Ranitidine | Caspian Tamin Pharmaceutical Company

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Ranitidine hydrochloride is a competitive, reversible inhibitor of the action of histamine at the histamine H2-receptors, including receptors on the gastric cells. Ranitidine hydrochloride does not lower serum Ca++ in hypercalcemic states. Ranitidine hydrochloride is not an anticholinergic agent.

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Ranitidine Injection is contraindicated for patients known to have hypersensitivity to the drug.

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Ranitidine Injection is contraindicated for patients known to have hypersensitivity to the drug.

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Ranitidine has been reported to affect the bioavailability of other drugs through several different mechanisms such as competition for renal tubular secretion, alteration of gastric pH, and inhibition of cytochrome P450 enzymes. such as Procainamide ,Warfarin ,Ketoconazole , Midazolam.

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Ranitidine has been reported to affect the bioavailability of other drugs through several different mechanisms such as competition for renal tubular secretion, alteration of gastric pH, and inhibition of cytochrome P450 enzymes. such as Procainamide ,Warfarin ,Ketoconazole , Midazolam.

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Ranitidine Injection is indicated in some hospitalized patients with pathological hypersecretory conditions or intractable duodenal ulcers, or as an alternative to the oral dosage form for short-term use in patients who are unable to take oral medication.

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Ranitidine Injection is indicated in some hospitalized patients with pathological hypersecretory conditions or intractable duodenal ulcers, or as an alternative to the oral dosage form for short-term use in patients who are unable to take oral medication.

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Ranitidine hydrochloride is absorbed very rapidly after intramuscular (IM) injection. Mean peak levels of 576 ng/mL occur within 15 minutes or less following a 50 mg IM dose. Absorption from IM sites is virtually complete, with a bioavailability of 90% to 100% compared with intravenous (IV) administration. Following oral administration, the bioavailability of ranitidine is 50%.
The volume of distribution is about 1.4 L/kg. Serum protein binding averages 15%.
In humans, the N-oxide is the principal metabolite in the urine; however, this amounts to <4% of the dose. Other metabolites are the S-oxide (1%) and the desmethyl ranitidine (1%). The remainder of the administered dose is found in the stool. Studies in patients with hepatic dysfunction (compensated cirrhosis) indicate that there are minor, but clinically insignificant, alterations in ranitidine half-life, distribution, clearance, and bioavailability.
Following IV injection, approximately 70% of the dose is recovered in the urine as unchanged drug. Renal clearance averages 530 mL/min, with a total clearance of 760 mL/min.
The elimination half-life is 2.0 to 2.5 hours.

[view] =>

Ranitidine hydrochloride is absorbed very rapidly after intramuscular (IM) injection. Mean peak levels of 576 ng/mL occur within 15 minutes or less following a 50 mg IM dose. Absorption from IM sites is virtually complete, with a bioavailability of 90% to 100% compared with intravenous (IV) administration. Following oral administration, the bioavailability of ranitidine is 50%.
The volume of distribution is about 1.4 L/kg. Serum protein binding averages 15%.
In humans, the N-oxide is the principal metabolite in the urine; however, this amounts to <4% of the dose. Other metabolites are the S-oxide (1%) and the desmethyl ranitidine (1%). The remainder of the administered dose is found in the stool. Studies in patients with hepatic dysfunction (compensated cirrhosis) indicate that there are minor, but clinically insignificant, alterations in ranitidine half-life, distribution, clearance, and bioavailability.
Following IV injection, approximately 70% of the dose is recovered in the urine as unchanged drug. Renal clearance averages 530 mL/min, with a total clearance of 760 mL/min.
The elimination half-life is 2.0 to 2.5 hours.

