No abstract

The effects of altered temperature in vivo on in vitro smooth muscle contractility of rainbow trout intestine were investigated. Initial analysis of the data revealed a seasonal variation in the maximal tension of intestinal smooth muscle attainable with 5-hydroxytryptamine (serotonin), carbachol, KCl, and transmural stimulation in vitro. Peaks occurred in spring and troughs in autumn. There was no seasonal cycling of the potency of the stimulants. All data regarding the efficacy of the stimulants were subsequently corrected for seasonal variation. The response of smooth muscle depends on the temperature of the water in which the fish are placed (2°C-20°C). There was a marked linear increase in efficacy and a slight increase in potency of the stimulants with increasing temperature. Changes in responsiveness of the intestinal smooth muscle occurred within 30 min of moving the fish between tanks. Smooth muscle reactivity returned to pretreatment values by 48h. Any changes in responsiveness with regards to time were unlikely to be as a consequence of water temperature, but may have been a result of handling stress.

Experiments were designed to determine whether contractility of trout smooth muscle in vitro varied with temperature and if changes occurred at the receptor or intracellular levels. The role of calcium in contractility at various temperatures was also investigated. Isolated trout intestinal segments, approximately 2 cm in length, were suspended isometrically under 2 g tension in 10-mL organ baths containing trout Ringer's solution aerated with O2 and CO2 (95:5). Contractions of trout intestine were not statistically different at 10 and 20 degrees C for carbachol, 5-hydroxytryptamine, and KCl. However, the efficacy, but not the potency, of each agonist was decreased at 2 degrees C. Receptor-induced contractions were reduced to a greater extent at 2 degrees C and did not recover to the same extent when returned to 10 degrees C in comparison with those induced by depolarization. The calcium source for contractility was also dependent on temperature. As temperatures increased, utilization of intracellular calcium increased, as indicated by increased contractility in the absence of extracellular calcium. Thus, low temperatures decrease smooth muscle contractility by affecting receptor-mediated events rather than the intracellular contractile mechanisms. Receptor-operated agonists appear to have a higher capability of using intracellular calcium than depolarizing agents.

Summary The heart rate changes during routine training in a group of 8 actively racing Standardbreds were used to simulate the training work on a treadmill (ST) and indices of exercise compared to maximal effort (MAX) on the treadmill. The following parameters were recorded during treadmill work: heart rate, velocity, O2 consumption, respiratory and stride frequency, and stride length. Blood lactate concentrations were measured before and after each work test. Heart rate during simulated training was mean ± s.d. 87.8 ± 5.5% heart rate in MAX, one of the 8 horses working <80% of maximal HR and 2 of the 8 horses working above 90% maximal heart rate. Mean ± s.d. oxygen consumption during the ST was 75.1% ± 8.4% MAX, but correlated poorly against percentage heart rate for individual horses (r2 = 0.02). At similar velocities for the ST and MAX, only respiratory frequency differed significantly (P>0.05), being higher during the ST. Most horses worked at intensities based on heart rate consistent with proposed guidelines of 80–90% of maximal heart rate. However, in 3 of the 8 horses work intensity of insufficient or excessive amounts may have occurred.

Mediators and mechanisms responsible for the inhibitory modulation of trout intestinal smooth muscle were examined using a series of putative mediators and substances known to modulate neurotransmission in mammalian systems. Frequency response relationships to transmural stimulation and concentration response relationships to 5-hydroxytryptamine, carbachol, and substance P were established on paired segments of rainbow trout intestinein vitro in the presence and absence of putative modulatory agents. Modulation of neurally-mediated contractions of trout intestine was achieved with dibutyryl cyclic AMP and forskolin, agents that increase intracellular levels of cyclic AMP. The effect appears to be at the level of the smooth muscle, since the adenylate cyclase activator, forskolin, inhibited muscarinic and serotoninergic contractions as well as transmurally stimulated contractions. Substance P-induced contractions were unaffected by forskolin. The endogenous agonists/neurotransmitters which would increase cyclic AMP levels in rainbow trout intestinal smooth muscle are as yet unknown. The effects do not appear to be modulated by vasoactive intestinal peptide (VIP), calcitonin, calcitonin gene-related peptide (CGRP), or agents that activate β-adrenoceptors. Prostaglandin E2 (PGE2) and α2-adrenergenic agonists are possible agents which will decrease contractility of the smooth muscle. They were only active in the proximal intestine and on transmurally stimulated contractions. The effects of both PGE2 and α2-agonists appear to be prejunctional, decreasing release of contractile neurotransmitters in the enteric nervous system.