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C R Honig

Publications and source records attributed to C R Honig.

12 recordsLinked to original sources
PubMed1979

Contributions of nerves and metabolites to exercise vasodilation: a unifying hypothesis.

Neuronal cell bodies exist in arterioles of skeletal muscle and appear to initiate vasodilation during phasic contraction. The following findings indicate that intrinsic nerves rather than metabolites maintain vasodilation during sustained phasic contraction with free flow. 1) Under certain conditions maximal vasodilation can occur without detectable release of metabolites. 2) When metabolites are released during exercise, their concentrations in blood or tissue do not always determine the extent of vasodilation. 3) Vasodilation during sustained contraction can be partly blocked by local anesthetics. The extent of block is inversely proportional to the concentration of metabolites. Dose, time course of block, and other tests of specificity indicate that local anesthetics act on the intrinsic nerves rather than smooth or striated muscle. When contraction stops, neurogenic vasodilation decays rapidly (half time less than 1 min). Sustained vasodilation during recovery is therefore fully accounted for by metabolites. A hypothesis is suggested that integrates the roles of extrinsic nerves, intrinsic nerves, and metabolites in support of muscle contraction.

Action Potentials↗
PubMed1978

Frequency analysis of coronary intercapillary distances: site of capillary control.

Frequency distributions for minimum intercapillary distance (ICD) and functional ICD were characterized for rat heart in situ. Minimum ICD denotes spacings between adjacent capillaries whether they contain erythrocytes or not. Functional ICD is defined as spacings between contiguous capillaries perfused with erythrocytes. Minimum ICD was well fitted by both the gamma and the lognormal distributions. Functional ICD was well fitted by the lognormal, but not by the gamma, or by any mixture of the gamma with another discrete distribution. The frequency analysis is interpreted to mean that: 1) A control site distal to the true arteriole exists. This is presumably the precapillary sphincter. 21 Intercapillary anastomoses help keep the diffusion path in myocardium short and comparatively uniform. 3) Complete closure of arterioles does not occur in the unstressed heart. 4) Blood flow and conditions for diffusion can be controlled independently.

Animals↗
PubMed1977

Capillary lengths, anastomoses, and estimated capillary transit times in skeletal muscle.

Total capillary length, capillary segment length, and number of anastomoses per capillary were measured in rat gracilis muscle at rest and after 2 min of phasic contraction. Mean values of the foregoing variables at rest (+/-SD) were, respectively, 1,012 micronm +/- 484, 409 micron +/- 274, and 0.83 +/- 1.09. Total capillary lengths are well described by the gamma distribution, number of anastomoses by the negative binomial distribution, and segment length by the Weibull distribution. Contraction has no significant effect on the means or the frequency distributions, indicating that: 1) pressure gradients between adjacent capillaries are small, and 2) intercapillary anastomoses do not improve flow distribution in exercise. Erythrocyte velocities observed in resting muscle (Burton, K. S., and P. C. Johnson. Am J. Physiol. 223: 517-524, 1972) were shown to be adequately characterized by the gamma distribution. From these velocities and the observed distribution of path lengths, we computed an estimated distribution of capillary transit times. Mean transit time was 4.29 s. The median was 2.45 s, and 11% of values exceeded 8 s. The range was 90 ms-43 s. This heterogeneity of transit times should profoundly affect calculations of O2 transport and the shape of indicator dilution curves.

Animals↗
PubMed1977

Intercapillary distance and capillary reserve in hypertrophied rat hearts beating in situ.

Functional intercapillary distance (ICD) was measured in stop-motion photomicrographs of hypertrophied, normally compensated, well oxygenated rat hearts beating in situ. Left ventricular hypertrophy was produced by salt loading and unilateral nephrectomy. Minimum ICD (when all capillaries are open) also was measured. Ventricular weight increased by 30-40% within 8-9 weeks after nephrectomy. To compare the effect of normal and pathological growth, ICD was also measured in normal rats. In normal animals, minimum ICD and functional ICD increased linearly and proportionately with left ventricular weight. Consequently, the extent to which capillary recruitment could decrease ICD was the same in large and small normal hearts (about 2 micrometer). In the hypertrophied hearts, capillary recruitment could have maintained ICD within normal limits at rest for several weeks. After 8-9 weeks, however, the capillary reserve in hypertrophy was fully utilized at rest, and mean functional ICD was 1.5-2.0 micrometer greater than normal for the age of the animal. An analysis of O2 transport indicates that anoxic foci would exist throughout the hypertrophied heart and particularly in subendocardium when the capillary reserve is exhausted. The calculated amount of anoxic tissue appears sufficient to account for the focal necrosis and fibrosis observed in hypertrophy and for the development of circulatory failure.

