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Biomedical subjects

R R Sonnenschein

Publications and source records attributed to R R Sonnenschein.

At least 19 recordsLinked to original sources
PubMed1985

Cortical acetylcholine efflux with hypercapnia and nociceptive stimulation.

In rabbits anesthetized with 70% N2O-30% O2, the rate of efflux of acetylcholine (ACh) from the cerebral cortex doubled during hypercapnia (increase of end-tidal CO2 from 4 to 8%), and during mild nociceptive stimulation of the tail. Under 0.7% halothane anesthesia, the control rate of ACh efflux was lower than that under N2O; the rate rose 2-fold during hypercapnia and 4-fold during tail stimulation. In the absence of systemic atropinization, increase in ACh efflux was correlated with a shift in EEG from high- to low-voltage ('activated'); after systemic atropinization EEG remained in the high-voltage state, but the changes in ACh efflux with hypercapnia and stimulation were not affected. Following transection of the midbrain, ACh efflux was markedly depressed and did not change during hypercapnia. Taken in context with the previously known facts that the cerebral hyperemia of hypercapnia is potentiated by cholinesterase inhibition and attenuated by atropine or decerebration, the present results support the concept of a cholinergic regulation of the cerebral vasculature.

Acetylcholine↗
PubMed1985

Cerebrovascular reactivity to CO2: modulation by arterial pressure.

Cerebrovascular reactivity to CO2 (CO2R), measured in halothane-anesthetized rabbits, decreased as arterial pressure was increased either pharmacologically or mechanically. On the other hand, hypotension, induced by bleeding, led to an increase in CO2R. These responses were unaffected by denervation of baroreceptors.

Animals↗
PubMed1983

Cholinergic cerebral vasodilatation: lack of involvement of cranial parasympathetic nerves.

Cerebral blood flow (CBF) was estimated by measurement of internal carotid blood flow (ICBF) and sagittal sinus blood flow (SSBF) in mechanically ventilated rabbits under 70% N2O/30% O2. Electrical stimulation of cranial nerves III, VII, IX, or X, with stimulus parameters adequate to excite other visceromotor outflows of these nerves, failed to elicit change in CBF. Combined bilateral section of nerves VII, VIII, IX, X, and XI had no effect on the reactivity of CBF to CO2, nor did the sectioning of these nerves affect the increases in CBF induced by physostigmine. Division of the sinus and aortic nerves and of the vagi in the neck failed to change CO2 reactivity, even though normocapnic CBF was reduced. Pentobarbital blocked the increase in CBF produced by physostigmine, but had no effect on that produced by pilocarpine. The results indicate that cranial parasympathetic nerves do not contain cerebral vasodilator fibers, and that they are not the source of acetylcholine which is presumably involved in CBF regulation.

Animals↗
PubMed1982

Cholinergic cerebral vasodilatation in the rabbit: absence of concomitant metabolic activation.

Cerebral blood flow (CBF) was estimated from measurements of internal carotid blood flow and sagittal sinus blood flow in mechanically ventilated rabbits under 70% N2O-30% O2. Intravenously administered physostigmine, a cholinesterase inhibitor, increased CBF under normocapnia and enhanced the cerebral vasodilatation of hypercapnia, but did not alter the cerebral metabolic rate of oxygen (CMRO2). The cerebrovascular effects of physostigmine were antagonized by atropine but not by dihydro-beta-erythroidine, a nicotinic blocker. Neostigmine, a quaternary cholinesterase inhibitor that does not cross the blood-brain barrier, showed no cerebrovascular effects. It is concluded that the cholinergic cerebral vasodilatation does not depend on cerebral metabolic activation, and that the cholinergic receptors involved are muscarinic and located beyond the blood-brain barrier.

Animals↗
PubMed1982

Cerebrovascular anatomy and blood flow measurements in the rabbit.

The arterial supply and venous drainage of the rabbit's brain were characterized by intravascular injection of casting material and intra-arterial administration of markers (crystal violet or dissolved hydrogen gas). The internal carotid artery supplies the homolateral cerebral cortex and subcortical structures except for the thalamus and the posterior portion of the nucleus caudatus; it also supplies the homolateral retina and optic nerve. No noncerebral structures are supplied by this artery. The dorsal sagittal sinus drains the dorsal and lateral parts of the frontal and parietal areas of the cerebral cortex, with no detectable extracerebral contamination. Electromagnetic measurement of flow in the internal carotid artery (ICBF), volumetric or H2-clearance measurement of flow in the dorsal sagittal sinus (SSBF), and H2-clearance determination in cerebral cortex yield comparable results on the cerebrovascular response to hyper- and hypocapnia. ICBF and SSBF are reliable and valid estimates of average blood flow through the homolateral cerebral hemisphere and the cerebral cortex, respectively.

Animals↗
PubMed1981

The electroencephalogram, blood flow, and oxygen uptake in rabbit cerebrum.

