following sympathetic denervation were determined by use of a photoelectric digital plethysmograph (pulse-wave monitor). Results in 20 cases of diagnostic sympathetic block, surgical sympathectomy, or both, are discussed. Pulse-wave changes were seen 3 to 5 minutes after block and 1/2 to 1 minute after sympathectomy. Use of a pulse-wave monitor permitted limiting the dosage of local anesthetic, usually to 5 to 10 ml. of 0.5 percent lidocaine for lumbar sympathetic block and 1 to 2 ml. of 0.5 percent lidocaine for stellate ganglion block. Pulse-wave monitoring was found to be simple and rapid.

Adult↗

Video endoscopic sympathectomy using a fiberoptic CO2 laser to treat palmar hyperhidrosis.

Palmar hyperhidrosis is a common disorder among orientals. A new therapeutic technique for this disorder has been designed by combining a computer compact disc video endoscopic system with a fiberoptic CO2 surgical laser unit. The operation is performed under general anesthesia with alternating one-lung ventilation. There are three important aids in localizing the correct sympathetic segment: 1) direct visualization of its magnified image on the television monitor; 2) identification with an electrode probe palpation at its presumed location; and 3) monitoring the microvasomotor changes on the skin of the finger resulting from electrical stimulation of the sympathetic trunk. Subsequently, the confirmed sympathetic target is vaporized using a low power CO2 laser under direct vision on the television monitor. The laser is delivered to the target by a small optical fiber passing through a throacoscope, which is introduced into the thoracic cavity via the intercostal space between the second and third ribs at the midclavicular line. Fourteen palmar hyperhidrosis patients were successfully treated by this method. No complications, such as Horner's syndrome, bleeding, or intercostal neuralgia, were encountered. Although the number of cases treated was small, and the follow-up period was short, the evidence indicates that a definite sympathectomy on a confirmed segment under magnified vision is possible with this procedure, and could warrant a definite and long-lasting therapeutic effect. Based on our experience, the method is considered a relatively minor and safe procedure, causing minimal discomfort and almost invisible scars. The operation time and hospital stay were remarkably shortened in comparison with other conventional sympathectomy procedures.

Adolescent↗

Coronary and cardiac responses to exercise after chronic ventricular sympathectomy.

This study examined the effects of chronic surgical ventricular sympathectomy on the relationships between left ventricular mechanical performance, coronary blood flow, and exercise workload in sham-operated control dogs and dogs which had been ventricular sympathectomized 8 wk earlier. During exercise, left ventricular global contractile state was less in sympathectomized ventricles than in control ventricles, as indicated by reduced systolic pressure and maximal rate of pressure generation. Regional contractile shortening was not different. Heart rate was significantly elevated in sympathectomized ventricles. Therefore, peak systolic pressure-heart rate product and tension-time index were not different in sympathectomized ventricles compared to control ventricles. However, at each level of exercise, mean coronary flow in sympathectomized ventricles was reduced by about 50% compared to control values. The slopes of coronary flow on pressure-rate product and tension-time index were also reduced. No difference in left ventricular oxygen extraction between control and sympathectomized hearts were observed. Thus, chronic ventricular sympathectomy altered the relationships between coronary flow and oxygen consumption, on the one hand, and ventricular oxygen-dependent performance and whole-body exercise level, on the other hand.

Animals↗

[Study of species differences on chemical sympathectomy: rats and guinea pigs].

Chemical sympathectomy induced by guanethidine or 6-hydroxydopamine (6-OHDA) and reserpinization were investigated by their influences on the cardiovascular system in urethane-anesthetized rats and guinea pigs and on nerve endings in the atrium or aorta and adrenaline-containing granules in the adrenal medulla. In rats, guanethidine and 6-OHDA significantly lowered the basal blood pressure, but reserpine did not. In guinea pigs, none of them affected the basal blood pressure, and with the exception of the potentiation of adrenaline-induced pressor responses, the influences of all 3 drugs on adrenaline- and tyramine-induced responses in blood pressure and heart rate were weaker than those in rats, but influences of treatments with guanethidine for 1 week were more striking than those for 5 weeks. There were significant differences between rats and guinea pigs in classified forms of nerve endings in the right atrium and of adrenaline-containing granules in the adrenal medulla or differences in the influences on the adrenal medulla by all 3 drugs. Only 6-OHDA induced injury in rat atrium. The above results suggest that there are species differences between rats and guinea pigs, not only in the chemical sympathectomized animals but also in the normal condition and that the pharmacodynamic effect of chemical sympathectomy is more prominent in rats than in guinea pigs.

Adrenal Medulla↗