RETRACTED ARTICLE: Dobutamine increases contractility of fatigued diaphragm in dogs: The relationship between dose and diaphragmatic contractility

The dose-related effects of dobutamine (DOB) on the contractility of fatigued diaphragm were studied in 16 anesthetized, mechanically ventilated dogs. The animals were divided into two groups of eight: the control (group C) and the DOB (group D). Diaphragmatic fatigue was induced by intermittent supramaximal electrophrenic stimulation at a frequency of 20 Hz applied for 30 min. Diaphragmatic contractility was assessed from changes in transdiaphragmatic pressure (P_di). After the induction of diaphragmatic fatigue, P_di at low-frequency (20-Hz) stimulation decreased significantly compared with the prefatigue values (P<0.05), whereas no change in P_di was observed at high-frequency (100-Hz) stimulation. In group D, after producing fatigue, P_di at 20-Hz stimulation increased significantly with a continuous infusion of DOB (5 and 10 μg·kg⁻¹·min⁻¹) i.v. (P<0.05). The P_di at 100-Hz stimulation increased significantly with administration of DOB 10 μg·kg⁻¹·min⁻¹ i.v. (P<0.05). There was a significant correlation between dose of DOB and P_di at both stimuli (P<0.05). In group C, the speed of P_di recovery at 20-Hz stimulation was relatively slower. The integrated diaphragmatic electric activity (E_di) in each group did not change at any frequency of stimulation throughout the study. It is concluded that DOB increases the contractility of fatigued diaphragm in a dose-dependent manner.     

RETRACTED ARTICLE: Amrinone improves contractility of fatigued diaphragm in dogs

The effects of amrinone, a bipyridine derivative, on diaphragmatic contractility and fatigue were examined in 36 anaesthetized, mechanically ventilated dogs divided into four groups. In Group Ia (n = 8), dogs without diaphragmatic fatigue were given a bolus injection (0.75 mg · kg^?1) followed by continuous infusion (10 μg · kg^?1 · min^?1) of amrinone iv. In Group Ib (n = 8), animals without fatigue received infusion only of maintenance fluid. In Group IIa (n = 10) and Group IIb (n = 10), diaphragmatic fatigue was induced by intermittent supramaximal bilateral electrophrenic stimulation at a frequency of 20 Hz applied for 30 min. After producing fatigue, amrinone (0.75 mg · kg^?1 loading dose plus 10 μg · kg^?1 · min^?1 maintenance dose) iv were administered in Group IIa. Only maintenance fluids were administered in Group IIb during this period. Diaphragmatic contractility was assessed in each group by measuring transdiaphragmatic pressure (Pdi). Compared with Group Ib, Pdi at any stimuli in Group Ia did not differ. After producing fatigue, in Group IIa and Group IIb, Pdi decreased at low-frequency (10–30 Hz) stimulation (P < 0.05), whereas no change in Pdi was observed at high-frequency (50–100 Hz) stimulation. In Group IIa, Pdi to each stimulus increased during amrinone infusion compared with Group IIb (P < 0.05). In Group IIb, the speed of recovery from fatigue was relatively slower at low-frequency stimulation. The integrated diaphragmatic electric activity (Edi) did not change throughout the experiment. These results indicate that amrinone improves contractility in the fatigued diaphragm.     

Comparative effects of xenon and nitrous oxide on diaphragmatic contractility in dogs

BACKGROUND: Xenon at two different concentrations (30%, 60%) has no effect on diaphragmatic contractility. This study was undertaken to compare the effects of xenon and nitrous oxide (N2O), a commonly used and well-established gas anesthetic, on diaphragmatic contractility in dogs. METHODS: Twenty-one pentobarbitone-anesthetized dogs were randomly divided into three groups of seven each: group 1 received xenon 30% (0.25 MAC) in oxygen; group 2 received N2O 47% (0.25 MAC) in oxygen; and group 3 received N2O 60% (0.32 MAC) in oxygen. Diaphragmatic contractility was assessed by transdiaphragmatic pressure (Pdi) at low- (20-Hz) and high-frequency (100-Hz) stimulation, after maintaining 60 min of stable condition. The integrated electrical activity of diaphragm (Edi) to each stimulus was measured. RESULTS: With an inhalation of xenon 30%, N2O 47%, or N2O 60%, Pdi and Edi at both stimuli did not change. No difference in Pdi or Edi was observed among the groups. CONCLUSION: When used at clinical concentration, xenon or N2O does not affect contractility and electrical activity of the diaphragm in dogs.     

