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PubMed1999

Cardiac sympathetic denervation after transmyocardial laser revascularization.

BACKGROUND: Transmyocardial laser revascularization (TMR) has been shown to improve refractory angina not amenable to conventional coronary interventions. However, the mechanism of action remains controversial, because improved myocardial perfusion has not been consistently demonstrated. We hypothesized that TMR relieves angina by causing myocardial sympathetic denervation. METHODS AND RESULTS: PET imaging of resting and stress myocardial perfusion with [13N]ammonia (NH3) and of sympathetic innervation with [11C]hydroxyephedrine (HED) was performed before and after TMR in 8 patients with class IV angina ineligible for CABG or PTCA. A mean of 50+/-11 channels were created in the left ventricle (LV) with a holmium:YAG laser. A semiautomated program was used to determine NH3 uptake and HED retention in the LV. Perfusion and innervation defects were defined as the percentage of LV with tracer uptake or retention >2 SD below normal mean values. All patients experienced improvement in their angina by 2.4+/-0.5 angina classes after surgery, P=0.008. Sympathetic innervation defects exceeded resting perfusion defects in all patients before TMR (34.6+/-27.3% for HED versus 9.4+/-10.8% for NH3, P=0.008). TMR did not significantly affect resting or stress myocardial perfusion but increased the extent of sympathetic denervation in 6 of 8 patients by 27.5+/-15.9%, P=0.03. In the remaining 2 patients, both sympathetic denervation and stress perfusion defects decreased after surgery. CONCLUSIONS: TMR causes decreased myocardial HED uptake in most patients without significant change in resting or stress myocardial perfusion, suggesting that the improvement in angina may be at least in part due to sympathetic denervation.

Aged↗
PubMed1980

Left ventricular response to isometric exercise in patients with denervated and innervated hearts.

Patients with cardiac denervation resulting from allograft transplantation have been observed to increase their diastolic and systolic blood pressure during isometric exercise without concomitant cardioacceleration. To determine the mechanism for the blood pressure increase, heart rate, blood pressure, and ventricular volumes (measured using fluoroscopy of tantalum midwall myocardial markers) were recorded before and after a 50% maximal voluntary contraction. Seven cardiac transplant recipients (denervated heart) and seven nontransplant patients (innervated heart) were studied. Innervated and denervated heart patients increased systolic blood pressure by 16% and 21% and total peripheral resistance by 20% and 12%, respectively. The percentage responses were not significantly different between groups, except for heart rate, which increased 17% in innervated heart patients and 2% in denervated heart patients (p less than 0.05). Neither group had enhanced contractility or increases in cardiac output, suggesting that the blood pressure increases resulted in both groups from increased peripheral resistance.

Adult↗
PubMed1987

Denervation supersensitivity of refractoriness in noninfarcted areas apical to transmural myocardial infarction.

Denervation supersensitivity was demonstrated in anesthetized dogs 5 to 10 days after transmural myocardial infarction produced by latex embolization of a diagonal branch of the left anterior descending coronary artery. Sympathetic efferent denervation in noninfarcted myocardium apical to the infarction was demonstrated by a 90% depletion of myocardial norepinephrine content in the apical (45 +/- 15 pg norepinephrine/g tissue) vs basal (437 +/- 76 pg/g tissue) regions and by the lack of effective refractory period (ERP) shortening during bilateral ansae subclaviae stimulation in 34% of sites apical to the infarction. Supersensitivity in the area apical to the infarction was manifested by an exaggerated shortening of the ERP during both norepinephrine and isoproterenol infusions, with an upward and leftward shift in the dose-response curves in the apical vs basal regions (p less than .001). The cellular mechanism for denervation supersensitivity did not involve detectable changes in the beta-adrenergic receptor adenylate cyclase system. There was no difference in the density of beta-adrenergic receptors ([125I]-cyanopindolol) in the apical (268.6 +/- 22.7 fmol/mg protein) vs the basal (253.5 +/- 24.8 fmol/mg protein) regions. Adenylate cyclase activity stimulated by guanosine triphosphate plus isoproterenol was slightly greater in the apical (58.7 +/- 17.4%) than in the basal (49.6 +/- 10.9%) region, but this difference did not reach statistical significance (p = .068). Muscarinic modulation of beta-receptor coupling (oxotremorine attenuation of guanosine triphosphate plus isoproterenol-stimulated adenylate cyclase activity) also was not significantly different at the apical (31.6 +/- 17.5% inhibition) and basal (21.4 +/- 20.9% inhibition) sites. These data show that a transmural myocardial infarction produces denervation supersensitivity in areas apical to the infarction, but in this preparation no differences in the total number or a redistribution of beta-adrenergic receptors or adenylate cyclase activity were detected.

