Comparison of [18F] FDG-PET/MRI and Clinical Findings for Assessment of Suspected Lumbar Facet Joint Pain: A Prospective Study to Characterize Candidate Nonanatomic Imaging Biomarkers and Potential Impact on Management.

BACKGROUND AND PURPOSE: Prior retrospective studies have suggested that both T2 hyperintensity and gadolinium enhancement on fat-suppressed MR imaging are associated with lumbar facet joint pain, but prospective evaluation of FDG-PET/MR imaging with a standardized protocol and correlation to clinical findings are lacking. The primary aim was to prospectively assess a standardized FDG-PET/MRI protocol in patients with suspected facetogenic low back pain, with determination of the concordance of imaging and clinical findings. MATERIALS AND METHODS: Ten patients with clinically suspected facetogenic low back pain were prospectively recruited with a designation of specific facet joints implicated clinically. Subsequently, patients underwent an FDG-PET/MR imaging examination with gadolinium. Each facet joint was graded for perifacet signal change on MR imaging and FDG activity. The frequency and correlation of MR imaging, FDG-PET, and clinical findings were determined. RESULTS: FDG activity showed high concordance with high overall MR imaging scores (concordance correlation coefficient = 0.79). There was concordance of the clinical side of pain with the side of high overall MR imaging scores and increased FDG activity on 12/20 (60%) sides. Both a high overall MR imaging score (concordance correlation coefficient = 0.12) and FDG-PET findings positive for increased activity (concordance correlation coefficient = 0.10) had low concordance with the specific clinically implicated facet joints. Increased FDG activity or high MR imaging scores or both were present in only 10/29 (34%) facet joints that had been clinically selected for percutaneous intervention. Eleven (11%) facet joints that had not been selected for treatment demonstrated these imaging findings. CONCLUSIONS: There was low concordance of perifacet signal change and FDG activity with clinically implicated facet joints. This could indicate either the potential to change patient management or a lack of biomarker accuracy. Therefore, additional larger randomized studies with the use of comparative medial branch blocks would be useful to further investigate the clinical utility of these findings.

FDG-PET appearance of pelvic Castleman's disease.

We report a case of Castleman's disease demonstrating 18F-fluorodeoxyglucose (FDG) localization by whole-body PET imaging in a pelvic soft-tissue mass shown on abdominopelvic CT. In this case, there is mild FDG localization within pelvic Castleman's disease with standard uptake values lower than in many cases of low-grade and intermediate-grade lymphomas previously reported. FDG-PET may be of value as an imaging modality for differentiating Castleman's disease from lymphoma.

Sedentism and child health among Rendille pastoralists of northern Kenya.

Many nomadic pastoralists of Africa are settling near towns and famine-relief centers in response to drought-induced livestock loss, loss of pasture land, increased involvement in market economies and political turmoil including civil war. The present study uses measurements of child health, particularly morbidity, dietary and growth patterns, to evaluate the consequences of sedentism for three Rendille communities of northern Kenya. A nutritional and health survey utilizing interviews, anthropometric measurements, physical examinations and hemoglobin measurements was conducted for 105 mothers and their 174 children under six years of age in three Rendille communities, one fully nomadic and two sedentary, in July 1990, a year of above average rainfall, and again in June 1992, a drought year. Results indicate that while the nomadic Rendille community of Lewogoso shares similar morbidity patterns with its sedentary counterparts and had similar numbers of malnourished children during the wet year, the sedentary communities had significantly more malnutrition among children under six during the dry year. Moreover, the children in the settled town of Korr had significantly higher levels of anemia. Differences in malnutrition are attributed to distinctive dietary regimes: during the drought, nomadic children consumed three times as much milk as the sedentary children, while settled children's diets concentrated on starches, fat and sugar. This study suggests that the pastoral nomadic diet, particularly one dependent on camels' milk, offers children better resistance to the pressures of drought and supports findings that the subsistence base of mixed-species pastoralism is superior to sedentary alternatives with respect to child health.

Colonic localization of labeled leukocytes in critically ill patients. Scintigraphic detection of pseudomembranous colitis.