RETRACTED ARTICLE: Nicardipine enhances diaphragmatic fatigue

The effects of nicardipine, a calcium channel blocker, on diaphragmatic fatigue were studied in 20 anaesthetized, mechanically ventilated dogs divided into two groups: control group (Group C, n = 10) and nicardipine group (Group N, n -10). Diaphragmatic fatigue was induced by intermittent supramaximal electric stimulation to bilateral phrenic nerves at a frequency of 20 Hz for 30 min. In Group N, 5 μg · kg^?1· min^?1 nicardipine iv was infused continuously during this fatigueproducing period. Transdiaphragmatic pressure (Pdi) produced by electrical stimulation (10–100 Hz) of the phrenic nerves was used as an index of diaphragmatic contractility. After a fatigueproducing period, the Pdi in both groups decreased at low frequency (10–30 Hz) stimulation compared with pre-fatigue values (P < 0.05), whereas no change in Pdi was observed at high-frequency (50–100 Hz) stimulation. The decrease of Pdi at low-frequency stimulation was larger in Group N (P < 0.05). The integrated diaphragmatic electric activity (Edi) in both groups did not change at any frequency of stimulation throughout the experiment. We conclude that nicardipine enhances diaphragmatic fatigue.     

RETRACTED ARTICLE: Dibutyryl cyclic AMP increases the contractility of fatigued diaphragm in dogs

The effects of dibutyryl cyclic AMP (DBcAMP) on the contractility of nonfatigued and fatigued diaphragms were studied in 36 anesthetized and mechanically ventilated dogs. The animals were divided into four groups. In group C₁ (n=8), dogs without fatigue received only Ringer's lactate solution. In group D₁ (n=8), dogs without fatigue were given a continuous infusion of DBcAMP 0.2 mg·kg⁻¹·min⁻¹. In groups C₂ and D₂ (n=10 each), diaphragmatic fatigue was induced by intermittent supramaximal bilateral electrophrenic stimulation at a frequency of 20 Hz applied for 30 min. In group D₂, after producing fatigue, DBcAMP 0.2 mg·kg⁻¹·min⁻¹ was administered. In groups C₂, only Ringer's solution was administered during this period. Diaphragmatic contractility was assessed by measuring the transdiaphragmatic pressure (P_di, cmH₂O). No difference in P_di was observed in groups C₁ and D₁. After diaphragmatic fatigue in groups C₂ and D₂, P_di at low-frequency (20-Hz) stimulation decreased significantly compared with the prefatigue values (group C₂; 9.3±1.9vs 12.5±2.4, group D₂; 9.3±2.1vs 12.5±2.6; mean±SD;P<0.05), whereas no change in P_di was observed at high-frequency (100-Hz) stimulation. In group D₂, P_di at both stimuli increased significantly with an infusion of DBcAMP compared with the fatigue values (20 Hz; 13.3±3.3vs 9.3±2.1, 100 Hz; 23.4±3.6vs 21.3±3.2;P<0.05). In group C₂, the speed of recovery from fatigue was relatively slower at 20-Hz stimulation than at 100-Hz stimulation. It is concluded that DBcAMP increases the contractility of fatigued diaphragm, but that this agent does not affect the contractility of nonfatigued diaphragm.     

RETRACTED ARTICLE: Different effects of olprinone on contractility in nonfatigued and fatigued diaphragm in dogs

PURPOSE: To evaluate the effects of low-dose olprinone, a phosphodiesterase III inhibitor, on contractility and its mechanism in nonfatigued and fatigued diaphragm in dogs. METHODS: Thirty six pentobarbitone-anesthetized dogs were studied. In Group Ia (n=6), animals without fatigue, received no study drug. In Group Ib (n=6), dogs were given a bolus injection (10 ug x kg(-1)) followed by continuous infusion (0.1 microg x kg(-1) x min(-1)) of olprinone. In Groups IIa, IIb, and IIc (n=8 each), diaphragmatic fatigue was induced by intermittent supramaximal bilateral electrophrenic stimulation at a frequency of 20-Hz applied for 30 min. After producing fatigue, Group IIa received no study drug; Group IIb was infused with olprinone (10 ug x kg(-1) loading dose plus 0.1 microg-kg(-1) min(-1) maintenance dose); Group IIc was infused with nicardipine (5 microg x kg(-1) x min(-1)) during olprinone administration. Diaphragmatic contractility was assessed by transdiaphragmatic pressure (Pdi). RESULTS: No difference in Pdi was observed between Groups Ia and Ib. After fatigue, in Groups IIa, IIb, and IIc, Pdi at low-frequency (20-Hz) stimulation decreased from prefatigued (baseline) values (P < 0.05), whereas there was no change in Pdi at high-frequency stimulation (100-Hz). In Group IIb, during olprinone administration, Pdi at both stimuli increased from fatigued values (P < 0.05). In Group IIc, the augmentation of Pdi to each stimulus in fatigued diaphragm by olprinone was abolished with an infusion of nicardipine. CONCLUSION: Low-dose olprinone does not affect contractility in nonfatigued diaphragm, but increases contractility in fatigued diaphragm via its effect on transmembrane calcium movement in dogs.     

