Wiley

The ascending monoamine pathways in the rat brain are demonstrated by the pile up of fluorescent material occurring in the axons after various types of lesions. The anatomy of the pathways is outlined in drawings of frontal sections of the brain and the origin and termination of several pathways is determined by studying the anterograde and retrograde degeneration occurring after well localised lesions. It is possible to separate the ascending NA pathways into a dorsal and a ventral bundle of axons. The dorsal bundle innervates the cortex and the hippocampus and the ventral bundle supplies NA nerve terminals to the medulla, the pons, the mesencephalon and the diencephalon. The dorsal bundle is found to originate in the locus coeruleus. Lesions of this nucleus abolish the nerve terminals in all cortical areas and in several other areas of the brain indicating a unique role for the locus coeruleus in influencing the activity of the entire brain. The 5‐HT pathways have a distribution similar to the ventral NA pathyway. The course of the nigro‐striatal and the meso‐limbic DA pathways is presented in detail.

The functional role of the nigro‐striatal dopamine (DA) system has been investigated on the basis of a recent detailed mapping of its path and a new method of lesioning the catecholamine systems selectively by intracerebral injection of 6‐hydroxydopamine (6‐OH‐DA). The investigation was especially focused on the symptoms of adipsia, aphagia, hypokinesia and catalepsia after lateral hypothalamic lesions as such lesions may interrupt the ascending DA axons. Electrocoagulations or 6‐OH‐DA lesions were performed bilaterally at several sites along the DA pathway and the behavioural effects were evaluated in relation to the histochemically detected lesion of the DA pathway. It was concluded that bilateral complete degeneration of the nigro‐striatal DA pathway produces severe, long lasting adipsia and aphagia, hypoactivity, difficulties to initiate activity and loss of exploratory behaviour and curiosity. Experiments with DA receptor stimulating and blocking drugs supported the lesion results. Catalepsia and somnolence were attributed to the interruption of other pathways. The results suggest an important role for the nigro‐striatal DA system and the striatum in the control of behaviour. A number of symptoms earlier related to the hypothalamus may in fact be due to disturbance of the nigro‐striatal DA system.

The pulmonary arterial blood pressure was recorded in anaesthetized cats by means of a special cannula, according to MELLIN's technique. In most experiments the thorax was closed and the animal was breathing spontaneously.

The pulmonary arterial pressure in 9 experiments averaged 23 cm water, or approximately 17 mm Hg, at an average systemic pressure of 132 mm Hg. The average ratio thus was about 1: 8, with the limits 1: 5 and 1: 14.

Pressure variations of 1–2 cm blood synchronous with the breathing were regularly recorded. In one case, slow large waves of 1–2 minutes duration and about 5 cm amplitude were observed.

Even great variations in the systemic blood pressure, elicited from the pressoregulating reflex mechanisms, were hardly accompanied by variations in the pulmonary arterial pressure.

During muscular work a moderate rise in pulmonary blood pressure generally occurred, greater when air was breathed than when oxygen alone was administered.

Clamping the pulmonary artery to one lung did not cause any change in systemic pressure (confirming LICHTHEIM and TIGERSTEDT) but caused a moderate rise in pulmonary arterial pressure.

Breathing of pure oxygen lowered the pulmonary arterial pressure and oxygen‐lack raised it. Carbon dioxide 6.5–20.5 per cent in oxygen raised the pressure sligthly, but constantly. These effects were not influenced by vagotomy.

The effect of injections of adrenaline, nor‐adrenaline, acetylcholine and histamine and of stimulation of pulmonary nerves were studied in some cases.

The experiments seem to warrant the conclusion, that the regulation of the pulmonary blood flow is mainly mediated by a local action of the blood and alveolar gases leading to an adequate distribution of the blood through the various parts of the lungs according to the effeciency of aeration.

Bài viết mô tả một phương pháp kiểm nghiệm hóa học cho một lượng nhỏ adrenaline và noradrenaline trong các mô. Các catecholamin được chiết xuất bằng axit perchloric. Các chiết xuất được đưa qua cột trao đổi cation (Dowex 50) nhằm hấp thụ catecholamin. Việc tách các amin khỏi cột được thực hiện bằng axit hydrochloric. Sự ước lượng của hai amin trong các dung dịch lọc được thực hiện thông qua phương pháp huỳnh quang sau khi thực hiện quá trình oxy hóa và tái cấu trúc trong kiềm. Phân biệt giữa adrenaline và noradrenaline được thực hiện bằng cách sử dụng sự khác biệt trong quang phổ kích hoạt của các chất gây huỳnh quang.