This study assesses the causes of colonic localization of labeled white blood cells (WBCs) in critically ill patients who had undergone leukocyte scintigraphy for suspected infection. Forty-two patients showed abdominal or pelvic WBC localization; 20 of these had a pattern of colonic localization, and some also showed a pattern of small bowel activity. Eight of the 20 patients had documented gastrointestinal bleeding. White blood cell scintigraphy in these eight patients showed a pattern of multifocal and/or regional bowel activity that changed in intensity and location from early (3-5-hour) to delayed (18-28-hour) images. In contrast, 5 of the 6 patients with documented pseudomembranous colitis (PMC) showed intense WBC localization involving most of the colon. In 3 of these 5 patients, early and delayed images were acquired and showed a relatively constant pattern of WBC localization. The sixth PMC patient had been treated with vancomycin before leukocyte scintigraphy and showed minimal distal small bowel activity on early images and only mild regional colonic activity on delayed images. As in the patients with gastrointestinal bleeding, the remaining six patients showed either focal or regional activity of variable intensity that changed over time. In critically ill patients, gastrointestinal bleeding and PMC accounted for 14 of the 20 patients in which labeled leukocyte scintigraphy exhibited colonic activity. A pattern of diffuse, intense colonic radiotracer activity which persists from early to delayed imaging strongly suggests the presence of PMC in this patient population.(ABSTRACT TRUNCATED AT 250 WORDS)

Diagnosis of recurrent brain tumor: value of 201Tl SPECT vs 18F-fluorodeoxyglucose PET.

OBJECTIVE: This prospective study was designed to compare the sensitivity and specificity of a relatively simple examination, 201Tl chloride single-photon emission CT (SPECT), with a more complex examination, 18F-fluorodeoxyglucose (FDG) positron emission tomography (PET), in patients thought to have recurrent brain tumor. Because both agents have been shown to be markers of viable tumor, we hypothesized that their sensitivity and specificity should be the same. SUBJECTS AND METHODS: Nineteen patients with evidence of recurrent tumor on CT or MR images were studied with both 201Tl SPECT and FDG PET imaging. Two patients were examined twice, so a total of 21 studies were evaluated. The 201Tl SPECT and FDG PET examinations were performed on the same day in 17 patients, and the remaining four examinations were done within 1 week of one another. Three reviewers independently interpreted each Tl SPECT and PET scan. Inappropriate regional increases in 201Tl or FDG activity were considered indicative of tumor recurrence. Sensitivity and specificity values were based on biopsy results and clinical follow-up. The final diagnosis was tumor recurrence in 16 cases and radiation necrosis in 5 cases. The relationship of scan results to survival was analyzed. RESULTS: The sensitivity and specificity of the 201Tl examination for detecting tumor recurrence were 11 (69%) of 16 and two (40%) of five, respectively; values for the FDG PET examination were 13 (81%) of 16 and 2 (40%) of 5, respectively. In patients with recurrent tumors less than 1.6 cm in size, results were false-negative in four 201Tl SPECT examinations and three FDG PET studies. All tumor lesions 1.6 cm or larger (n = 8) were detected. Agreement among the three nuclear medicine specialists was complete for each of the 201Tl SPECT scans. There was disagreement on the interpretation of five (24%) of the 21 FDG PET scans, which was resolved by consensus. Scintigraphic findings did not correlate with patients' survival times. CONCLUSION: We were unable to detect a statistically significant difference in sensitivity or specificity between the 201Tl SPECT and FDG PET scans. Both techniques were sensitive for tumor recurrence with lesions less than 1.6 cm or larger. However, given the greater availability, simplicity, and ease of interpretation and the lower cost of the 201Tl SPECT studies, this technique should be considered for detection of tumor recurrence with lesions that are demonstrated to be 1.6 cm or larger on CT or MR examinations.

Crossed cerebellar diaschisis associated with balloon test occlusion of the carotid artery.