Adenylyl Cyclases↗
PubMed1989

Cellular abnormalities in chronically denervated myocardium. Implications for the transplanted heart.

Heart transplantation involves chronic effects due to denervation, rejection, and treatment of rejection. The chronically denervated dog heart provides a model for the effects of denervation alone. These hearts have been shown to contain intrinsic neurons with VIP and NPY as possible neurotransmitters. Myocardial tissue noradrenaline concentration falls to very low levels after degeneration of postganglionic sympathetic neurons, but dopamine remains in near-normal concentration and is probably synthesized extraneuronally. ANP is present and released normally; however, the natriuretic response to atrial distension is blunted, suggesting that this response is mainly due to a reflex mechanism. Chronically denervated myocardial tissue exhibits increased oxygen consumption in vitro and increased Na-K, ATPase activity but has normal tissue levels of ATP and creatine phosphate. Glucose oxidation is inhibited in vivo, associated with increased levels of fructose-6-phosphate but normal glucose-6-phosphate, suggesting inhibition of phosphofructokinase activity. However, the enzyme protein concentration of phosphofructokinase, as judged by maximal in vitro activity, is normal. Maximal in vitro activities of succinate dehydrogenase, cytochrome oxidase, monoamine oxidase, calcium-dependent ATPase, and glyceraldehyde-3-dehydrogenase are also normal. From these findings, we would predict that patients with transplanted hearts are likely to show myocardial metabolic inefficiency.

Animals↗
PubMed1992

Changes in vascular resistance during carotid occlusion in normal and baroreceptor-denervated rats.

In the present study, we investigated changes in mesenteric, renal, and hindquarter vascular resistance during the pressor response produced by bilateral carotid occlusion (BCO) in conscious, freely moving normal and denervated (aortic, carotid, or both) rats. BCO was performed using special previously implanted cuffs. In control normal rats, the increase in mean arterial pressure (MAP) during early and late responses (37 +/- 4 and 21 +/- 2 mm Hg, respectively) was related to increased renal (125 +/- 12% and 45 +/- 10%) and mesenteric (38 +/- 13% and 41 +/- 5%) but not hindquarter (14 +/- 4% and 8 +/- 7%) vascular resistance. In aortic-denervated rats, the greater MAP increase in early and late responses (57 +/- 4 and 44 +/- 4 mm Hg, respectively) compared with normal rats was related to a marked increase in hindquarter (137 +/- 26% and 106 +/- 26%) and mesenteric (104 +/- 14% and 66 +/- 9%) vascular resistance. In carotid-denervated rats, MAP increase and change in vascular resistance were similar to those values observed in control rats. Sinoaortic-denervated rats showed a greater MAP increase (34 +/- 4 mm Hg) during late response and a reduced increase in renal vascular resistance (46 +/- 6%) during early response.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Renal denervation normalizes pressure and baroreceptor reflex in high renin hypertension in conscious rats.