Amphetamine induced vigorous rotational behaviour in rats where the nigrostriatal dopamine (DA) system was unilaterally degenerated by an intracerebral injection of 6‐hydroxydopamine (6‐OH‐DA). The rotational behaviour was analysed in a specially designed “rotometer” and found highly reproducable. The intensity of the rotation was proportional to the extent of degeneration in the DA system. The amphetamine site of action was in all probability presynaptic as amphetamine caused a rotation in the opposite direction as compared to the DA receptor stimulating drug apomorphine. Tyrosine hydroxylase inhibition abolished the amphetamine effect, while reserpine potentiated the effect. Evidence was also obtained that the amphetamine induced release of DA was dependent upon nerve impulses. The rotational behaviour reflected the degree of DA receptor stimulation, but changes in the noradrenaline (NA) transmission seemed to modulate the behaviour. Decreased NA transmission after dopamine‐β‐hydroxylase inhibition increased the rotational behaviour. The unilateral degeneration of the DA system was studied by the changes in posture and movements that occurred during the degeneration. After inhibition of the monoamine oxidase the rats showed a strong rotation beginning on the 23d and ending on the 33d hour after the operation. The rotational behaviour was probably due to degeneration release of DA and equivalent to the degeneration contraction of the nictitating membrane in the peripheral nervous system Amphetamine greatly potentiated the spontaneous degeneration release during this period.

It is shown that for a free ion diffusing through a membrane the ratio between the flux in one direction and the simultaneous flux in the opposite direction is independent of the structure of the membrane. This ratio , which can be evaluated through tracer experiments, is equal to the ratio between the electrochemical activities of the ion on the two sides of the membrane.

Muscle biopsy samples were obtained from healthy subjects in order to evaluate quantitative differences in single fibres of substrate (glycogen and triglyceride) and ion concentrations (Na⁺ and K⁺) as well as enzyme activity levels (succinate‐dehydrogenase, SDH; phosphofructokinase, PFK; 3‐hydroxyacyl‐CoA‐dehydrogenase, HAD; myosin ATPase) between human skeletal muscle fibre types. After freeze drying of the muscle specimen fragments of single fibres were dissected out and stained for myofibrillar‐ATPase with preincubations at pH's of 10.3, 4.6, and 4.35. Type I (“red”) and II A, B, and C (“white”) fibres could then be identified. Glycogen content was the same in different fibres, whereas triglyceride content was highest in Type I fibres (2–3 × Type II). No significant differences were observed for Na⁺ and K⁺ between fibre types. The activity for the enzymes studied were quite different in the fibre types (SDH and HAD, Type I ≊ 1.5 × Type II; PFK Type I ≊ 0.5 × Type II; Myosin ATPase Type I ≊ 0.4 × Type II). The subgroups of Type II fibres were distinguished by differences in both SDH and PFK activities (SDH, Type II C > A > B; PFK, Type II B > A ≊ C). It is concluded that contractile and metabolic characteristics of human skeletal fibres are very similar to many other species. One difference, however, appears to be that no Type II fibres have an oxidative potential higher than Type I fibres.

Electrical stimulation of the cat cervical sympathetic trunk caused submandibular salivary secretion and vasoconstriction simultaneously with a contraction of the nictitating membrane. Following α‐ and β‐adrenoceptor blockade by phentolamine or phenoxybenzamine combined with propranolol, the salivary response and the nictitating membrane contraction upon sympathetic stimulation were almost abolished. A considerable vasoconstrictor response (up to 40% of control) however still remained in the submandibular gland. This yasoconstriction, which persisted after α‐adrenoceptor blockade, was rather slow in onset and had a long duration without any poststimulatory hyperemia. Local intra‐arterial infusions of noradrenaline caused submandibular vasoconstriction, salivary secretion and nictitating membrane contraction. The blood flow response to exogenous noradrenaline did, however, not mimic the effects of sympathetic nerve stimulation with regard to vascular escape. Whereas the vascular escape after nerve stimulation was followed by a prolonged vasoconstriction with a gradual decline, the escape after noradrenaline infusions was accompanied by a normalization of blood flow. Local intra‐arterial infusions of pancreatic polypeptide (PP)‐related peptides caused a slowly developing vasoconstriction with a long duration in the submandibular gland, but no salivary secretion or contraction of the nictitating membrane. The relative molar potencies as vasoconstrictory agents were about PYY: 1, neuropeptide Y (NPY): 5, avian and bovine pancreatic polypeptid 100. The vasoconstrictor effects of PP‐related peptides were resistant to α‐adrenoceptor blockade and present also in sympathectomized animals, suggesting a direct action on vascular smooth muscle. Combined local infusions of noradrenaline and NPY caused a vascular response in the submandibular salivary gland which was similar to that seen upon sympathetic nerve stimulation. PYY and NPY caused increase in systemic arterial blood pressure upon systemic administration which indicates general vasoconstrictor actions. This effect was accompanied by a transient bradycardia which was due to inhibition of sympathetic tone, since it was absent in animals treated with propranolol.

In conclusion, the present findings illustrate the differential sensitivity to α‐adrenoceptor antagonists of the submandibular vasoconstriction and salivation as well as smooth muscle contraction of the nictitating membrane induced by sympathetic nerve stimulation. This remaining vasoconstriction may be explained by release of a nonadrenergic, PP‐related transmitter such as NPY which may be present together with noradrenaline in the vascular nerves. Release of an additional vasoconstrictory factor may also account for the finding that infusions of noradrenaline do not mimic the vascular effects of sympathetic nerve stimulation in vivo.