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C T Frantzides

Publications and source records attributed to C T Frantzides.

46 records · Page 3Linked to original sources

Morphine effects on human colonic myoelectric activity in the postoperative period.

Colonic myoelectrical activity was studied in 25 patients, 18 of whom received morphine sulfate, using bipolar electrodes placed in the ascending and descending colon during laparotomy. Baseline myoelectrical activity was recorded daily, then morphine (3 to 15 mg) was administered intravenously, intramuscularly, or epidurally, and recordings continued. Seven activity patterns were observed during recovery from postoperative ileus. During the first 2 postoperative days, morphine at any dose did not affect colon myoelectrical activity. From the third postoperative day on, morphine given intravenously or intramuscularly initiated clusters of short, nonmigrating, phasic spike bursts occurring on each successive slow wave in 14 of 18 patients, which lasted for 30 to 45 minutes. When morphine was administered epidurally, there was no colonic response in any patient. These findings suggest that: (1) morphine intravenously or intramuscularly induces predominantly nonmigrating colonic spike bursts; (2) morphine-induced activity alters the normal pattern of colonic motility during recovery from postoperative ileus; and (3) these phenomena are not due to direct action of morphine on the spinal cord since epidural morphine had no effect.

Colon↗

Prostaglandins and modulation of small bowel myoelectric activity.

We explored the effects of prostaglandins (PG) F2 alpha and E2 on the motor and myoelectric activity of the small intestine using closed intra-arterial injections in conscious chronically instrumented dogs. PGF2 alpha (0.125-5 micrograms) and PGE2 (1-10 micrograms) were injected via a T tube into a branch of the superior mesenteric artery perfusing a 15-cm segment of jejunum. Experiments were performed on four dogs in which the recording devices had been implanted above, below, and within the perfused segment. PGF2 alpha given during phase I of the migrating myoelectric complex cycle induced phasic contractions in the perfused segment of intestine in a dose-dependent manner. Atropine (50-100 micrograms), hexamethonium (15 mg), or TTX (10-15 micrograms) administered before the injection of PGF2 alpha failed to inhibit the effects of PGF2 alpha. In contrast pretreatment of the perfused segment with verapamil (2.5 mg) or PGE2 (1-5 micrograms) abolished the effects of PGF2 alpha. Moreover, PGE2 injected 5 min after the administration of PGF2 alpha inhibited the PGF2 alpha-induced contractions. Administration of PGE2 alone (3-10 micrograms) before the arrival of phase III activity in the perfused segment abolished phase III from this segment of intestine. Our studies indicate opposing effects of PGF2 alpha and PGE2 on small intestinal myoelectric and contractile activities. PGF2 alpha has a direct excitatory effect on the intestinal smooth muscle, which is calcium channel dependent but independent of intrinsic nerves. PGE2 has an inhibitory effect both on the spontaneous and PGF2 alpha-induced small intestinal myoelectric and contractile activity.

Animals↗

Laparoscopic highly selective vagotomy: technique and case report.

As the advantages of minimally invasive surgical techniques become more apparent, new applications are being identified. Here we describe the technique and our initial experience with laparoscopic highly selective vagotomy. The ability to perform this effective antiulcer operation laparoscopically with minimal resultant pain, reduced hospital time, less cost, and diminished morbidity may make surgical therapy a more attractive option in the management of peptic ulcer disease.

Duodenal Ulcer↗

Effects of morphine on colonic myoelectric and motor activity in subhuman primates.

We investigated the effects of numerous doses of morphine on colonic myoelectric and motor activity in monkeys. In each of four monkeys (Macaca arctoides), combined strain gauge transducers and bipolar electrodes were chronically implanted at four defined sites in the colon and recordings were made for 3 h in fasted, unanesthetized animals before and after intravenous administration of morphine sulfate (10-1,000 micrograms/kg). The basal fasting pattern of colonic motility was characterized by random contractions, nonmigrating clusters of contractions, and migrating individual contractions. Morphine at very low doses (10-25 micrograms/kg) had no effect on colonic motility at any site. At doses of 50-200 micrograms/kg, clusters and migrating contractions were eliminated, but there was an overall increase in the frequency of random contractions without an alteration in contraction amplitude or duration. At morphine doses of 500 and 1,000 micrograms/kg, contraction clusters and migrating contractions also were not seen, but there was a decrease in the colonic motility index caused entirely by a decreased frequency of random contractions. Both stimulation and inhibition were most marked in the sigmoid colon. Morphine has a dose-dependent biphasic effect on colonic myoelectric and contractile activity and alters colonic motility patterns by inhibiting migrating contractions and clusters of contractions.