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1. Symptomatic response to therapy with ranitidine hydrochloride does not preclude the presence of gastric malignancy.
2. Since ranitidine hydrochloride is excreted primarily by the kidney, dosage should be adjusted in patients with impaired renal function . Caution should be observed in patients with hepatic dysfunction since ranitidine hydrochloride is metabolized in the liver.
3. In controlled studies in normal volunteers, elevations in SGPT have been observed when H2-antagonists have been administered intravenously at greater-than-recommended dosages for 5 days or longer. Therefore, it seems prudent in patients receiving IV ranitidine at dosages ≥100 mg 4 times daily for periods of 5 days or longer to monitor SGPT daily (from day 5) for the remainder of IV therapy.
4. Bradycardia in association with rapid administration of Ranitidine Injection has been reported rarely, usually in patients with factors predisposing to cardiac rhythm disturbances. Recommended rates of administration should not be exceeded.
5. Rare reports suggest that ranitidine hydrochloride may precipitate acute porphyric attacks in patients with acute porphyria. Ranitidine hydrochloride should therefore be avoided in patients with a history of acute porphyria.

[view] =>

1. Symptomatic response to therapy with ranitidine hydrochloride does not preclude the presence of gastric malignancy.
2. Since ranitidine hydrochloride is excreted primarily by the kidney, dosage should be adjusted in patients with impaired renal function . Caution should be observed in patients with hepatic dysfunction since ranitidine hydrochloride is metabolized in the liver.
3. In controlled studies in normal volunteers, elevations in SGPT have been observed when H2-antagonists have been administered intravenously at greater-than-recommended dosages for 5 days or longer. Therefore, it seems prudent in patients receiving IV ranitidine at dosages ≥100 mg 4 times daily for periods of 5 days or longer to monitor SGPT daily (from day 5) for the remainder of IV therapy.
4. Bradycardia in association with rapid administration of Ranitidine Injection has been reported rarely, usually in patients with factors predisposing to cardiac rhythm disturbances. Recommended rates of administration should not be exceeded.
5. Rare reports suggest that ranitidine hydrochloride may precipitate acute porphyric attacks in patients with acute porphyria. Ranitidine hydrochloride should therefore be avoided in patients with a history of acute porphyria.

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Transient pain at the site of IM injection has been reported. Transient local burning or itching has been reported with IV administration of ranitidine hydrochloride.
The following have been reported as events in clinical trials or in the routine management of patients treated with oral or parenteral ranitidine hydrochloride. The relationship to therapy with ranitidine hydrochloride has been unclear in many cases. Headache, sometimes severe, seems to be related to administration of ranitidine hydrochloride.

[view] =>

Transient pain at the site of IM injection has been reported. Transient local burning or itching has been reported with IV administration of ranitidine hydrochloride.
The following have been reported as events in clinical trials or in the routine management of patients treated with oral or parenteral ranitidine hydrochloride. The relationship to therapy with ranitidine hydrochloride has been unclear in many cases. Headache, sometimes severe, seems to be related to administration of ranitidine hydrochloride.

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Ranitidine hydrochloride is a competitive, reversible inhibitor of the action of histamine at the histamine H2-receptors, including receptors on the gastric cells. Ranitidine hydrochloride does not lower serum Ca++ in hypercalcemic states. Ranitidine hydrochloride is not an anticholinergic agent.

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Ranitidine hydrochloride is absorbed very rapidly after intramuscular (IM) injection. Mean peak levels of 576 ng/mL occur within 15 minutes or less following a 50 mg IM dose. Absorption from IM sites is virtually complete, with a bioavailability of 90% to 100% compared with intravenous (IV) administration. Following oral administration, the bioavailability of ranitidine is 50%.
The volume of distribution is about 1.4 L/kg. Serum protein binding averages 15%.
In humans, the N-oxide is the principal metabolite in the urine; however, this amounts to <4% of the dose. Other metabolites are the S-oxide (1%) and the desmethyl ranitidine (1%). The remainder of the administered dose is found in the stool. Studies in patients with hepatic dysfunction (compensated cirrhosis) indicate that there are minor, but clinically insignificant, alterations in ranitidine half-life, distribution, clearance, and bioavailability.
Following IV injection, approximately 70% of the dose is recovered in the urine as unchanged drug. Renal clearance averages 530 mL/min, with a total clearance of 760 mL/min.
The elimination half-life is 2.0 to 2.5 hours.

