Suppressive effect of acetylcholine on automaticity of cannine atrioventricular node

The effects of acetylcholine on the spontaneous activity of the AV node of dog hearts were studied by recording transmembrane potentials of its fibers. Action potentials of most nodal fibers were characterized by prominent phase 4 depolarization and a smooth transition from phases 4 to 0. On the isolated AV nodes, acetylcholine at 1.0 μg/m1 suppressed the rate of phase 4 depolarization and increased the amplitude of the maximum diastolic potential, resulting in a slowing of spontaneous activity. At 2.0 μg/m1, spontaneous activity was completely suppressed. In comparison, spontaneous activity of the isolated His bundle was relatively insensitive to the suppressive effect of acetylcholine at the same concentrations. In the AV node-His bundle preparations in which the AV node was the pacemaker, acetylcholine decreased spontaneous activity by suppressing the phase 4 depolarization of the nodal fibers and shifted the pacemaker of the preparation to the His bundle. The findings provide a basis for predicting that under strong vagal influence, the automaticity of the AV node will be suppressed and the pacemaker of the junctional rhythm will be located at the His bundle.     

Arterial pulse waves and velocity and systolic time intervals in diabetic children

Arterial pulse wave velocities, pulse wave contours, and systolic time intervals were recorded in thirty-nine diabetic children and were compared with recordings taken in twenty-seven normal children. Systolic time intervals were similar in the two groups of subjects. However, brachial and aortic pulse wave velocities were significantly greater in the diabetic than in the normal children (p < 0.025 and < 0.005, respectively). Also, in the diabetic children the time interval from the incisura to the midpoint of the dicrotic wave (I-D) was significantly shortened in both the brachial (p < 0.005) and carotid (p < 0.05) pulse waves as compared to the normal children. These changes in pulse wave velocity and contour are associated with increased wall stiffness that occurs with aging and suggest that the large arteries of diabetic children may exhibit acceleration of the aging process. The severity of these changes bore no direct correlation with the degree of carbohydrate intolerance as judged by insulin requirement.     

Plasma beta-thromboglobulin as a measure of platelet activity: Effect of risk factors and findings in ischemic heart disease and after acute myocardial infarction

The plasma concentration of beta-thromboglobulin (BTG), a platelet-specific protein released during platelet aggregation, is considered a sensitive marker of in vivo platelet activity. The mean plasma level in 133 asymptomatic individuals was 32.3 ± 1.1 ng/ml, and there was no difference between those with no risk factors (32.2 ± 1.2 ng/ml, n = 56), those who smoked (31.8 ± 1.8 ng/ml, n = 45), those with hyperlipidemia (32.8 ± 1.7 ng/ml, n = 15), and those exposed to both of these risk factors (34.1 ± 2.7 ng/ml, n = 17). The mean plasma BTG level in 104 patients with symptomatic ischemic heart disease was significantly elevated (40.9 ± 1.4 ng/ml, p < 0.01), but there was considerable overlap with normal levels. Although no difference was found between patients with no risk factors (38.1 ± 4.0 ng/ml, n = 13) and those with only 1 risk factor (37.0 ± 1.8 ng/ml, n = 44), patients with 2 or more risk factors had a significantly elevated plasma BTG level (45.2 ± 2.2 ng/ml, n = 47, p < 0.01). It is concluded that risk factors themselves do not increase platelet activity, but that patients with vascular disease have activated platelets that may contribute to the progression of the disease. Plasma BTG was also measured serially for 10 days in 29 patients after hospitalization with acute ischemic cardiac pain. Although the median plasma level was elevated above normal there were no acute changes in plasma BTG after either acute infarction (n = 22) or acute ischemia (n = 7), except in 2 patients in whom pericardial friction rubs developed. Thus, measurement of systemic plasma BTG did not detect platelet involvement in acute coronary occlusion or acute ischemia.     

Neutropenia as a Complication of Tumefactive Demyelinating Disease: A Case Report

Tumefactive demyelination is an aggressive, localized, generally solitary area of demyelination that often mimics a neoplasm. We present a case of a 13-year-old female patient who presented with sudden-onset progressive hemiplegia and hemianopsia. Magnetic resonance imaging of the brain showed tumefactive demyelination with partial rim of enhancement. During inpatient rehabilitation, she developed myalgias, rash, and abdominal and mouth pain with evidence for severe neutropenia. The neutropenia was determined to be a secondary complication of the tumefactive disease process. This scenario may be concerning in an inpatient rehabilitation setting, as patients share common areas, increasing the risk of acquired infection while neutropenic.

