Comparative study between atropine and hyoscine-N-butylbromide for reversal of detomidine induced bradycardia in horses

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Cardiorespiratory and neuroendocrine changes induced by methadone in conscious and in isoflurane anaesthetised dogs

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

AT1 receptor blockade attenuates insulin resistance and myocardial remodeling in rats with diet-induced obesity

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Is gender crucial for cardiovascular adjustments induced by exercise training in female spontaneously hypertensive rats?

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Opiate activation suppresses the drinking, pressor and natriuretic responses induced by cholinergic stimulation of the medial septal area

The present study investigates the participation and interaction between cholinergic and opiate receptors of the medial septal area (MSA) in the regulation of Na+, K+ and water excretion, drinking and blood pressure regulation. Male Holtzman rats were implanted with stainless steel cannulae opening into the MSA. Na+, K+ and water excretion, water intake and blood pressure were measured after injection of carbachol (cholinergic agonist), FK-33824 (an opiate agonist) + carbachol or naloxone (an opiate antagonist) + carbachol into MSA. Carbachol (0.5 or 2.0 nmol) induced an increase in Na+ and K+ excretion, water intake and blood pressure and reduced the urinary volume. FK-33824 reduced the urinary volume and Na+ and K+ excretion. Previous injection of FK-33824 (100 ng) into the MSA blocked the increases in Na+ and K+ excretion, water intake and blood pressure induced by carbachol. Naloxone (10 μg) produced no changes in the effect of 2.0 nmol carbachol, but potentiated the natriuretic effect induced by 0.5 nmol dose of carbachol. These data show an inhibitory effect of opiate receptors on the changes in cardiovascular, fluid and electrolyte balance induced by cholinergic stimulation of the MSA in rats. © 1992.

Effect of AV3V lesion on the cardiovascular, fluid, and electrolytic changes induced by activation of the lateral preoptic area

In this study we investigated the effect of the anteroventral third ventricle (AV3V) lesion on the pressor, bradycardic, natriuretic, kaliuretic, and dipsogenic responses induced by the injection of the cholinergic agonist carbachol into the lateral preoptic area (LPOA) in rats. Male Holtzman rats with sham or electrolytic AV3V lesion were implanted with stainless steel cannula directly into the LPOA. Injection of carbachol (7.5 nmol) into the LPOA of sham rats induced natriuresis (405 ± 66 μEq/120 min), kaliuresis (234 ± 44 μEq/120 min), water intake (9.5 ± 1.7 ml/60 min), bradycardia (-47 ± 11 bpm), and increase in mean arterial pressure (28 ± 3 mmHg). Acute AV3V lesion (1-5 days) reduced the natriuresis (12 ± 4 μEq/120 min), kaliuresis (128 ± 27 μEq/120 min), water intake (1.7 ± 0.9 ml/60 min), and pressor responses (14 ± 4 mmHg) produced by carbachol into the LPOA. Tachycardia instead of bradycardia was also observed. Chronic (14-18 days) AV3V lesion reduced only the pressor response (10 ± 2 mmHg) induced by carbachol. These results showed that acute, but not chronic, AV3V lesion reduced the natriuretic, kaliuretic, and dipsogenic responses to carbachol injection into the LPOA. The pressor response was reduced in acute or chronic AV3V-lesioned rats. The results suggest that the lateral areas may control the fluid and electrolyte balance independently from the AV3V region in chronic AV3V-lesioned rats. © 1992.

Different effects on rat arterial pressure and heart rate when losartan is injected into the third or fourth ventricle

Cardiovascular responses to central losartan (LOS), a non-peptide angiotensin II (ANG II) receptor antagonist, were investigated by comparing the effects of LOS injection into the 3rd and 4th cerebral ventricles (3rdV, 4thV) on mean arterial pressure (MAP) and heart rate (HR). Adult male Holtzman rats were used (N=6 animals per group). Average basal MAP and HR were 114±3 mmHg and 343±9 bpm (N=23), respectively. LOS (50, 100 or 200 nmol/2 μl) injected into the 3rdV induced pressor (peak of 25±3 mmHg) and tachycardic (peak of 60±25 bpm) responses. LOS injected into the 4thV had no effect on MAP, but it induced bradycardia (peak of -35±15 bpm). KCl (200 nmol/2 μl) injected into the 3rdV or into the 4thV had no effect on either MAP or HR compared to 0.9% saline injection. The results indicate that LOS injected into the third ventricle acts on forebrain structures to induce its pressor and tachycardic effects and that bradycardia, likely dependent on hindbrain structures, is obtained when LOS is injected into the fourth ventricle.

