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Biomedical subjects

M A Nathan

Publications and source records attributed to M A Nathan.

At least 19 recordsLinked to original sources
PubMed1989

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.

Angiotensin II↗
PubMed1988

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.

Animals↗
PubMed1988

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.

Anesthetics↗
PubMed1987

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.

Animals↗
PubMed1986

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.

Animals↗
PubMed1986

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.

Animals↗
PubMed1986

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.

Animals↗
PubMed1978

Enhancement of conditioned arterial pressure responses in cats after brainstem lesions.

Cats were classically conditioned after the baroreceptor reflexes were abolished by bilateral placement of electrolytic lesions in the nucleus tractus solitarii. The conditioned increases in arterial pressure were more than five times larger than the responses obtained in similarly trained controls. This finding suggests that the baroreceptor reflexes actively inhibit conditioned increases of arterial pressure.

Animals↗
PubMed1977

Chronic labile hypertension produced by lesions of the nucleus tractus solitarii in the cat.

Bilateral electrolytic lesions of the nucleus tractus solitarii (NTS) were made at the level of the obex in seven cats. Within 1 hour the mean arterial pressure (MAP) rose to a maximum of 144 mm Hg (141% of control), and by 7 hours heart rate reached a peak of 236 beats/min (148% of control). The baroreceptor reflexes were abolished. After 24 hours the arterial pressure became extremely labile, with variations of 80-100 mm Hg observed. The lability occurred spontaneously and during behaviors that were self-initiated or elicited by environmental stimuli. The MAP in the lesion group was 144 mm Hg (180% of control) during the day, and 96 mm Hg (120% of control) at night. The lability, measured by the standard deviation, during the day in the lesion group was 4 times greater than in the control group and at night there were no differences. The heart rate of the lesion group was always higher than that of the control group but the lability of both groups was the same. We conclude that lesions of the NTS produced labile hypertension, probably by disinhibition of sympathetic activity through central interruption of the baroreceptor reflexes. The higher, more labile arterial pressures during the day may be caused by uninhibited increases in sympathetic activity elicited by environmental stimuli that are present during the day and absent at night. The daily variation of pressure may also be caused by somatomotor activity or by a daily rhythm of sympathetic activity which is unmasked by the lesions.

Acute Disease↗
PubMed1975

Fulminating arterial hypertension with pulmonary edema from release of adrenomedullary catecholamines after lesions of the anterior hypothalamus in the rat.

Bilateral electrolytic lesions of the anterior hypothalamus in unrestrained rats resulted in the development, within 2 hours, of arterial hypertension, tachycardia, hyperthermia, and increased locomotor activity, often leading to pulmonary edema and death. Similar lesions in paralyzed, artificially ventilated rats produced comparable changes in arterial blood pressure and body temperature with a similar time course. The arterial hypertension was a consequence of an increase in total peripheral resistance to 15% of control with a reduction in cardiac output to 49% of control. Arterial hypertension, elevated peripheral resistance, and diminished cardiac output were reversed toward normal by alpha-receptor blockade with phentolamine (1 mg/kg, iv). Bilateral adrenalectomy, adrenal demedullation, or adrenal denervation performed prior to lesion placement prevented the development of arterial hypertension and pulmonary edema as well as the changes in peripheral resistance, cardiac output, and body temperature. We conclude that arterial hypertension following lesions of the anterior hypothalamus is due to a neurally mediated increase in peripheral resistance initiated by the release of adrenal medullary catecholamines and that pulmonary edema is due to myocardial failure secondary to the ensuing ventricular overload. Structures originating in or passing through the anterior hypothalamus may exert selective control over the adrenal medulla independent of vasomotor neurons.

Adrenal Medulla↗
PubMed1973

Predatory attack, grooming, and consummatory behaviors evoked by electrical stimulation of cat cerebellar nuclei.

Electrical stimulation at single sites in the rostral fastigial nucleus elicits hypertension, grooming, feeding, and attack behaviors in the cat. The stimulus intensity and availability of suitable goal objects determines the behavior. Bilateral lesions of the area fail to produce motor deficits. The rostral fastigial nucleus may be a cerebellar area for behavioral and autonomic regulation.

Aggression↗