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Ranitidine hydrochloride is absorbed very rapidly after intramuscular (IM) injection. Mean peak levels of 576 ng/mL occur within 15 minutes or less following a 50 mg IM dose. Absorption from IM sites is virtually complete, with a bioavailability of 90% to 100% compared with intravenous (IV) administration. Following oral administration, the bioavailability of ranitidine is 50%.
The volume of distribution is about 1.4 L/kg. Serum protein binding averages 15%.
In humans, the N-oxide is the principal metabolite in the urine; however, this amounts to <4% of the dose. Other metabolites are the S-oxide (1%) and the desmethyl ranitidine (1%). The remainder of the administered dose is found in the stool. Studies in patients with hepatic dysfunction (compensated cirrhosis) indicate that there are minor, but clinically insignificant, alterations in ranitidine half-life, distribution, clearance, and bioavailability.
Following IV injection, approximately 70% of the dose is recovered in the urine as unchanged drug. Renal clearance averages 530 mL/min, with a total clearance of 760 mL/min.
The elimination half-life is 2.0 to 2.5 hours.

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Ranitidine hydrochloride is absorbed very rapidly after intramuscular (IM) injection. Mean peak levels of 576 ng/mL occur within 15 minutes or less following a 50 mg IM dose. Absorption from IM sites is virtually complete, with a bioavailability of 90% to 100% compared with intravenous (IV) administration. Following oral administration, the bioavailability of ranitidine is 50%.
The volume of distribution is about 1.4 L/kg. Serum protein binding averages 15%.
In humans, the N-oxide is the principal metabolite in the urine; however, this amounts to <4% of the dose. Other metabolites are the S-oxide (1%) and the desmethyl ranitidine (1%). The remainder of the administered dose is found in the stool. Studies in patients with hepatic dysfunction (compensated cirrhosis) indicate that there are minor, but clinically insignificant, alterations in ranitidine half-life, distribution, clearance, and bioavailability.
Following IV injection, approximately 70% of the dose is recovered in the urine as unchanged drug. Renal clearance averages 530 mL/min, with a total clearance of 760 mL/min.
The elimination half-life is 2.0 to 2.5 hours.

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Ranitidine hydrochloride is absorbed very rapidly after intramuscular (IM) injection. Mean peak levels of 576 ng/mL occur within 15 minutes or less following a 50 mg IM dose. Absorption from IM sites is virtually complete, with a bioavailability of 90% to 100% compared with intravenous (IV) administration. Following oral administration, the bioavailability of ranitidine is 50%.
The volume of distribution is about 1.4 L/kg. Serum protein binding averages 15%.
In humans, the N-oxide is the principal metabolite in the urine; however, this amounts to <4% of the dose. Other metabolites are the S-oxide (1%) and the desmethyl ranitidine (1%). The remainder of the administered dose is found in the stool. Studies in patients with hepatic dysfunction (compensated cirrhosis) indicate that there are minor, but clinically insignificant, alterations in ranitidine half-life, distribution, clearance, and bioavailability.
Following IV injection, approximately 70% of the dose is recovered in the urine as unchanged drug. Renal clearance averages 530 mL/min, with a total clearance of 760 mL/min.
The elimination half-life is 2.0 to 2.5 hours.

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Ranitidine Injection is indicated in some hospitalized patients with pathological hypersecretory conditions or intractable duodenal ulcers, or as an alternative to the oral dosage form for short-term use in patients who are unable to take oral medication.

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Ranitidine Injection is indicated in some hospitalized patients with pathological hypersecretory conditions or intractable duodenal ulcers, or as an alternative to the oral dosage form for short-term use in patients who are unable to take oral medication.