High renin hypertension is usually accompanied by impairment of the baroreceptor reflexes. This feature has been mostly ascribed to overactivity of the renin-angiotensin system. However, renal nerves could also modulate the baroreceptor reflexes. In the present experiments, the effect of renal denervation on the depressed baroreceptor reflexes was studied in rats subjected to aortic ligation between the renal arteries. Renal denervation of the ischemic kidney was performed at the same time as aortic ligation. The resulting effects on arterial pressure, heart rate, plasma renin activity, and baroreceptor reflex control of heart rate were studied 10-12 days after ligation and denervation. Aortic ligation induced high levels of mean arterial pressure (166 +/- 6 versus 110 +/- 3 mm Hg in controls), heart rate (380 +/- 9 versus 352 +/- 8 beats per minute in controls), and plasma renin activity (44 +/- 5 versus 6 +/- 1.2 ng angiotensin I/ml/hr). The baroreceptor reflex sensitivity for bradycardia and tachycardia was significantly reduced (-0.18 +/- 0.04 and -0.18 +/- 0.05, respectively, versus -2.3 +/- 0.01 and -2.4 +2- 0.1 beats per minute per mm Hg in controls). Denervation of the ischemic kidney attenuated the development of hypertension in aortic-ligated rats (122 +/- 3 mm Hg), lowering heart rate (319 +/- 8 beats per minute) and normalizing baroreceptor reflex sensitivity to bradycardia (-2.0 +/- 0.2 beats per minute per mm Hg) and to tachycardia (-4.0 +/- 0.1 beats per minute per mm Hg). Plasma renin activity was also normalized (4.3 +/- 2.4 ng angiotensin I/ml/hr).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Salt-dependent hypertension in the sinoaortic-denervated rat.

To determine the extent to which baroreceptor function is a determinant of salt-dependent hypertension, we studied the cardiovascular and renal responses to increasing dietary sodium chloride in sinoaortic-denervated (n = 9) and sham-denervated (n = 9) Sprague-Dawley rats. Rats were instrumented with an arterial catheter for measurement of arterial pressure and were individually housed for daily measurements of water intake, sodium intake, urinary output, and urinary sodium excretion. Arterial pressure was monitored daily over a 30-minute period by computer. After 3 days of control measurements (0.4% sodium chloride diet), dietary sodium chloride was increased to 8.0% for 21 days, followed by a 3-day recovery period (0.4% sodium chloride). Ingestion of an 8.0% sodium chloride diet resulted in a 20- to 25-fold increase in sodium intake and a fivefold increase in water intake in both groups. In sinoaortic-denervated rats, arterial pressure increased approximately 10 mm Hg on days 5-10, 20 mm Hg on days 11-18, and 30 mm Hg on days 19-21 of 8.0% sodium chloride. Arterial pressure returned to control levels within the first 24 hours of the recovery period. Elevated sodium intake had no significant effect on arterial pressure in the sham-denervated group. Finally, there were no significant differences between groups in urine output or urinary sodium excretion at any time during the study. We conclude that a primary impairment in the afferent limb of the arterial baroreceptor reflex results in salt-dependent hypertension in the Sprague-Dawley rat.

Animals↗
PubMed1998

Renal denervation prevents and reverses hyperinsulinemia-induced hypertension in rats.

Experiments were performed to evaluate the role of the renal nerves in hyperinsulinemia-induced hypertension. Male Sprague-Dawley rats were made hyperinsulinemic by insulin infusion via osmotic minipumps implanted subcutaneously (3.0 mU/kg per minute for 6 weeks). Rats with vehicle infusion served as controls. Bilateral renal denervation was performed either at the beginning of or 4 weeks after insulin infusion. The systolic blood pressure was measured by the tail-cuff method twice a week. Food and water intake and urine flow were measured daily. The results showed that sustained insulin infusion significantly increased plasma insulin concentrations from 277.7+/-25.8 pmol/L to 609.9+/-22.2 and 696.7+/-23.0 pmol/L by the end of weeks 4 and 6, respectively (P<0.05). Systolic blood pressure was significantly increased from 135+/-3 to 157+/-3 and 159+/-2 mm Hg (P<0.05) at the corresponding time points. There was a significant increase in the plasma norepinephrine concentration after insulin infusion, whereas no significant changes in plasma triglyceride and glucose concentrations, water intake, urine flow, sodium excretion, sodium gain, and body weight gain were observed. Bilateral renal denervation depleted renal norepinephrine stores and prevented the development of hyperinsulinemia-induced hypertension. After hyperinsulinemia-induced hypertension had been fully established (from 134+/-2 to 157+/-2 mm Hg), bilateral renal denervation reversed the elevated systolic blood pressure to normotensive levels within 2 weeks. Transient denervated diuresis and natriuresis were observed. These results indicate that chronic hyperinsulinemia-induced hypertension requires the presence of intact renal nerves in rats.

Animals↗
PubMed1980

Inhibition of glycolysis in the denervated dog heart.