99Tcm-hexamethylpropyleneamine oxime (99Tcm-HMPAO) single photon emission computed tomographic (SPECT) brain imaging performed in conjunction with balloon test occlusion of the carotid artery has been used to assess risk of neurologic sequelae that might follow permanent surgical ligation of the artery. The predictive value of cortical hypoperfusion during temporary carotid occlusion for adverse neurologic events has been debated in previous publications. We believe that the risk of an adverse event is greater when a reduction in cortical perfusion during balloon test occlusion is associated with crossed cerebellar diaschisis (CCD). To test our hypothesis we evaluated the results of 27 99Tcm-HMPAO SPECT brain studies obtained in association with balloon test occlusions of the carotid artery. In each case we correlated clinical outcome with the presence or absence of regional decreases in cerebral perfusion and CCD. All of the 27 patients were free of neurologic symptoms during the balloon test occlusion. Seventeen of the 27 scintigraphic studies were felt to be abnormal, showing cortical perfusion defects all on the side of the occlusion. Among these 17 patients, five demonstrated CCD. Four of these five CCD patients showed evidence for cerebral cortical ischaemia on the side of the temporary carotid occlusion either shortly after the procedure or following carotid artery sacrifice. Of the remaining 12 patients with regionally reduced cerebral perfusion and no CCD, none showed evidence for cortical ischaemia in association with balloon test occlusion, and five of these 12 patients had carotid ligation without subsequent neurologic sequelae.(ABSTRACT TRUNCATED AT 250 WORDS)

Pressor systems involved in the maintenance of arterial pressure after lesions of the rostral ventrolateral medulla.

The current study examined three pressor systems which might support mean arterial pressure (MAP) after lesions of the rostral ventrolateral medulla (RVLM). In two protocols, bilateral electrolytic lesions or sham lesions were placed in the RVLM of rats anesthetized with sodium pentobarbital. In the first protocol, the following drugs were given sequentially after placement of the lesions: captopril (5 mg/kg) and d-pentamethylene methylated tyrosine (30 micrograms/kg), a vascular arginine-vasopressin antagonist (AVPX). A final procedure consisted of spinal-cord transection. The second protocol was identical to the first except that the order of drug administration was reversed. In the first protocol, RVLM lesions caused a slight, but statistically significant, decrease in MAP from 118 +/- 3 mmHg to 103 +/- 5 mmHg. After captopril and AVPX, MAP further decreased to 87 +/- 5 mmHg and 62 +/- 4 mmHg, respectively. The MAP fell to 38 +/- 2 mmHg after spinal-cord transection. In the sham-lesion group, MAP rose slightly from 127 +/- 6 mmHg to 134 +/- 7 mmHg after placement of the sham lesions. A significant reduction in MAP was not seen until after administration of AVPX, which decreased MAP to 103 +/- 6 mmHg. Spinal-cord transection substantially lowered MAP to 36 +/- 4 mmHg. In the second protocol, RVLM lesions had no effect on MAP. Administration of AVPX had little effect on MAP (before: 117 +/- 5 mmHg; after: 102 +/- 7 mmHg). In contrast, sequential administration of captopril substantially decreased MAP to 55 +/- 5 mmHg. Spinal cord transection lowered MAP to 33 +/- 1 mmHg. A decrease in MAP in the companion sham-lesion group was not seen until after administration of captopril (before: 109 +/- 8 mmHg; after: 89 +/- 11 mmHg). The greatest fall in MAP followed spinal cord transection (to 39 +/- 6 mmHg). These results demonstrate normotension after RVLM lesions despite a marked reduction in sympathetic vasomotor activity. They also indicate that, after RVLM lesions, arterial pressure is maintained mainly by activity of the renin-angiotensin system and by AVP secretion.

An emission-based technique for obtaining attenuation correction data for myocardial SPECT studies.

In this paper, a technique is described for obtaining the information needed to perform attenuation correction in the thorax entirely from an emission study. This technique is based on the observation that the variation in soft tissue and lung attenuation coefficients is small among individuals. Thus only the outer contours of the body and lungs need be determined for obtaining the attenuation map. The contours are determined by using 99Tcm-macroaggregated albumin (MAA) to locate the lungs and an external source wrapped about the chest to locate the body boundary. Simulation studies were performed to investigate how errors in the presumed tissue attenuation coefficients affect the accuracy of the correction. Body and lung attenuation coefficients were varied from 20% less to 20% more than the coefficients used in the corrections. Over this range, there was less than a 15% alteration in the relative distribution of counts in the left ventricle. To test clinical feasibility, seven patients referred for clinical myocardial perfusion studies were scanned before and after the placement of the body source and the administration of 99Tcm-MAA. Reconstructed images from these studies showed clear demarcation of all body and lung boundaries. The presence of 99Tcm-MAA in the lungs had no significant effect on the clinical interpretation of the single photon emission computed tomographic (SPECT) studies. It is concluded that this technique is feasible for clinical application and that it offers important advantages over other current methods.

