Contractile tissues development

The force generated by a muscle is proportional to the contraction time. The longer the contraction time, the greater the force development up to the point of maximum tension. Slower contraction leads to greater force production because more time is allowed for the tension produced in contractile elements to be transferred through the noncontractile components to the tendon. This is the force-time relationship. Tension in the tendon will reach the maximum tension developed by the contractile tissues only if the active contraction process is of adequate (even up to 300 msec) duration [Sukop and Nelson, 1974). 

The individual modules of the in situ heart can be coupled together to compute a whole sequence from ventricular pressure development, coronary perfusion, tissue supply of metabolites, cell energy consumption, and electrophysiology, to contractile activity and ventricular pressure development in the subsequent beat. The starting point (here chosen as ventricular pressure development) can be freely selected, and drug effects on the system can be simulated. Inserted into a virtual torso, these models allow one to compute the spread of excitation, its cellular basis, and the consequences for an ECG under normal and pathological conditions. 

Histamine receptors have been classified into two major subtypes, H, and H2, on the basis of quantitative studies on isolated peripheral tissues. Histamine H,-receptors mediate the contractile actions of histamine on numerous visceral smooth muscles, most notably from the trachea, ileum and uterus of the guinea-pig [36-39]. These responses are antagonized by the classical -antihistamines [36-39] such as mepyramine (1) [36] and diphenhydramine (3) [40] (see Figure 2.1). Histamine also stimulates the secretion of acid by stomach, increases the rate of contraction of guinea-pig isolated atria and inhibits electrically evoked contractions of rat isolated uterine horn [41 ]. However, these responses are not affected by H, -receptor antagonists and have been defined as histamine H2-receptor responses following the development of specific antagonists to these responses such as burimamide [41], cimetidine [42] and ranitidine [43]. The distribution and classification of histamine H,-and H2-receptors in various mammalian peripheral tissues have been reviewed elsewhere [44-46a]. 

CARDIAC EFFECTS Epi is a powerful cardiac stimulant. Direct responses to Epi include increase in the rate of tension development, peak contractile force, and rate of relaxation decreased time to peak tension increased excitability, acceleration of the rate of spontaneous beating, and induction of automaticity in speciahzed regions of the heart. Epi acts directly on the predominant /3 receptors of the myocytes and of the cells of the pacemaker and conducting tissues. The heart rate increases, and the rhythm often is altered. Cardiac systole is shorter and more powerful, cardiac output is enhanced, and the work of the heart and its Oj consumption are markedly increased. Cardiac efficiency (work done relative to Oj consumption) is lessened. 

Because of the qualitative similarities of the mechanical properties in smooth and striated muscles, much research over the past several decades has focused on determining whether the functional behavior of these muscles can be explained on the basis of simUar mechanisms. However, the unique structural features of smooth muscle are likely to underly some aspects of its contractile properties which differ significantly from those of striated muscles. In addition, smooth muscle tissues possess a number of distinctive functional properties that are not easily accounted for on the basis of models developed to account for the properties of striated muscles. 

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