We measured glucose metabolism in five dogs before and 3 weeks after cardiac denervation; after this time myocardial norepinephrine is depleted. The discharge by the myocardium, of 14CO2 from infused 14C-D-glucose (U), decreased following denervation (P = 0.05). The ratio of 14CO2 to total CO2 production, which measured the proportion of glucose to total substrate oxidized, also decreased following denervation (P = 0.05). The inhibition of glucose oxidation by denervation was not due to an increase in arterial lactate concentration. There was an associated increase in myocardial content of fructose-6-phosphate in an additional seven dogs (P < 0.01). We postulate that myocardial tissue norepinephrine is one of the controllers of the activity of phosphofructokinase.

Animals↗
PubMedDate not supplied

Upper limit of cerebral autoregulation during development of hypertension in spontaneously hypertensive rats--effect of sympathetic denervation.

The upper limit of cerebral autoregulation was studied in pre- or early established hypertension in spontaneously hypertensive rats (SHR). Cerebral blood flow (CBF) was measured with the hydrogen clearance method, and wall/lumen ratio of cerebral arteries was morphometrically measured with the freeze-substitution technique. To test autoregulation, phenylephrine was intravenously infused to cause stepwise increments of blood pressure. Unilateral superior cervical ganglionectomy was carried out to examine the effects of sympathetic denervation on CBF autoregulation and thickness of vascular wall. Resting blood pressure at 4 weeks, 3 months and 6 months of age were 89 +/- 3 mm Hg (mean +/- SEM), 140 +/- 6 and 165 +/- 6, respectively. Baseline CBF was slightly diminished with age; 50.6 +/- 9.2 ml/100 g/min at 4 weeks, 49.8 +/- 8.1 at 3 months and 44.1 +/- 5.6 at 6 months. The upper limit of autoregulation was markedly raised with age; 118 +/- 5 mm Hg at 4 weeks, 180 +/- 7 at 3 months and 208 +/- 10 at 6 months. Acute sympathetic denervation lowered the upper limits to 105 +/- 2, 162 +/- 4 and 185 +/- 7 mm Hg, respectively. On the other hand, in chronic denervation which was made at 4 weeks of age, the upper limit of autoregulation in the denervated hemisphere was slightly lower than that in innervated hemisphere at 2 months (165 +/- 5 and 178 +/- 6 mm Hg), and at 5 months (202 +/- 8 and 215 +/- 8 mm Hg) after ganglionectomy.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMedDate not supplied

Regional cerebral blood flow autoregulation in normotensive and spontaneously hypertensive rats--effects of sympathetic denervation.

The present study was designed to investigate the effect of acute sympathetic denervation on the regional cerebral blood flow (CBF) autoregulation during acute elevation of blood pressure in spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto rats (WKY). CBF to the parietal cortex and thalamus was measured by the hydrogen clearance method and, to test autoregulation, systemic arterial blood pressure was elevated by intravenous infusion of phenylephrine. Superior cervical ganglia were removed on both sides to interrupt sympathetic innervation in the deeper structures of the brain. Acute bilateral sympathetic denervation did not alter the resting blood pressure or CBF in either SHR or WKY. In innervated SHR, resting mean arterial pressure (MAP) was 165 +/- 5 mm Hg (mean +/- SEM) and the upper limit of autoregulation in the cortex was 210 +/- 3 mm Hg, which was significantly lower than that in the thalamus (229 +/- 3 mm Hg, p less than 0.02). In bilaterally denervated SHR, the upper limits were lowered to 193 +/- 4 mm Hg in the cortex (p less than 0.02 vs. innervated SHR) and to 207 +/- 5 mm Hg in the thalamus (p less than 0.02 vs. innervated). In WKY, resting MAP was approximately 55 mm Hg lower than that in SHR. Acute denervation reduced the upper limits from 142 +/- 3 mm Hg to 130 +/- 4 in the cortex (p less than 0.05) and from 158 +/- 4 to 145 +/- 4 in the thalamus (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Does cerebral vasospasm result from denervation supersensitivity?