Cardiovascular effects of lesions of the rostral ventrolateral medulla and the nucleus reticularis parvocellularis in rats.

This study explored the possibility that the nucleus reticularis parvocellularis (NRP) acts in concert with the rostral ventrolateral medulla (RVLM) in the maintenance of mean arterial pressure (MAP). Bilateral electrolytic or chemical lesions (kainic acid) were placed in three groups of rats anesthetized with sodium pentobarbital. In the different groups, lesions were placed only in the NRP or RVLM or in both the NRP and RVLM (NRPRVLM). Captopril (5 mg/kg, i.v.) and an arginine vasopressin antagonist (AVPX), d-pentamethylene methylated tyrosine (30 micrograms/kg, i.v.), were sequentially administered. A final procedure consisted of spinal cord transection. The RVLM lesions did not significantly alter MAP (before: 116 +/- 3 mmHg; after: 106 +/- 5 mmHg). Sequential administration of captopril and AVPX each reduced MAP to 87 +/- 5 mmHg and 62 +/- 4 mmHg, respectively. Spinal-cord transection lowered MAP to 38 +/- 2 mmHg. Lesions of the NRP also did not alter MAP (before: 113 +/- 4 mmHg; after: 118 +/- 5 mmHg). Captopril reduced MAP to 109 +/- 7 mmHg, AVPX had no effect, and spinal-cord transection decreased MAP to 31 +/- 3 mmHg. In contrast to the lack of effect of lesions of the RVLM or NRP on MAP, profound hypotension was observed after NRPRVLM lesions (before: 113 +/- 3 mmHg; after: 51 +/- 3 mmHg). Subsequent administration of captopril decreased MAP to 39 +/- 2 mmHg, and AVPX lowered MAP to 32 +/- 1 mmHg. Spinal-cord transection reduced MAP to 23 +/- 1 mmHg. Several conclusions can be drawn from this study. First, lesions of the RVLM do not decrease MAP because of compensation by the renin-angiotensin system and AVP secretion which is mediated by the NRP. Second, lesions of the NRP do not affect MAP because the intact RVLM can maintain sympathetic tone. Third, the profound hypotension observed after NRPRLVM lesions occurred because of the simultaneous impairment of sympathetic vasomotor activity and the neuroendocrine vasoconstrictor effects of the renin-angiotensin system and AVP secretion.

Malignant hyperthermia: perioperative considerations.

In no situation is perioperative patient advocacy more important than when a smoothly running case is interrupted by an episode of malignant hyperthermia (MH). An understanding of the demographics, manifestations, and clinical interventions can enable the perioperative nurse to respond in an appropriate manner.

Normotension in conscious rats after placement of bilateral electrolytic lesions in the rostral ventrolateral medulla.

The effects of bilateral electrolytic lesions of the rostral ventrolateral medulla (RVLM) on mean arterial pressure (MAP) and heart rate (HR) were examined in 8 rats at one and 5 days after placement of the lesions. The MAP (111 +/- 2 mm Hg) and HR (393 +/- 17 bpm) of the lesion group were similar to the values recorded in the control group (117 +/- 3 mm Hg, 405 +/- 11 bpm; n = 18). Blockade of the synthesis of angiotensin II with captopril in the lesion group significantly decreased MAP to 93 +/- 2 mm Hg on the first postlesion day. In contrast, the MAP of the control group after captopril fell slightly to 111 +/- 4 mm Hg. Captopril did not alter MAP or HR on postlesion day 5 in either group. Administration of chlorisondamine, an autonomic ganglionic blocking agent, reduced MAP in the lesion and control groups to similar values of 59 +/- 2 mm Hg and 64 +/- 2 mm Hg, respectively. Baroreflex-mediated tachycardia to a decrease in MAP was abolished in the lesion group at one day postlesion and attenuated at 5 days postlesion. In contrast, the baroreflex-mediated bradycardia to an increase in MAP was unaffected by the lesions. Plasma renin activity (PRA) in the lesion group was elevated by nearly 50% as compared to the control group on the first postlesion day (7.3 +/- 0.8 and 4.9 +/- 0.5 ng AI/ml/h, respectively). A 90% elevation in plasma norepinephrine (NE) concentration was also observed in the lesion group as compared to the control group (437 +/- 80 pg/ml and 228 +/- 22 pg/ml, respectively) on postlesion day one. By postlesion day 5, the PRA of the lesion and control groups were nearly identical (4.4 +/- 0.7 and 4.0 +/- 1.0 ng AI/ml/h, respectively), and the plasma NE concentrations were also very similar (201 +/- 41 pg/ml and 175 +/- 22 pg/ml, respectively). We conclude that bilateral destruction of the RVLM does not cause hypotension or bradycardia in conscious rats. Therefore, areas other than the RVLM are capable of maintaining MAP and HR. Sympathetic vasomotor and cardiomotor tone appears unaffected by the lesions. However, increased activity of the renin-angiotensin system may contribute transiently to the maintenance of vasomotor tone and, consequently, MAP after lesion of the RVLM. The RVLM may be important in mediating baroreflex increase in HR.