) [#title] => [#description] => [#children] =>

Ranitidine Injection is indicated in some hospitalized patients with pathological hypersecretory conditions or intractable duodenal ulcers, or as an alternative to the oral dosage form for short-term use in patients who are unable to take oral medication.

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Ranitidine Injection is indicated in some hospitalized patients with pathological hypersecretory conditions or intractable duodenal ulcers, or as an alternative to the oral dosage form for short-term use in patients who are unable to take oral medication.

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Ranitidine Injection is contraindicated for patients known to have hypersensitivity to the drug.

[#delta] => 0 ) [#title] => [#description] => [#theme_used] => 1 [#printed] => 1 [#type] => [#value] => [#prefix] => [#suffix] => [#children] =>

Ranitidine Injection is contraindicated for patients known to have hypersensitivity to the drug.

) [#title] => [#description] => [#children] =>

Ranitidine Injection is contraindicated for patients known to have hypersensitivity to the drug.

[#printed] => 1 ) [#single] => 1 [#attributes] => Array ( ) [#required] => [#parents] => Array ( ) [#tree] => [#context] => full [#page] => 1 [#field_name] => field_contraindications [#title] => Contraindications [#access] => 1 [#label_display] => above [#teaser] => [#node] => stdClass Object *RECURSION* [#type] => content_field [#children] =>

Ranitidine Injection is contraindicated for patients known to have hypersensitivity to the drug.

[#printed] => 1 ) [#title] => [#description] => [#children] => [#printed] => 1 ) [field_precautions] => Array ( [#type_name] => product [#context] => full [#field_name] => field_precautions [#post_render] => Array ( [0] => content_field_wrapper_post_render ) [#weight] => 8 [field] => Array ( [#description] => [items] => Array ( [0] => Array ( [#formatter] => default [#node] => stdClass Object *RECURSION* [#type_name] => product [#field_name] => field_precautions [#weight] => 0 [#theme] => text_formatter_default [#item] => Array ( [value] => 1. Symptomatic response to therapy with ranitidine hydrochloride does not preclude the presence of gastric malignancy. 2. Since ranitidine hydrochloride is excreted primarily by the kidney, dosage should be adjusted in patients with impaired renal function . Caution should be observed in patients with hepatic dysfunction since ranitidine hydrochloride is metabolized in the liver. 3. In controlled studies in normal volunteers, elevations in SGPT have been observed when H2-antagonists have been administered intravenously at greater-than-recommended dosages for 5 days or longer. Therefore, it seems prudent in patients receiving IV ranitidine at dosages ≥100 mg 4 times daily for periods of 5 days or longer to monitor SGPT daily (from day 5) for the remainder of IV therapy. 4. Bradycardia in association with rapid administration of Ranitidine Injection has been reported rarely, usually in patients with factors predisposing to cardiac rhythm disturbances. Recommended rates of administration should not be exceeded. 5. Rare reports suggest that ranitidine hydrochloride may precipitate acute porphyric attacks in patients with acute porphyria. Ranitidine hydrochloride should therefore be avoided in patients with a history of acute porphyria. [format] => 1 [safe] =>

1. Symptomatic response to therapy with ranitidine hydrochloride does not preclude the presence of gastric malignancy.
2. Since ranitidine hydrochloride is excreted primarily by the kidney, dosage should be adjusted in patients with impaired renal function . Caution should be observed in patients with hepatic dysfunction since ranitidine hydrochloride is metabolized in the liver.
3. In controlled studies in normal volunteers, elevations in SGPT have been observed when H2-antagonists have been administered intravenously at greater-than-recommended dosages for 5 days or longer. Therefore, it seems prudent in patients receiving IV ranitidine at dosages ≥100 mg 4 times daily for periods of 5 days or longer to monitor SGPT daily (from day 5) for the remainder of IV therapy.
4. Bradycardia in association with rapid administration of Ranitidine Injection has been reported rarely, usually in patients with factors predisposing to cardiac rhythm disturbances. Recommended rates of administration should not be exceeded.
5. Rare reports suggest that ranitidine hydrochloride may precipitate acute porphyric attacks in patients with acute porphyria. Ranitidine hydrochloride should therefore be avoided in patients with a history of acute porphyria.