Animals↗
PubMed1976

Effect of Ca++ on Vmax measured in absence of external or internal load.

Myofibrils 1 sarcomere wide (single myofibrils) were prepared from rat heart. Mean initial sarcomere length was 2.68 mu. Contraction was initiated with 20, 25 or 100 muM MgATP and terminated with EGTA and EDTA. Single fibrils shortened at the theoretical Vmax for the in vitro conditions until sarcomere length reached 2.05 mu. At this length they encountered a significant internal afterload. Reaction time, substrate, and temperature were adjusted so that final sarcomere length was greater than or equal to 2.05 mu in most experiments. Ca++ increased Vmax of single fibrils 2- 4-fold. Results were similar at 20 and 100 muM MgATP, and in reaction mixture containing 100 or 140 mM KCI. We conclude that Ca++ controls not only the number of cross-bridges, but also the rate at which the cross-bridges turn over.

Animals↗
PubMed1975

Ganglion cells in arterioles of skeletal muscle: role in sympathetic vasodilation.

Ganglion cells were found in arterioles of gracilis muscles of dogs 2 wk after complete extrinsic denervation. We tested the possibility that they function in active sympathetic vasodilation (SVD) induced in isolated gracilis muscles by hypothalamic stimulation. To this end various drugs were injected into the gracilis perfusate. (Drugs did not reach the systemic circulation, and exerted their effects within the gracilis itself). C6 had no effect. Submaximal doses of atropine or l-hyoscyamine delayed and slowed SVD; higher doses blocked completely. d-Hyoscyamine did not change SVD or acetylcholine vasodilation, but when administered prior to l-hyoscyamine, threshold for blockade of SVD by the l-isomer increased 10,000-fold. Blockade by l-hyoscyamine of acetylcholine vasodilation was unaltered by d-hyoscyamine. Eserine partly blocked SVD, but enhanced and prolonged acetylcholine vasodilation. The foregoing and certain features of the time course of SVD are interpreted to mean that: a) atropine blocks SVD at muscarinic sites on peripheral ganglion cells; b) transmission at the ganglion cells depends on slow excitatory postsynaptic potentials; c) the final mediator of SVD at the vascular muscle cell is unknown.

Acetylcholine↗
PubMed1975

Halothane decreases actomyosin ATPase activity: a possible mechanism of the negative inotropic effect.

Like all inhalation anesthetics, halothane (CF3CHBrCl) has a dose-dependent negative inotropic effect on cardiac muscle. The mechanism of the action has not been determined, although effects on glycolysis, mitochondrial respiration and calcium kinetics, and sarcoplasmic reticulum ATPase activity have been suggested. Previous studies of the effect of halothane on the ATPase of contractile protein suffered from design and dosing defects. We have measured ATP splitting by canine cardiac natural actomyosin using extraction and equilibration procedures described previously (Honig, C. R. and Reddy, Y. C. 1973, J. Pharmacol. 184: 330-338). Drug dosing calculations were facilitated by measurement of the partition coefficient of halothane in protein. Halothane shifted the Ca++ concentration effect curve for actomyosin ATPase activity to the right. The maximum depression occurred at pCa 7.0 or 6.5. The effect was dose dependent with less than 10 percent depression at threshold and 50-60 percent depression at peak. Enzyme inhibition was antagonized by high Ca++ concentration, and was reversed by removing halothane from the reaction mixture. We suggest that inhibition of ATP utilization by the contractile system may be a mechanism of the in vivo myocardial depression produced by halothane.

Actomyosin↗