Hypotensive effects of lesions of the rostral ventrolateral medulla in rats are anesthetic-dependent.

These studies were designed to determine if the hypotensive effects of bilateral electrolytic lesions of the rostral ventrolateral medulla are dependent on the type of anesthetic agent used. The lesions caused an immediate fall in mean arterial pressure (MAP) in rats anesthetized with urethane, alpha-chloralose or sodium pentobarbital. At 30 min after placement of the lesions, severe hypotension (MAP = 54 +/- 5 mm Hg) persisted in the rats anesthetized with urethane. However, 30 min after placement of the lesions, the MAP of rats anesthetized with alpha-chloralose or sodium pentobarbital was 87 +/- 9 mm Hg and 99 +/- 10 mm Hg, respectively. Subsequent transection of the cervical spinal cord produced a much greater decrease in MAP in rats anesthetized with alpha-chloralose and sodium pentobarbital as compared to rats anesthetized with urethane. Heart rate was significantly lower after placement of the lesions in all 3 groups. We conclude that the magnitude of the hypotensive effect caused by placement of lesions in the rostral ventrolateral medulla is anesthetic-dependent and that the rostral ventrolateral medulla is not the only area of the central nervous system capable of maintaining vasomotor tone.

Changes in plasma catecholamines and plasma renin activity during hypotension in conscious rats with lesions of the nucleus tractus solitarii.

The purpose of the present study was to examine the effects of lesions of the nucleus tractus solitarii on the reflex control of sympathetic activity and renin release in the conscious rat. Two doses of the arteriolar vasodilator hydralazine (0.3 and 1 mg/kg, i.v.) were used to activate reflexively the sympathetic nervous system in nucleus tractus solitarii lesion and control rats. Administration of 1 mg/kg of hydralazine to the control rats caused mean arterial pressure to fall from 120 +/- 2 mm Hg to 84 +/- 2 mm Hg and elicited an 11.2-fold increase in plasma renin activity and a 2.7-fold increase in plasma norepinephrine concentration. Administration of 0.3 mg/kg of hydralazine caused the arterial pressure of the lesion group to fall from 118 +/- 3 mm Hg to a comparable value of 85 +/- 4 mmg Hg, but plasma renin activity and plasma norepinephrine concentration did not rise significantly. However, administration of 1 mg/kg of hydralazine to the lesion group caused arterial pressure to fall from 128 +/- 6 mm Hg to 64 +/- 2 mm Hg, in association with a 12.4-fold increase in plasma renin activity and a 1.6-fold elevation in plasma norepinephrine concentration. Atenolol, a beta 1-adrenoceptor antagonist, blocked 70% of the rise in plasma renin activity caused by 1 mg/kg of hydralazine in both groups of rats. In addition, prior renal denervation also markedly attenuated the rise in plasma renin activity caused by hydralazine in the lesion group. Finally, electrical stimulation of the vagus nerves, which caused a large vasodepressor response in the control group, failed to lower the arterial pressure of the lesion group. Based on these observations, we conclude that in the conscious rat (1) nucleus tractus solitarii lesions eliminate the arterial baroreflexes as well as the cardiopulmonary baroreflex, and (2) severe hypotension induces sympathetically mediated renin release in the apparent absence of arterial and cardiopulmonary baroreflex function.