Effect of sevoflurane on diaphragmatic contractility in dogs.

The effect of sevoflurane on diaphragmatic contractility was investigated in 12 anesthetized, mechanically ventilated dogs with the thorax opened. Animals were divided into two groups of six each: the sevoflurane and time control groups. We assessed contractility by the transdiaphragmatic pressure (Pdi) during supramaximal stimulation of the phrenic nerve at frequencies of 0.5, 10, 20, 50, and 100 Hz under quasiisometric conditions. The integrated electrical activity (Edi) of the crural and costal parts of the diaphragm (Edi cru, Edi cost) was also measured. In the sevoflurane group, diaphragmatic contractility was determined during three levels of anesthesia, specifically 0, 1.0, and 1.5 minimum alveolar anesthetic concentration (MAC). Measurements were made at the start of the stimulation (initial) and at the end of the 2-s period (2-s). Increasing the depth of sevoflurane anesthesia did not cause any significant differences in Pdi and Edi at 0.5-, 10-, and 20-Hz stimulation. By contrast, at 50- and 100-Hz stimulation, initial Pdi during 1.0 and 1.5 MAC sevoflurane exposure decreased significantly compared with the 0 MAC value (P less than 0.05). In addition, there was a statistical difference in 2-s Pdi between 1.0 and 1.5 MAC at 100-Hz stimulation (P less than 0.05). The Edi cru showed similar changes in Pdi at both measurements, whereas there was no remarkable change in Edi cost. There was no significant change either in Pdi or in Edi with respect to time in the time control group. We conclude from these results that sevoflurane impairs diaphragmatic contractility through its inhibitory effect on neuromuscular transmission, predominantly of the crural part.     

RETRACTED ARTICLE: Nicardipine inhibits amrinone-enhanced contractility in fatigued diaphragm

The purpose of this study was to examine the effect of amrinone, a bipyridine derivative, with and without nicardipine, a calcium channel blocker, on the contractility of fatigued diaphragm in dogs. Twenty dogs were divided into two groups of ten each: amrinone group (group A) and combined amrinone and nicardipine group (group AN). Diaphragmatic fatigue was induced by intermittent supramaximal bilateral electrophrenic stimulation at a frequency of 20 Hz applied for 30 min. Diaphragmatic contractility was assessed from changes in transdiaphragmatic pressure (P_di). In group A, after producing fatigue, amrinone (0.75 mg·kg⁻¹ loading dose plus 10 μg·kg⁻¹·min⁻¹ maintenance dose) was administered iv. In group AN, nicardipine 5 μg·kg⁻¹·min⁻¹ was infused iv simultaneously with amrinone during this period. After diaphragmatic fatigue, P_di at low-frequency (10–30 Hz) stimulation decreased compared with the prefatigue values (P<0.05), whereas no change in P_di was observed at high-frequency (50–100 Hz), stimulation. The P_di at each stimulus were increased compared with the fatigued values (P<0.05) by administering amrinone, and returned to these values after this agent was discontinued. The P_di values at any frequency of stimulation did not change when amrinone was administered with nicardipine. Our results suggest that amirinone may enhance contractility in fatigued diaphragm via its effect on transmembrane calcium movement.     