In the present study, the relationships among electroencephalographic (EEG) amplitude shifts, cerebral blood flow (CBF), and cerebral oxygen uptake (CMRO2) have been characterized in halothane-anesthetized rabbits. CBF was measured by timed collection of venous effluent from the superior sagittal sinus. CMRO2 was calculated as the product of CBF and the arteriovenous difference in oxygen content. The depth of anesthesia in the first series of experiments was maintained at a constant level that was characterized by spontaneous EEG shifts from high- to low-voltage states (HV-LV shifts). These shifts were associated with transient decreases in mean arterial pressure (MAP), which averaged 23 +/- 2 mm Hg (n = 17). Ninety seconds after spontaneous HV-LV shifts, MAP had returned to its original value, CBF had increased by 26 +/- 7% (n = 8), and CMRO2 had increased 22 +/- 4% (n = 7). In a second series of experiments, HV-LV shifts were induced by a 90-s application of a standardized nociceptive stimulus (n = 13). Following these stimulation-induced HV-LV shifts, CBF increased 28 +/- 5% and CMRO2 increased 27 +/- 4%. Under scopolamine (0.35 mg/kg, i.v., n = 8), no change in CBF was observed following HV-LV shifts induced by 90-s of stimulation, although CMRO2 increased significantly by 14 +/- 3%. After 300 s of post-scopolamine stimulation, however, both CBF and CMRO2 had significantly increased by 12 +/- 3 and 15 +/- 3% (n = 8) of control, respectively. These results demonstrate that HV-LV shifts, whether spontaneous or stimulation-induced, are associated with significant increases in both CBF and CMRO2. Because the early (90-s) increases in CBF but not those in CMRO2 could be blocked by scopolamine, we suggest that the cerebral vasodilatation that occurs during the early phase of HV-LV shifts involves cholinergic mechanisms. Because scopolamine could not block the increase in CBF observed after 300 s of stimulation, we suggest that the final value of CBF obtained after an HV-LV shift is determined by a combination of both cholinergic and noncholinergic factors.

Animals↗
PubMed1979

Abolition of hypoxic vagal bradycardia by lateral mesencephalic lesions in spinal cats.

To examine central sites that integrate the vagal bradycardia induced by hypoxia, heart rates were recorded continuously in spinal, precollicular, decerebrated cats during transient hypoxia induced by ventilation with 100% nitrogen. Bilateral lesions in the lateral mesencephalic reticular formation either decreased the extent of bradycardia or caused a reversal to tachycardia; anesthesia induced the same change. In contrast, bilateral lesions in the medial mesencephalic reticular formation failed to alter the bradycardia. Hence, the lateral mesencephalic reticular formation is essential for the appearance of hypoxia-induced vagal bradycardia.

Anesthesia↗
PubMed1978

Mechanisms of vascular changes in skeletal muscle during asphyxia in the cat.

Vascular responses in the hindlimb muscles of anesthetized paralyzed cats during systemic asphyxia were studied. The cats were ventilated with 10% O2-10% CO2-80% N2 for 10-20 min periods, while blood flow to the skinned hindlimb was monitored (electromagnetic flowmeter). Mean arterial pressure rose and hindlimb flow typically fell during asphyxia, implying increased vascular resistance. After sympathetic denervation of the hindlimb, resistance increased in some groups of animals, and did not change in others during asphyxia. Functional adrenalectomy did not alter these response characteristics. Resistance also did not changes significantly if the control resistance was first increased to the predenervation level by electrically pacing the lumbar sympathetic chain. In contrast, pronounced vasodilatation occurred during asphyxia after blocking of the alpha receptors in the hindlimb (phenoxybenzamine) or after systemic catecholamine depletion (reserpine). We conclude that the vasoconstriction in innervated muscle during asphyxia was caused in part by increased discharge of sympathetic constrictor nerves to the muscle vasculature, with augmentation from a humoral alpha agonist of nonadrenal origin, possibly norepinephrine released from sympathetic nerves throughout the body.

Adrenal Medulla↗
PubMed1978

Sympathetic vasomotor outflows to hindlimb muscles of the cat.

Blood flow to the hindlimb muscles of chloralose-anesthetized, paralyzed cats was monitored with an electromagnetic flowmeter on the femoral artery. The functional pathways of the sympathetic constrictor and dilator innervations to the vasculature of these muscles were determined by measuring changes in vascular conductance during electrical stimulation of 1) ventral roots T12-L7 (exit of preganglionic fibers from the spinal cord and entrance into the sympathetic chain), 2) the distally intact sympathetic chain at successive levels between the L1 and L7 ganglia (presence of caudally running vasomotor fibers in the chain at each level), and 3) isolated sympathetic ganglia L2-L7 (exit of postganglionic vasomotor fibers from the chain at each level). Our results indicate that vasoconstrictor fibers emerge from ventral roots T12-L4 with maximum functional outflow at L1-L3; the fibers course downward through the sympathetic chain to exit from the chain mainly at L5-L7 or below. In contrast, the preganglionic origin of cholinergic vasodilator fibers, tested after blocking the constrictor fibers with bretylium, is limited to ventral roots L2-L5, with maximum outflow at L4. The vasodilator fibers leave the sympathetic chain to enter the spinal nerves at the same levels as the vasoconstrictor fibers.

Animals↗
PubMed1976

Vascular response to short-term systemic hypoxia, hypercapnia, and asphyxia in the cat.

Acute systemic hypoxia, hypercapnia, or asphyxia was produced in ketamine-anesthetized, paralyzed cats by ventilating them for 2-4 min with appropriate gas mixtures. A sustained rise in arterial pressure occurred in all cases. Vascular responses to hypoxia (7% O2, 10% 02, or 14% O2) included muscle constriction, cutaneous (hindpaw) dilatation (no change with 14% O2), renal constriction (unchanged flow), and unchanged intestinal resistance. Asphyxia (hypoxia + 10% CO2) produced a similar pattern, except that intestinal dilatation occurred. Hypercapnia (10% CO2 + 21% O2) produced muscle constriction, renal constriction (unchanged flow), intestinal dilatation, and no change in cutaneous resistance. Intestinal dilatation seemed in all cases a response to elevated CO2 only. Hypercapnia augmented the effects of hypoxia in skin and skeletal muscle. The variation of responses in different vascular beds suggests a patterning of sympathetic discharge, and varying responsivity to local and humoral factors.

Animals↗