Xiangbinfang granules enhance gastric antrum motility via intramuscular interstitial cells of Cajal in mice

BACKGROUND Interdigestive migrating motor complexes(MMC)produce periodic contractions in the gastrointestinal tract,but the exact mechanism of action still remains unclear.Intramuscular interstitial cells of Cajal(ICC-IM)participate in gastrointestinal hormone and neuromodulation,but the correlation between ICCIM and MMC is also unclear.We found that xiangbinfang granules(XBF)mediated the phase III contraction of MMC.Here,the effects of XBF on gastric antrum motility in W/Wv mice and the effects of ICC-IM on gastric antrum MMC are reported.AIM To observe the effects of ICC-IM on gastric antrum motility and to establish the mechanism of XBF in promoting gastric antrum motility.METHODS The density of c-kit-positive ICC myenteric plexus(ICC-MP)and ICC-IM in the antral muscularis of W/Wv and wild-type(WT)mice was examined by confocal microscopy.The effects of XBF on gastric antrum slow waves in W/Wv and WT mice were recorded by intracellular amplification recording.Micro-strain-gauge force transducers were implanted into the gastric antrum to monitor the MMC and the effect of XBF on gastric antrum motility in conscious W/Wv and WT mice.RESULTS In the gastric antrum of W/Wv mice,c-kit immunoreactivity was significantly reduced,and no ICC-IM network was observed.Spontaneous rhythmic slow waves also appeared in the antrum of W/Wv mice,but the amplitude of the antrum slow wave decreased significantly in W/Wv mice(22.62±2.23 mV vs 2.92±0.52 mV,P<0.0001).MMCs were found in 7 of the 8 WT mice but no complete MMC cycle was found in W/Wv mice.The contractile frequency and amplitude index of the gastric antrum were significantly increased in conscious WT compared to W/Wv mice(frequency,3.53±0.18 cpm vs 1.28±0.12 cpm;amplitude index,23014.26±1798.65 mV·20 min vs 3782.16±407.13 mV·20 min;P<0.0001).XBF depolarized smooth muscle cells of the gastric antrum in WT and W/Wv mice in a dose-dependent manner.Similarly,the gastric antrum motility in WT mice was significantly increased after treatment with XBF 5 mg(P<0.05).Atropine(0.1 mg/kg)blocked the enhancement of XBF in WT and W/Wv mice completely,while tetrodotoxin(0.05 mg/kg)partially inhibited the enhancement by XBF.CONCLUSION ICC-IM participates in the regulation of gastric antrum MMC in mice.XBF induces MMC III-like contractions that enhance gastric antrum motility via ICCIM in mice.     

Variable susceptibility to dynamic coronary obstruction: An elusive link between coronary atherosclerosis and angina pectoris

Growing evidence suggests that dynamic coronary obstructions play an important but elusive role in the genesis of ischemic events. Dynamic coronary obstructions can develop during certain phases of coronary disease as a result of a variable combination of vasoconstriction, arterial wall lesions, and increased thrombotic tendency. In a certain phase of their disease some patients develop dynamic coronary obstruction, while others with a similar degree of fixed atherosclerotic obstruction do not.     

Glucose and alanine metabolism during bacterial infections in rats and rhesus monkeys

To investigate the effects of bacterial infection on glucose and alanine metabolism, a variety of studies were carried out in rat and monkey models. These included glucose turnover by a pulse-dose technique in infected rats; alanine and glucose production and utilization in control and septic monkeys; in vivo measurement of gluconeogenesis in rats, with and without an alanine load; the in vitro rate of glucose formation from various substrates by isolated liver perfusion and hepatic cells; and in vivo rates of oxidation of glucose labeled with ¹⁴C at the 1 or 6 carbon position. In rats, glucose turnover was markedly accelerated 24 hr after inoculation of either 10⁴ or 10⁷Streptococcus pneumoniae. Glucose utilization and production were also accelerated during illness and early recovery from a pneumococcal infection in monkeys. The rates of gluconeogenesis as measured by either a pulse technique in rats or continuous infusion of labeled alanine in monkey were significantly elevated during pneumococcal septicemia. During the agonal stages (10⁷) of the pneumococcal infection in rat, an alanine load resulted in a decreased rate of labeled glucose production and an increase in plasma glucose when compared to values of fasted control rats. However, early illness caused similar or increased rates of glucose production from alanine in vivo. Similar reduced rates of glucose formation were observed when the isolated livers or hepatocytes from rats during the agonal stages of infection were perfused with excess quantities of gluconeogenic substrates. Thus, in the rat, gluconeogenic capacity (ability to form glucose from excess substrates) appears to decrease only during the agonal stages of pneumococcal infection. During acute pneumococcal sepsis in the rhesus monkey, alanine production and utilization were significantly elevated and it was estimated that over 90% of the newly produced alanine was utilized for glucose synthesis. When arterial-venous differences were measured across the hindquarters, significantly more alanine was released, presumably from skeletal muscle of the septic monkey, compared to the recovery period or in the control groups. Thus, the increase in glucose synthesis in both rat and monkey appears to be correlated with substrate availability and kinetic rate, rather than gluconeogenic capacity of the liver. The major increase in glucose utilization during both S. pneumoniae and Francisella tularensis live vaccine strain (LVS) infections in rat was a progressive elevation in the rate of oxidation via the pentose phosphate shunt in the rat. Further, the rate of oxidation appeared to be correlated with the magnitude of the bacteremia, which is an indication of the severity of the infection. Therefore, since glucose oxidation is necessary for a number of metabolic processes of various cells (such as phagocytosis and RNA synthesis), the increased glucose production during pneumococcal sepsis in the rat or rhesus monkey may not represent functional wastage to remove the excess alanine produced in skeletal muscle but a necessary process in the host defense mechanism against infectious disease.