Effects of intracerebroventricular injections of losartan or PD123319 on arterial pressure and heart rate of sodium replete and sodium deplete rats

Angiotensin II (Ang II) non-peptide antagonists were injected i.c.v. (6.25-200 nmol, n = 5-8 rats/group): In sodium replete rats, losartan (AT1 receptor antagonist) induced an increase in mean arterial pressure (MAP) and in heart rate (HR) by 3rd ventricular (3rdV) injection, and a weaker pressor response and bradycardia by 4th ventricular (4thV) injection. PD123319 (AT2 receptor antagonist) induced an increase in MAP and in HR by 3rdV injection, and an increase in MAP and no alteration in HR by 4thV injection. In sodium deplete (furosemide plus removal of ambient sodium for 24 h) rats, losartan induced an increase in MAP and no alteration in HR by 3rdV injection, and no alteration in MAP and bradycardia by 4thV injection. PD123319 induced an increase in MAP and in HR by 3rdV injection, and an increase in MAP and bradycardia by 4thV injection. Thus, there was no fall in MAP by central injections of Ang II antagonists. Intravenous injection of losartan, but not of PD123319, induced a fall in MAP in both sodium replete and sodium deplete animals. Therefore, losartan and PD123319 can have similar effects on MAP and HR when injected intracerebroventricularly, although some differences are also present. The bradycardia is consistent with an withdrawal of Ang II inhibitory action on baroreflex.

Toxic effects of nickel exposure on heart and liver of rats

The role of air pollution as a health risk factor is of special interest. Numerous toxic pollutants, such as nickel, are being released to the environment as a result of combustion of fossil fuels, crude oil, and coal. Nickel in the atmosphere can be combined with other environmental pollutants, producing various nickel compounds, which have varying animal toxicity. A rat biossay validated for the identification of toxic effects of nickel revealed increased serum activities of total lactate dehydrogenase (LDH) and alanine transaminase (ALT) in rats that received intratracheal injection of Ni2+ in .09% saline solution of NiCl2. The total LDH activity was also increased in the heart, and the isoenzyme pattern showed the LDH1/LDH2 ratio elevated to greater than 1. We conclude that intratracheal administration of nickel induced cardiac and hepatic damage. The development of cardiac and hepatic damage and of increased enzymes' activities was only demonstrated when nickel had accumulated in these tissues, indicating that nickel depot is essential to its toxicity. Intratracheal administration of NiCl2 induced changes in LDH and ALT activities.

Food restriction-induced myocardial dysfunction demonstrated by the combination of in vivo and in vitro studies

The aim of this study was to test the hypothesis that protein-calorie undernutrition decreases myocardial contractility jeopardizing ventricular function, and that ventricular dysfunction can be detected noninvasively. Five-month-old male Wistar-Kyoto rats were fed with regular rat chow ad libitum for 90 days (Control group, n = 14). A second group of rats received 50% of the amount of diet consumed by de control group (Food restricted group, n = 14). Global LV systolic function was evaluated in vivo, noninvasively, by transthoracic echocardiogram. After echocardiographic study, myocardial contractility was assessed in vitro in the isovolumetrically beating isolated heart in eight animals from each group (Langendorff preparation). The in vivo LV fractional shortening showed that food restriction depressed LV systolic function (p < 0.05). Myocardial contractility was impaired as assessed by the maximal rate of rise of LV pressure (+dP/dt), and developed pressure at diastolic pressure of 25 mmHg (p < 0.05). Furthermore, food restriction induced eccentric ventricular remodeling, and reduced myocardial elasticity and LV compliance (p < 0.05). In conclusion, food restriction causes systolic dysfunction probably due to myocardial contractility impairment and reduction of myocardial elasticity. © 2002 Elsevier B.V. All rights reserved.

Hepatic bleeding induced by streptokinase and heparin in a patient with acute myocardial infarction