Parabrachial lesions increase plasma norepinephrine concentration, plasma renin activity and enhance baroreflex sensitivity in the conscious rat.

Electrolytic lesions of the parabrachial nucleus (PBN) caused significant increases in basal plasma renin activity (+433%) and basal plasma norepinephrine concentration (+98%) in conscious rats. Plasma epinephrine concentration, mean arterial pressure, heart rate, hematocrit, plasma osmolality and plasma sodium and potassium concentrations were not significantly affected by the lesions. Atenolol reduced the elevated plasma renin activity in the lesion group to a value similar to that of a control group (sham lesions or lesions in areas adjacent to the PBN). Captopril significantly lowered mean arterial pressure in the lesion group, but it had no effect on arterial pressure in the control group. Lesions of the PBN also increased the baroreflex-mediated bradycardia evoked by an abrupt elevation of arterial pressure. We propose that the PBN tonically inhibits sympathetic activity, sympathetically mediated renin release and baroreflex sensitivity.

Comparison of 1-hour and 24-hour blood pressure recordings in central or peripheral baroreceptor-denervated rats.

We compared the mean arterial pressure and heart rate activity of conscious, unrestrained rats during 1-hour and 24-hour continuous recording sessions, 3 to 4 weeks after either sinoartic denervation, placement of electrolytic lesions in the nucleus tractus solitarii, or sham operations. Sinoaortic denervation and nucleus tractus solitarii lesions both eliminated the reflex bradycardia to a phenylephrine-induced pressor response. No difference was found in the average level and lability of the mean arterial pressure between 1-hour and 24-hour recordings for any group. No elevation in the average mean arterial pressure of rats with nucleus tractus solitarii lesions was observed, although a mild hypertension was noted in half the sinoarotic-denervated rats, while the other half were normotensive. Group differences were not found for heart rate or heart rate variability; however, 24-hour recordings yielded significantly higher values than 1-hour recordings for all groups. Both medullary lesions and sinoaortic denervation significantly increased the lability of the mean arterial pressure, but the magnitude of the increase was significantly greater in the rats with lesions. The lability of the mean arterial pressure in sinoaortic-denervated rats depended largely on movement-related depressor responses that produced a negative skew in the frequency distribution of their mean arterial pressure. Rats with nucleus tractus solitarii lesions exhibited both pressor and depressor responses that resulted in pressure distributions that had a slight positive skew similar to that displayed by control rats. It is concluded that short-term continuous recordings of mean arterial pressure and heart rate accurately estimate the altered cardiovascular activity of baroreceptor-denervated rats. The differences in the cardiovascular responses of central and peripheral baroreceptor-denervated rats are believed to be due to the more extensive destruction by nucleus tractus solitarii lesions of central neurons and pathways involved in cardiovascular regulation.

Cardiovascular and neuroendocrine responses to behavioral stress after central or peripheral barodenervation in rats.

The cardiovascular and neuroendocrine responses to acute behavioral stress were evaluated in rats after disruption of the baroreflexes by electrolytic lesions of the nucleus tractus solitarii (NTS) or sinoaortic denervation (SAD). Rats with NTS lesions or SAD showed significantly greater increases in mean arterial pressure (MAP) and plasma norepinephrine (NE) concentrations than control rats during a single 30-min escape-avoidance test. In addition, the increases in MAP and plasma NE concentration of NTS lesion rats were significantly greater than those of SAD rats. However, NTS lesion rats showed no increase in plasma renin activity (PRA), as observed in the other groups. Thus, disruption of the baroreflexes by NTS lesions or SAD augments the arterial pressure and plasma NE responses to stress. Additionally, NTS lesions appeared to eliminate the neurons or fibers of passage participating in the sympathetically mediated increase in PRA.

Plasma norepinephrine concentration reflects pharmacological alteration of sympathetic activity in the conscious cat.

This study provides the first comprehensive set of basal values for hemodynamic variables, plasma norepinephrine (NE) and epinephrine concentrations and plasma renin activity in the conscious cat and demonstrates that changes in plasma NE concentration in the conscious cat accurately reflect the alterations in sympathetic discharge caused by hydralazine, yohimbine, chlorisondamine and clonidine.