RETRACTED ARTICLE: The dose-response relationship of amrinone in increasing the contractility of fatigued diaphragm in dogs

We studied the dose-related effects of amrinone on the contractility of a fatigued diaphragm in 16 anesthetized, mechanically ventilated dogs. The animals were divided into two groups: the control group (Group C,n=8) and the amrinone group (Group A,n=8). Diaphragmatic fatigue was induced by intermittent supramaximal bilateral electrophrenic stimulation at a frequency of 20 Hz applied for 30 min. The contractility of the diaphragm was assessed from changes in transdiaphragmatic pressure (P _di). After inducing fatigue,P _di at low-frequency (20 Hz) stimulation decreased significantly compared with the pre-fatigue values (P<0.05), whereas no change was observed at high-frequency (100 Hz) stimulation. In Group A, after producing fatigue,P _di at 20 Hz stimulation increased significantly with a bolus injection (0.75 mg·kg⁻¹) followed by continuous infusion of amrinone (2.5, 5 and then 10μg·kg⁻¹min⁻¹) IV (P<0.05).P _di at 100 Hz stimulation increased significantly with an administration of amrinone (10μg·kg⁻¹min⁻¹ IV (P<0.05). There was a significant positive correlation betweenP _di at both stimuli and amrinone dose (P<0.01). In Group, C, the speed of recovery ofP _di at 20 Hz stimulation was relatively slower. The integrated electric activity of the diaphragam (E _di) in each group did not change at any frequency of stimulation throughout the experiment. We conclude that amrinone exerts a dose-dependent enhancement of the contractility of a fatigued diaphragm in dogs.     

Propofol decreases diaphragmatic contractility in dogs

Volatile anesthetics depress diaphragmatic muscle function; however, no data are available regarding the effect of propofol on diaphragmatic contractility. We therefore studied this effect in dogs. Pentobarbital-anesthetized animals were divided into three groups of 10 each. Group I received only maintenance fluid; Group II was infused with a subhypnotic dose of propofol (0.1-mg/kg initial dose plus 1.5-mg x kg(-1) x h(-1) maintenance dose); Group III was infused with an anesthetic dose of propofol (0.1-mg/kg initial dose plus 6.0-mg x kg(-1) x h(-1) maintenance dose). We assessed diaphragmatic contractility by transdiaphragmatic pressure (Pdi). With an infusion of propofol in Groups II and III, Pdi at low-frequency (20-Hz) stimulation decreased from the baseline values (P < 0.05), whereas Pdi at high-frequency (100-Hz) stimulation did not change. Compared with Group I, Pdi at 20-Hz stimulation decreased during propofol administration in Groups II and III (P < 0.05). The decrease in Pdi was more in Group III than in Group II (P < 0.05). We conclude that propofol is associated with a dose-related inhibitory effect on diaphragmatic contractility in dogs. IMPLICATIONS: Propofol is an effective IV anesthetic for the induction and maintenance of anesthesia. Subhypnotic and anesthetic doses of propofol decrease diaphragmatic contractility in dogs.     

Dobutamine increases diaphragmatic contractility in dogs

The effects of dobutamine on diaphragmatic contractility were studied in 24 dogs anaesthetized with secobarbital and receiving mechanical lung ventilation. The phrenic nerves were stimulated supramaximally for two seconds with electrodes placed around the fifth and sixth cervical roots when the airway was closed at the level of FRC. The stimulating frequency ranged from 10 to 100 Hz. Transdiaphragmatic pressure gradient (Pdi) generated by the electrophrenic stimulation was used as an index of diaphragmatic contractility. The electrical activity of the diaphragm during the stimulation (Edi) was also measured with needle electrodes inserted in the right hemidiaphragm percutaneously. During an infusion of dobutamine (10 micrograms.kg-1.min-1 for 20 min), Pdi increased by 15 +/- 2.1% of control value at 20 Hz stimulation (P less than 0.01), and by 13 +/- 1.2% at 100 Hz stimulation (P less than 0.01). The Edi was not altered by dobutamine infusion. This enhancement of Pdi by dobutamine was abolished by simultaneous infusion of nicardipine, a Ca-channel blocker, but was not affected by prostaglandin E1. These results suggest that dobutamine has a stimulating effect on canine diaphragmatic contraction, and this action may be related to the increased inward movement of extracellular calcium.     