This study examined the role of denervation supersensitivity in the development of cerebral vasospasm. Adrenergic denervation of cat basilar artery was accomplished by resection of the superior cervical ganglia or by injection of 6-hydroxydopamine into the cisterna magna. In vivo dose-response characteristics were determined for normal and for denervated arteries, and no significant differences were found between topical applications of serotonin, norepinephrine, epinephrine, fresh blood, or incubated blood. In addition, analysis of cat blood incubated in vitro revealed that the levels of serotonin, norepinephrine, and epinephrine diminished over time, whereas levels of hemoglobin and methemoglobin increased up to Day 14. The results of this study indicate that adrenergic denervation is not the cause of cerebral vasospasm and that, whatever the mechanism, hemoglobin is far more likely to play a role than are the other agents.

Animals↗
PubMed2002

Long-term effects of carotid sinus denervation on arterial blood pressure in humans.

BACKGROUND: After experimental carotid sinus denervation in animals, blood pressure (BP) level and variability increase markedly but normalize to preoperative levels within 10 to 14 days. We investigated the course of arterial BP level and variability after bilateral denervation of the carotid sinus baroreceptors in humans. METHODS AND RESULTS: We studied 4 women (age 41 to 63 years) who were referred for evaluation of arterial baroreflex function because of clinical suspicion of carotid sinus denervation attributable to bilateral carotid body tumor resection. The course of BP level and variability was assessed from repeated office and 24-hour ambulatory measurements (Spacelabs/Portapres) during 1 to 10 years of (retrospective) follow-up. Rapid cardiovascular reflex adjustments to active standing and Valsalva's maneuver were assessed. Office BP level increased from 132/86 mm Hg (range, 118 to 148/80 to 92 mm Hg) before bilateral surgery to 160/105 mm Hg (range, 143 to 194/90 to 116 mm Hg) 1 to 10 years after surgery. During continuous 24-hour noninvasive BP recording (Portapres), a marked BP variability was apparent in all 4 patients. Initial symptomatic hypotension on change to the upright posture and abnormal responses to Valsalva's maneuver were observed. CONCLUSIONS: Acute carotid sinus denervation, as a result of bilateral carotid body tumor resection, has a long-term effect on the level, variability, and rapid reflex control of arterial BP. Therefore, in contrast to earlier experimental observations, the compensatory ability of the baroreceptor areas outside the carotid sinus seems to be of limited importance in the regulation of BP in humans.

Adult↗
PubMed2003

Aging of skeletal muscle does not affect the response of satellite cells to denervation.

Satellite cells (SCs) are the main source of new fibers in regenerating skeletal muscles and the key contributor to extra nuclei in growing fibers during postnatal development. Aging results in depletion of the SC population and in the reduction of its proliferative activity. Although it has been previously determined that under conditions of massive fiber death in vivo the regenerative potential of SCs is not impaired in old muscle, no studies have yet tested whether advanced age is a factor that may restrain the response of SCs to muscle denervation. The present study is designed to answer this question, comparing the changes of SC numbers in tibialis anterior (TA) muscles from young (4 months) and old (24 months) WI/HicksCar rats after 2 months of denervation. Immunostaining with antibodies against M-cadherin and NCAM was used to detect and count the SCs. The results demonstrate that the percentages of both M-cadherin- and NCAM-positive SCs (SC/Fibers x 100) in control TA muscles from young rats (5.6 +/- 0.5% and 1.4 +/- 0.2%, respectively) are larger than those in old rats (2.3 +/- 0.3% and 0.5 +/- 0.1%, respectively). At the same time, in 2-month denervated TA muscles the percentages of M-cadherin and NCAM positive SC are increased and reach a level that is comparable between young (16.2 +/- 0.9% and 7.5 +/- 0.5%, respectively) and old (15.9 +/- 0.7% and 10.1 +/- 0.5%, respectively) rats. Based on these data, we suggest that aging does not repress the capacity of SC to become activated and grow in the response to muscle denervation.

Aging↗
PubMed1992

Fever in young lambs: carotid denervation alters the febrile response to a small dose of bacterial pyrogen.