Chronic lability of the arterial blood pressure produced by electrolytic lesions of the nucleus tractus solitarii in the rat.

The purpose of this study was to assess the chronic effects of lesions of the nucleus tractus solitarii on the cardiovascular activity of rats. Arterial pressure and heart rate were recorded in conscious, unrestrained rats 7-216 days following placement of electrolytic lesions in the nucleus tractus solitarii. To assess the impact of environmental stimuli on the mean level and lability of the mean arterial pressure, cardiovascular activity was recorded under conditions of controlled and uncontrolled environmental stimulation. Nucleus tractus solitarii lesions abolished the reflex bradycardia to a phenylephrine-induced elevation in arterial pressure. A marked increase in the lability of the mean arterial pressure was produced with nucleus tractus solitarii lesions. The standard deviation of the mean arterial pressure, an index of lability, was 380% greater in rats with lesions than in control rats. The average mean arterial pressure, heart rate and heart rate variability were not significantly different between the lesion and control groups, regardless of the environmental conditions under which the measurements were made. Nucleus tractus solitarii lesions also greatly exaggerated the arterial pressure response to naturally occurring behaviors, such as eating and drinking. Vagal and beta-adrenergic blockade with methyl atropine and propranolol did not alter the average level or lability of the mean arterial pressure, although heart rate responses were similar in both groups. alpha-Receptor blockade with prazosin significantly lowered the mean arterial pressure in both lesion and control rats, but the decrease in mean arterial pressure was significantly greater in rats with nucleus tractus solitarii lesions (42 +/- 6 mm Hg, 38.5%) than in control rats (27 +/- 4 mm Hg, 23.2%). Prazosin also reduced the lability of the mean arterial pressure to control levels in rats with lesions. Thus, the chronic effects of nucleus tractus solitarii lesions in rats are to abolish the cardiomotor component of the baroreflexes and to produce extreme lability of the arterial pressure without altering the average level of the mean arterial pressure. Exaggerated blood pressure responses are seen in association with various behaviors. These effects are mediated primarily by changes in sympathetic discharge to the vasculature and are independent of the ambient level of environmental stimuli.

Arterial hypertension elicited either by lesions or by electrical stimulations of the rostral hypothalamus in the rat.

Bilateral anodal lesions performed with stainless steel electrodes placed either in the anterior medial (AMH) or lateral (ALH) hypothalamus, or in the ventromedial nucleus (VMH), induced in unrestrained rats the rapid development of arterial hypertension, tachycardia and death. Similarly placed cathodal lesions performed with platinum electrodes failed to elicit the cardiovascular syndrome. The electrical stimulation of the AMH, ALH or VMH caused an increased in the arterial blood pressure in anesthetized rats. This pressor response was characteristically biphasic and consisted of a sharp increase in arterial pressure at the onset of the stimulation, followed by a second elevation at the end of the stimulation. The hypertension evoked either by lesions or by stimulations of the hypothalamus, appeared to depend largely on a neurally mediated release of adrenal medullary catecholamines, and to some extent on the activation of the sympathetic vasoconstrictor fibers. Bilateral adrenalectomy, or adrenal demedullation, prevented the hypertension evoked by lesions, and selectively blocked the important secondary phase of the pressor response elicited by stimulation, but did not affect the primary phase. The latter was specifically eliminated by the destruction of the sympathetic vasomotor axons with 6-hydroxydopamine (6-OHDA). On the other hand, the tachycardia evoked by lesions or stimulations of the medial hypothalamus, resulted from an increase in sympathetic neural discharges to the heart, and it was abolished either by beta-receptor blockade with sotalol or by chemical sympathectomy with 6-OHDA. In contrast, the tachycardia occurring after lesions of the lateral hypothalamus was entirely due to circulating adrenal medullary catecholamines and it was eliminated by adrenalectomy. It is concluded that acute hypertension and tachycardia produced by anodal lesions performed with stainless steel electrodes results from the excitation of the hypothalamus, possibly due to the irritative action of the metallic ions deposited at the lesion sites. The observations of cardiovascular responses entirely due to adrenomedullary secretions suggests that the control of the adrenal medulla is at least partially distinct from that of the sympathetic vasoconstrictor and cardiac fibers, at the rostral hypothalamic level.