High-dose colforsin daropate increases diaphragmatic contractility in dogs

PURPOSE: To evaluate the effects of colforsin daropate, a water-soluble derivate known to improve contractility in fatigued canine diaphragm, at two different doses (low-dose and high-dose) on contractility of the non-fatigued diaphragm of dogs. METHODS: Twenty-four pentobarbitone-anesthetized dogs were divided into three groups of eight each: Group I received no study drug; Group II received low-dose (0.2 microg x kg-1 x min-1) colforsin daropate; Group III received high-dose (0.5 microg x kg-1 x min-1) colforsin daropate. Diaphragmatic contractility was assessed by transdiaphragmatic pressure (Pdi). RESULTS: In Group III, with an infusion of high-dose colforsin daropate, Pdi at low-frequency (20 Hz) and high-frequency (100 Hz) stimulation increased from baseline values (P < 0.05). Compared with Group I, Pdi at both stimuli increased during colforsin daropate administration in Group III (P < 0.05). In Group II, with an infusion of low- dose colforsin daropate, Pdi to each stimulus did not change. CONCLUSION: Colforsin daropate, only when administered at high-dose, increases contractility of non-fatigued diaphragm in dogs.     

RETRACTED ARTICLE: Effects of nicardipine on diaphragmatic fatigue in the dog: The relationship between dosage and fatigability

We examined the dose-related effects of nicardipine on the diaphragmatic fatigability in 24 anesthetized, mechanically ventilated dogs. Animals were divided into three groups of eight each: the control group (group C), the nicardipine 3 μg·kg⁻¹ I.V. group (group N₁) and the nicardipine 5 μg·kg⁻¹·min⁻¹ I.V. group (group N₂). Diaphragmatic fatigue was induced by intermittent supramaximal bilateral electrophrenic stimulation at a frequency of 20 Hz applied for 30 min. In groups N₁ and N₂, nicardipine was continuoulsy infused intravenously during this fatigueproducing period. Diaphragmatic contractility was assessed by changes in transdiaphragmatic pressure (P_di). After induction of diaphragmatic stimulation at low-frequency (20 Hz), P_di decreased significantly in all groups compared with the prefatigue value (P<0.05), whereas no change was observed in P_di at high-frequency (100 Hz) stimulation. The P_di at 20 Hz stimulation was significantly lower in groups N₁ and N₂ compared with that in group C (P<0.05). The decrease in P_di at 20 Hz stimulation was significantly larger in group N₂ than in group N₁ (P<0.05). The speed of recovery of P_di at 20 Hz stimulation was dose dependent. The integrated diaphragmatic electric activity (E_di) in each group did not change at any frequency of stimulation throughout the study. Our results demonstrate that nicardipine causes a dose-dependent reduction of the contractility of the fatigued diaphragm.     

The effect of sedative drugs on diaphragmatic contractility in dogs: propofol versus midazolam

Implications: a sedative dose (0.1 mg x kg(-1) x h(-1)) of midazolam, compared with a subhypnotic dose (1.5 mg x kg(-1) x h(-1)) of propofol, decreases the contractility of the diaphragm in dogs.     

The recovery profile of reduced diaphragmatic contractility induced by propofol in dogs

Propofol decreases contractility of the diaphragm, but no data are available for its effects on recovery. We studied the recovery profile of reduced diaphragmatic contractility induced by propofol in dogs. Animals were divided into 4 groups of 7 each. Group I, without fatigue, received only maintenance fluid; Group II, without fatigue, was infused with propofol; Group III, with fatigue, received no study drug; Group IV, with fatigue, was infused propofol. Propofol at an anesthetic dose (0.1 mg/kg initial dose plus 6.0 mg x kg(-1) x h(-1)) was administered for 60 min. In Groups III and IV, diaphragmatic fatigue was induced by intermittent supramaximal bilateral electrophrenic stimulation at 20-Hz for 30 min. We assessed diaphragmatic contractility by transdiaphragmatic pressure (Pdi). In group II, Pdi at low-frequency (20-Hz) stimulation decreased to less than baseline (P < 0.05), whereas there was no change in Pdi at high-frequency (100-Hz) stimulation. At 10 min after the end of propofol administration, Pdi at 20-Hz stimulation returned to baseline. When fatigue was established, in Groups III and IV, Pdi at 20-Hz stimulation decreased to less than baseline (P < 0.05), whereas Pdi at 100-Hz stimulation did not change. After administering propofol in Group IV, Pdi at 20-Hz stimulation decreased from fatigued values (P < 0.05). At 20 min after the end of propofol administration, Pdi at 20-Hz stimulation returned to fatigued values. We conclude that reduced contractility in nonfatigued and fatigued canine diaphragm induced by propofol recovers within 20 min after the cessation of administration.     

RETRACTED ARTICLE: Conservative Management of Acute Appendicitis

Background  

The acute appendicitis is the most common abdominal emergency, and the primary treatment has been appendicectomy. Antibiotics are started preoperatively and continued postoperatively as needed.