[Vasoconstrictor responses of isolated pig coronary arteries].

In helical strips of pig coronary arteries, histamine, serotonin, acetylcholine and a stable analogue of thromboxane A2 (9, 11-epithio-11, 12-methano TXA2: s-TXA2) produced a dose-dependent contraction. The histamine-induced contraction was suppressed by treatment with chlorpheniramine, suggesting an involvement of H1 receptors. Contractile responses to serotonin were attenuated by not only ketanserin, an S2 antagonist, but also by cinanserin and methysergide. Relaxation induced by serotonin in preparations treated with high concentrations of ketanserin were inhibited by cinanserin and methysergide. Norepinephrine contracted coronary arteries treated with propranolol. Contractile responses to norepinephrine were reversed to relaxations by prazosin, which were abolished by treatment with yohimbine. Contractile responses to histamine were potentiated by treatment with low concentrations of serotonin or s-TXA2. Contractile responses to serotonin were also potentiated by low concentrations of histamine or s-TXA2. Removal of the endothelium from pig coronary arterial strips potentiated contractions induced by serotonin, histamine and norepinephrine. These results suggest that, in addition to damaged endothelium, integrating action of endogenous vasoconstrictors, including histamine, serotonin, TXA2 and norepinephrine, may play an important role in producing coronary vasospasm.

Periaqueductal gray inhibition of viscerointercostal and galvanic skin reflexes.

In adult cats anesthetized with urethan-chloralose, effects of descending volleys from the mesencephalic periaqueductal gray (PAG) upon the viscerointercostal and galvanic skin reflexes were studied. The viscerointercostal reflex (VIR) was evoked by electrical stimulation of the greater splanchnic nerve and was recorded from the 11th, 12th or 13th intercostal nerve. Conditioning stimuli applied to the PAG inhibited the VIR. The inhibition was particularly marked when the nucleus raphe dorsalis (NRD) or its immediately adjacent ventromedial PAG was stimulated. A train of pulses was required in order to produce a recognizable PAG/NRD inhibition of the VIR. When the PAG/NRD was stimulated at 300-500 Hz, stimulation-produced inhibition became more pronounced in parallel with increase in number of pulses in each train and levelled off at about 5 pulses. The most effective frequency of PAG/NRD stimulation was found within this frequency range. Degree of PAG/NRD stimulation-produced inhibition of the VIR was dependent upon the strength of the test stimulus applied to the splanchnic nerve; the weaker the test stimulus, the more marked the inhibition. PAG/NRD stimulation-produced inhibition of the VIR was completely eliminated by bilateral section of the dorsolateral funiculi. The same section enhanced the VIR per se. It was suggested that PAG/NRD stimulation-produced inhibition of the VIR is mediated by descending pathways in the ipsi- as well as contralateral dorsolateral funiculi, and that the VIR per se is tonically inhibited by descending impulses in these pathways. PAG/NRD stimulation inhibited the segmental polysynaptic reflex in the intercostal nerve, but had little effect on the segmental monosynaptic reflex in the same nerve. Intravenous administration of morphine suppressed the VIR. The suppression was antagonized by intravenous naloxone. In contrast, PAG/NRD stimulation-produced inhibition of the VIR was unaffected by intravenous naloxone. Electrical stimulation of the splanchnic nerve evoked the galvanic skin reflex (GSR) from the forepaw pad. The GSR was inhibited by electrical stimulation of the PAG/NRD. The PAG/NRD stimulation-produced inhibition of the GSR was completely eliminated by intravenous administration of naloxone (0.4 mg/kg).