Animals↗

Chemical degeneration of intestinal nerves.

In 15 dogs, cobalt chloride solutions were infused close intra-arterially to perfuse a short segment of the jejunum. In an additional four dogs, the jejunum was perfused with the aqueous vehicle (perfusion control). All animals were killed after 1 mo and tissue samples from cobalt-treated and from nonperfused intestine (tissue comparison control) were obtained for electron microscopic and immunohistochemical studies. Segments infused with 0.25 g/dl cobalt solution showed minimal changes; the most striking feature was an increase of vasoactive intestinal polypeptide (VIP)- and substance P-containing neurosecretory granules. Cobalt chloride at higher concentrations (0.75-1.5 g/dl) induced degeneration of ganglion cells and axons in both the myenteric and submucosal plexi. In contrast, the smooth muscle and the mucosal cells of the cobalt-perfused intestine showed no histological abnormalities. Immunohistochemical staining of tissues treated with 0.75-1.5 g/dl cobalt solutions revealed absence of substance P, Met-enkephalin, and VIP immunoreactivity in all section studied; control segments showed the presence of all three peptides. Cobalt chloride in concentrations of 0.75-1.5 g/dl causes degeneration of intestinal intramural nerves and provides an experimental model suitable for studying the role of these nerves in small intestinal function.

Animals↗

Effects of enteric neural defunctioning on small bowel motility.

In this study, we investigated the role of intrinsic nerves of the small intestine on phase III migration of the migrating myoelectric complex. Fasting myoelectric activity was recorded from the small bowel in chronically instrumented dogs. Once control experiments were completed, the animals were divided into two groups and were reoperated. In the first group of five dogs, a 1.5-g/dl aqueous solution of cobaltous chloride (shown to induce degeneration of intestinal intrinsic nerves) was infused close intra-arterially to perfuse a 15-cm segment of jejunum. In the second group of dogs, a catheter was implanted in a branch of the superior mesenteric artery supplying a 15-cm segment of intestine. Tetrodotoxin (0.3-1 micrograms/kg) was infused through the catheter just before the arrival of phase III activity in the perfused segment. Subsequent to the fifth postcobalt perfusion day, phase III traversed but did not occur in the cobalt-treated segment. When tetrodotoxin was injected through the catheter, spontaneous phasic myoelectric and contractile activities in the perfused jejunal segment were inhibited, but phase III migration was not blocked. These findings suggest 1) acute or chronic defunctioning of enteric nerves does not interrupt phase III migration, but 2) phase III expression is dependent on the integrity of intrinsic nerves.

Animals↗

An intrinsic neural pathway for long intestino-intestinal inhibitory reflexes.

We studied the mechanisms of initiation and pathways for the propagation of intestino-intestinal inhibitory reflexes induced by close intraarterial injections of neostigmine in conscious dogs. Two or three T-shaped catheters were surgically implanted in the intestinal branches of the superior mesenteric artery to inject pharmacologic agents locally in 10-15-cm-long segments. Migrating myoelectric complexes were recorded by a set of 10 electrodes and strain-gauge transducers. Close intraarterial injection of neostigmine initiated strong contractions of long duration in the perfused segment that terminated phase III activity in progress 90-150 cm distal or proximal to the cannulated sites and stopped its further migration. Atropine or 4-diphenylmethoxy-N-methylpiperidine methiodide injected just before neostigmine administration through the same catheter blocked both the local contractile effects and the reflex inhibition of phase III activity. Pirenzepine or hexamethonium injected in a similar manner did not affect the local response to neostigmine but blocked the reflex inhibition of phase III activity. A transection and reanastomosis in the mid-small intestine blocked the reflex inhibition by close intraarterial injection of neostigmine beyond the transection site. Pirenzepine, atropine, or hexamethonium injected through a middle catheter also blocked the reflex inhibition of phase III activity beyond the site perfused with these cholinergic antagonists. Close intraarterial administration of 4-diphenylmethoxy-N-methylpiperidine methiodide at a middle site had no effect on reflex inhibition. We concluded that strong spasmodic contractions in the small intestine initiate an intestino-intestinal inhibitory reflex in both directions. This reflex is mediated through an intrinsic neural pathway involving nicotinic and M1 muscarinic receptors.