Experiments were done on 13 young lambs to determine if carotid denervation influences the cardiovascular and metabolic responses to i.v. administration of bacterial pyrogen [Salmonella abortus equi (SAE) 0.3 micrograms]. Each lamb was anesthetized with halothane and prepared for measurements of cardiac output, arterial and mixed venous oxygen saturations, and body core temperature. No sooner than 3 d after surgery, measurements were made during a control period and at 10-min intervals for 120 min after i.v. administration of SAE in seven carotid-intact lambs and six carotid-denervated lambs. Administration of SAE produced a short-lived fever of about 1 degrees C in the carotid-intact lambs, whereas no change in body core temperature was observed in the carotid-denervated lambs. In carotid-intact lambs, the rise in body core temperature began approximately 40 min after administration of SAE and continued for approximately 50 min. This rise in body core temperature was preceded by the onset of shivering and an increase in total body oxygen consumption. Carotid denervation produced changes in some of the cardiovascular variables during the control period (i.e. arterial oxygen content, cardiac index, heart rate, and pulmonary blood pressure); however, there were no additional significant changes in any of the metabolic or cardiovascular variables after administration of SAE. The mechanism of these unexpected findings remains to be determined.

Animals↗
PubMed1977

The effect of denervation on subsequent in vitro induction of myotonia.

In order to study the influence of innervation on myotonia, an attempt was made to induce myotonia in previously denervated rat hemidiaphragm preparations in vitro with use of 2,4-dichlorophenoxy acetic acid (2,4-D) and low chloride solutions. Prior denervation prevented the onset of myotonia in both media except during the first 24 hours after nerve section. On the basis of already available data, we propose that the reduced potassium conductance accompanying denervation may be the main factor preventing induciton of myotonia in denervated muscle.

2,4-Dichlorophenoxyacetic Acid↗
PubMed1998

Denervation of eccrine glands in patients with familial amyloidotic polyneuropathy type I.

OBJECTIVE: To study the alterations in the structure and innervation of eccrine glands in familial amyloidotic polyneuropathy (FAP) type I with Val 30 Met transthyretin mutation. BACKGROUND: Anhidrosis of the distal lower limbs is a prominent feature of FAP type I. METHODS: Qualitative and morphometric study of amyloid deposition, eccrine glands, and their innervation in nine patients with FAP type I (duration of sensory symptoms, 8.4 +/- 3.9 years [mean +/- SD]; range, 3 to 15 years) and seven control subjects. RESULTS: On light microscopy, the endoneurium of cutaneous nerve fascicles had no definite amyloid deposition. Amyloid deposition was observed around eccrine glands in seven of nine patients. On electron microscopy, no focal destruction and degeneration of eccrine glands or ducts and of Schwann cell processes with or without nerve terminals or unmyelinated axons were observed in relation to adjacent amyloid deposition. Secretory vacuoles and granules of dark cells were markedly decreased in some secretory coils. Nerve terminals and unmyelinated axons of eccrine glands were considerably fewer in patients than in control subjects, and denervation was prominent in all patients. A few nerve terminals and unmyelinated axons of eccrine glands were present in patients who had experienced sensory symptoms for 3, 5, and 6 years, but were absent in patients with sensory symptoms for more than 7 years. CONCLUSIONS: Eccrine glands are markedly to totally denervated in patients with FAP type I and chronic sensory symptoms. The extent of denervation indicates the severity of autonomic denervation and therefore may suggest the timing of liver transplantation.

Adult↗
PubMed1986

Contribution of vasopressin to hypertension caused by baroreceptor denervation and nucleus tractus solitarius lesions in rats.

The purpose of this study was to examine, using pentobarbital-anesthetized rats, whether vasopressin contributes to hypertension caused by denervation of baroreceptors, in comparison to the contribution of vasopressin to hypertension caused by nucleus tractus solitarius (NTS) lesions. Bilateral baroreceptor denervation caused acute hypertension which was inhibited by intravenous injection of an antagonist of the vasoconstrictor action of vasopressin. Lesions of the NTS also produced an increased in blood pressure which was reduced by the vasopressin antagonist. The magnitude of the antagonist-induced hypotension was significantly greater in NTS hypertension than that in baroreceptor denervation hypertension. It is concluded, that in rats, vasopressin contributes to the neurogenic hypertension caused by baroreceptor denervation and NTS lesions. Thus, it appears that interruption of baroreceptor afferents at the NTS level is responsible for the vasopressin-mediated hypertension caused by NTS lesions but that it is not the only factor involved.

Animals↗