ABSTRACTS 231

on the time constant of relaxation (7) during repeated contractions and with recovery. Two stimulation protocols were used: a high-tension time index (TTI, 60 Hz, 160 ms, 2/s) and a low TTI (25 Hz, 160 ms, l/s). In the high TTI protocol an early increase in the r was noted in theophylline but not in caffeine or control. In the low TTI protocol there was no difference in r with theophylline. The combination of theophylline (100 mg/l) and verapamil (5 PM) was also studied. Verapamil decreased force in contractions of 300-ms duration but not in those lasting 160 ms and had no effect on 7. It did not block the prolongation of 7 seen with theophyl- line. These studies suggest that theophylline has a direct effect on relaxation of skeletal muscle, which is not prevented by verapamil, and also that external calcium may be impor- tant for sustained contractions of skeletal muscle. (Reprinted with permission.)

Comparison of Diaphragmatic Fatigue in Newborn and

Older Rabbits. SouZf PN, England SJ, Stogryn HAF, et al. J Appl Physiol65:1040, 1988.

The ability to maintain occlusion pressure (i.e., fatigabili- ty) during activation of the diaphragm via phrenic nerve stimulation was compared in newborn (~14 days old) and older (>30 days old) rabbits. The younger animals had lower maximum inspiratory pressures (MIP) and markedly greater falls in pressure during sustained diaphragmatic contractions at >40% MIP than did the older animals. Histological analysis showed a paucity of high-oxidative type I fibers in the diaphragms of the young animals. We therefore conclude that the newborn rabbit diaphragm is extremely susceptible to fatigue and that this susceptibility correlates with the distribution of muscle fiber types. (Reprinted with permis- sion.)

NMR Study of Rat Diaphragm Exposed to Metabolic and Compensated Metabolic Acidosis. Fitzgerald RS, Howell S, Pike MM, et al. J Appl Physiol65:2218, 1988.

When exposed to hypercapnia, several muscles deteriorate with respect to their mechanical performance. Exposure to metabolic acidosis and, perhaps surprisingly, to compensated metabolic acidosis has the same effect on the diaphragm. The mechanisms involved in these effects remain unclear. If the diaphragmatic intracellular pH (pHi) is assumed to decrease with hypercapnia, to remain unchanged during metabolic acidosis, and to increase during compensated metabolic aci- dosis, it would appear that different mechanisms must be responsible for the depreciation in the diaphragm’s mechani- cal performance. The present experiments using “P nuclear magnetic resonance (“P-NMR) spectroscopy were under- taken to determine the effect of metabolic acidosis and compensated metabolic acidosis on pHi and on high-energy phosphate metabolites in the resting rat diaphragm. A whole diaphragm was slightly stretched while being stitched onto a fiberglass mesh. The area approximated that at functional residual capacity. It was superfused in the NMR sample tube with a phosphate-free Krebs-Ringer bicarbonate solution ([HCO;] = 6 me@) equilibrated with either 95% 02-5% CO, or 98.75% O,-1.25% CO*). Spectra were acquired during 15min intervals for control (30 min of normal Krebs- Ringer bicarbonate superfusate, equilibrated with 95% 02- 5% CO*), for 120 min of exposure to either form of acidosis

and for 60 min of recovery with normal superfusate. The pHi decreased rapidly during metabolic acidosis but did not change significantly during compensated metabolic acidosis. In both forms of acidosis, phosphocreatine declined gradually but not significantly, whereas ATP and inorganic phosphate did not change at all. The results suggest that HCO; passes freely through the diaphragmatic sarcolemma, very much like the cardiac sarcolemma. Overall, it seems unlikely that the previously observed decrease in mechanical force during acidosis is due to any loss of high-energy phosphate stores. (Reprinted with permission.)

“‘P-NMR Study of Resting in Vitro Rat Diaphragm Exposed to Hypercapnia. Fitzgerald RS, Howell S, Jacobus WE. J Appl Physiol65:2270, 1988.

We have reported previously that, when exposed to hyper- capnia of various intensities, the diaphragm reduces its force of twitch and tetanic contractions in the in vitro rat prepara- tion as well as in the in vivo dog preparation. The experiments reported here with “P nuclear magnetic resonance (3’P- NMR) spectroscopy attempt to examine cellular mecha- nisms that might be responsible for this deterioration in mechanical performance. Specifically they describe certain characteristics of this preparation and cautions needed to study the resting in vitro rat diaphragm with such techniques. Second, they report the response of intracellular pH (pHi), phosphocreatine (PCr), ATP, and inorganic phosphate (Pi) in the resting in vitro rat diaphragm exposed to long-term normocapnia or to long-term hypercapnia. The results show that I) to maintain a viable preparation, it was necessary to keep the diaphragm extended to an area approximating that at functional residual capacity, 2) the diaphragm seemed quite capable of maintaining a constant pH, and constant contents of ATP and Pi during normocapnia, but there was a gradual decline in PCr, and 3) during hypercapnia there was a significant decrease in pHi, but the behavior of the phos- phate metabolites was exactly as during normacapnia. The results suggest that the decrease in mechanical performance of the diaphragm is probably not due to a decrease in the availability of the high-energy phosphates, although they do not completely exclude this possibility or possibilities related to regional compartmentation. (Reprinted with permission.)

Muscle Perfusion and Oxygenation During Local Hyperoxia. Bredle DL, Bradley WE, Chapler CK, et al. J Appl Physiol 65:2057, 1988.

Ventilation with O2 was previously shown to decrease whole-body and hindlimb muscle 0, uptake (~oJ in anesthe- tized dogs, particularly during anemia. To determine whether this was a purely local effect of hyperoxia (HiOx), we pump perfused isolated dog hindlimb muscles with autolo- gous blood made hyperoxic (PO* > 500 Torr) in a membrane oxygenator while the animals were ventilated with room air. Both constant-flow and constant-pressure protocols were used, and half the dogs were made anemic by exchange transfusion of dextran to hematocrit (Hct) -15%. Thus there were four groups of n = 6 dogs each. A 30-min period of HiOx was preceded and followed by similar periods of perfusion with normoxic blood. In HiOx all four groups showed increased leg hindrance, increased leg venous PO*, and no significant changes in leg O2 inflow. Limb blood flow