Animals↗

Radionuclide visualization of acute occlusive and nonocclusive intestinal ischemia.

A noninvasive radionuclide technique to visualize ischemic small intestine was evaluated. Vascular ligation of 20-30 cm ileum was done in rabbits. After induction of ischemia, technetium (99mTc) methylene diphosphonate (TMDP) was injected IV at intervals up to 24 hours. Images were recorded 1 and 3 hours after injection of radioisotope and showed preferential (9:1) uptake by ischemic bowel. Positive scans were present in all animals up to 4 hours and in 75% at 10-12 hours, but in none 24 hours after induction of ischemia. Nonocclusive intestinal ischemia was simulated in 4 dogs by infusing norepinephrine into a jejunal mesenteric arterial branch. After 1 hour, an IV bolus of TMDP was injected and images recorded at intervals up to 3 hours. Selective uptake of isotope by the ischemic segment was observed in all animals. Angiography confirmed that isotope uptake was confined to the infused segment. These studies show that occlusive intestinal ischemia can be detected, by radionuclide imaging up to 12 hours, and nonocclusive (low flow) ischemia for at least 4 hours, after onset.

Acute Disease↗

Resolution of postoperative ileus in humans.

Bipolar electrodes were placed in the ascending and descending colon of 13 patients during laparotomy. The magnitude of their operations varied from exploratory laparotomy to total gastrectomy. The magnitude and length of the operations performed did not correlate positively with the duration of postoperative ileus. Signals were recorded for up to 4 hours daily for up to 8 days after operation during periods of rest and, in some patients, after administration of epidural or parenteral morphine sulfate. Power spectrum analyses of electrical control activity (ECA) showed dominant frequencies in both lower (2-9 cpm) and higher (9-14 cpm) ranges. During postoperative recovery, the mean ECA frequencies in right and left colon were relatively constant, but a variety of dominant ECA frequency relationships were observed. The modal pattern in the right colon was a shift in the dominant frequency from the higher to the lower range as recovery progressed, while the modal pattern in the left colon was persistent dominance of ECA in the higher frequency range. Electrical response activity (ERA) initially was comprised of only random, disorganized single bursts but became progressively more complex through the initial 3 postoperative days with the appearance of more organized bursts and clusters, some of which propagated very slowly (about 5 cm/min) both orad and aborad. ERA recovery culminated, typically on the third or fourth postoperative day, with the return of long bursts of continuous ERA, some of which propagated at a higher velocity (about 80 cm/min) and exclusively in the aborad direction and which were accompanied by passage of flatus or by defecation.

Adolescent↗

Streptococcus milleri group (Streptococcus anginosus): recovery from intra-abdominal and soft tissue sites.

One hundred thirty-three Streptococcus milleri group (S. anginosus) isolates were recovered from 487 surgical patients. The streptococci were recovered from 33 percent of intra-abdominal infection cultures (84/257). 22 percent of samples from penetrating visceral trauma (19/86), 52 percent of perirectal abscess specimens (13/25), 13 percent of nonpuerperal breast abscess cultures (8/60), and 15 percent of diabetic foot lesions (9/59). Ninety-eight percent of the S. milleri (131/133) were recovered as companion flora in polymicrobial cultures. The organisms were highly susceptible to the beta-lactam antibiotics. The precise pathogenic role of the S. milleri group (S. anginosus) is unknown. However, intrinsic virulence may be expressed in patients with severe infection or other predisposing factors.

Abdomen↗