Although rare, major bleeding is the most important side effect of thrombolytic therapy in acute myocardial infarction (AMI) (Levine et al., 1995). Spontaneous hepatic bleeding in normal liver after thrombolytic administration has rarely been reported in literature. To our knowledge, there are only three cases of hepatic bleeding related to thrombolytic therapy in AMI. In these, the used drugs were anisolylated plasminogen streptokinase activator complex (APSAC) (Garcia-Jiménez et al., 1997; Fox et al., 1991) and rt-PA (Garcia-Jiménez et al., 1997). We report a case of hepatic bleeding after streptokinase followed by units over 60 minutes). The next day, the patient developed third-degree atrioventricular block and a temporary pacemaker was inserted. Twenty-seven hours after streptokinase infusion, the patient complained of refractory chest pain that was interpreted as post-myocardial infarction angina; clotting screen was normal and intravenous heparin was started (80 U/kg followed by 18 U/kg/hour). After four hours of heparin administration, the patient presented abdominal pain and distension, and his blood pressure and hematocrit level dropped. Abdominal ultrasonography revealed free fluid in the peritoneal cavity (about 3,000 mL). A laparotomy disclosed blood in the abdominal cavity with bleeding from the right lateral hepatic segment, which was removed. The remaining abdominal viscera were normal and there was no other evidence of hemorrhage. The partial liver resection presented subcapsular hemorrhage with small parenchymal hemorrhage. Histopathological examination also revealed focal areas of ischemic centrilobular necrosis. The patient died of multiple organ system failure 21 days after admission. Copyright © 2002 By PJD Publications Limited.

Plication of the free wall of the left ventricle in dogs with doxorubicin-induced cardiomyopathy

Objective - To evaluate plication of the free wall of the left ventricle, which reduces the left ventricular area and volume, as a method to improve the left ventricular systolic function without cardiopulmonary bypass. Animals - 8 mixed-breed adult dogs. Procedure - Dilated cardiomyopathy (DCM) was induced in each dog by administration of doxorubicin (30 mg/m2, IV, q 21 d for 168 days). Two dogs died during induction of cardiomyopathy. Plication surgery was performed in 4 dogs. Two dogs did not ondergo to surgery (control group). Values for cardiac output (CO), 2-dimensional and M-mode echocardiography, arterial blood pressure, electrocardiography, blood cell counts, and serum biochemical analyses were recorded after induction of DCM (baseline) and 1, 2, 7, 15, 21, 30, 60, 90, 120, 150, and 180 days after plication surgery. Ambulatory ECG (Holter) recordings were conducted for 24 hours on the day of surgery. Results - 1 dog died after plication surgery. The remaining dogs undergoing ventricular plication had a significant improvement in CO, ejection fraction, and fractional shortening and reductions of left ventricular area and volume after surgery. Electrocardiographic and Holter recordings revealed premature ventricular complexes, which resolved without treatment during the first week after surgery. Clinical condition of the control dogs declined, and these 2 dogs died approximately 40 days after induction of cardiomyopathy. Conclusions and Clinical Relevance - Plication of the free wall of the left ventricle improved left ventricular systolic function in dogs with doxorubicin-induced cardiomyopathy. Additional studies are needed to evaluate its application in dogs with naturally developing DCM.

Heart failure alters MyoD and MRF4 expressions in rat skeletal muscle

Heart failure (HF) is characterized by a skeletal muscle myopathy with increased expression of fast myosin heavy chains (MHCs). The skeletal muscle-specific molecular regulatory mechanisms controlling MHC expression during HF have not been described. Myogenic regulatory factors (MRFs), a family of transcriptional factors that control the expression of several skeletal muscle-specific genes, may be related to these alterations. This investigation was undertaken in order to examine potential relationships between MRF mRNA expression and MHC protein isoforms in Wistar rat skeletal muscle with monocrotaline-induced HF. We studied soleus (Sol) and extensor digitorum longus (EDL) muscles from both HF and control Wistar rats. MyoD, myogenin and MRF4 contents were determined using reverse transcription-polymerase chain reaction while MHC isoforms were separated using polyacrylamide gel electrophoresis. Despite no change in MHC composition of Wistar rat skeletal muscles with HF, the mRNA relative expression of MyoD in Sol and EDL muscles and that of MRF4 in Sol muscle were significantly reduced, whereas myogenin was not changed in both muscles. This down-regulation in the mRNA relative expression of MRF4 in Sol was associated with atrophy in response to HF while these alterations were not present in EDL muscle. Taken together, our results show a potential role for MRFs in skeletal muscle myopathy during HF. © 2006 Blackwell Science Ltd.

Marine catfish sting causing fatal heart perforation in a fisherman

Many marine catfish have serrated bony stings (spines), which are used in defense against predators, on the dorsal and pectoral fins. While catfish-induced injuries are generally characterized by the pain associated with envenomation, the stings in some species are sufficiently long and sharp to cause severe penetrating trauma. Most injuries are to the hands of victims, commonly fishermen. We report the death of a fisherman caused by myocardial perforation from a catfish sting. To our knowledge, this is the first such description in the medical literature.