[#delta] => 0 ) [#title] => [#description] => [#theme_used] => 1 [#printed] => 1 [#type] => [#value] => [#prefix] => [#suffix] => [#children] =>

1. Symptomatic response to therapy with ranitidine hydrochloride does not preclude the presence of gastric malignancy.
2. Since ranitidine hydrochloride is excreted primarily by the kidney, dosage should be adjusted in patients with impaired renal function . Caution should be observed in patients with hepatic dysfunction since ranitidine hydrochloride is metabolized in the liver.
3. In controlled studies in normal volunteers, elevations in SGPT have been observed when H2-antagonists have been administered intravenously at greater-than-recommended dosages for 5 days or longer. Therefore, it seems prudent in patients receiving IV ranitidine at dosages ≥100 mg 4 times daily for periods of 5 days or longer to monitor SGPT daily (from day 5) for the remainder of IV therapy.
4. Bradycardia in association with rapid administration of Ranitidine Injection has been reported rarely, usually in patients with factors predisposing to cardiac rhythm disturbances. Recommended rates of administration should not be exceeded.
5. Rare reports suggest that ranitidine hydrochloride may precipitate acute porphyric attacks in patients with acute porphyria. Ranitidine hydrochloride should therefore be avoided in patients with a history of acute porphyria.

) [#title] => [#description] => [#children] =>

1. Symptomatic response to therapy with ranitidine hydrochloride does not preclude the presence of gastric malignancy.
2. Since ranitidine hydrochloride is excreted primarily by the kidney, dosage should be adjusted in patients with impaired renal function . Caution should be observed in patients with hepatic dysfunction since ranitidine hydrochloride is metabolized in the liver.
3. In controlled studies in normal volunteers, elevations in SGPT have been observed when H2-antagonists have been administered intravenously at greater-than-recommended dosages for 5 days or longer. Therefore, it seems prudent in patients receiving IV ranitidine at dosages ≥100 mg 4 times daily for periods of 5 days or longer to monitor SGPT daily (from day 5) for the remainder of IV therapy.
4. Bradycardia in association with rapid administration of Ranitidine Injection has been reported rarely, usually in patients with factors predisposing to cardiac rhythm disturbances. Recommended rates of administration should not be exceeded.
5. Rare reports suggest that ranitidine hydrochloride may precipitate acute porphyric attacks in patients with acute porphyria. Ranitidine hydrochloride should therefore be avoided in patients with a history of acute porphyria.

[#printed] => 1 ) [#single] => 1 [#attributes] => Array ( ) [#required] => [#parents] => Array ( ) [#tree] => [#context] => full [#page] => 1 [#field_name] => field_precautions [#title] => Precautions [#access] => 1 [#label_display] => above [#teaser] => [#node] => stdClass Object *RECURSION* [#type] => content_field [#children] =>

1. Symptomatic response to therapy with ranitidine hydrochloride does not preclude the presence of gastric malignancy.
2. Since ranitidine hydrochloride is excreted primarily by the kidney, dosage should be adjusted in patients with impaired renal function . Caution should be observed in patients with hepatic dysfunction since ranitidine hydrochloride is metabolized in the liver.
3. In controlled studies in normal volunteers, elevations in SGPT have been observed when H2-antagonists have been administered intravenously at greater-than-recommended dosages for 5 days or longer. Therefore, it seems prudent in patients receiving IV ranitidine at dosages ≥100 mg 4 times daily for periods of 5 days or longer to monitor SGPT daily (from day 5) for the remainder of IV therapy.
4. Bradycardia in association with rapid administration of Ranitidine Injection has been reported rarely, usually in patients with factors predisposing to cardiac rhythm disturbances. Recommended rates of administration should not be exceeded.
5. Rare reports suggest that ranitidine hydrochloride may precipitate acute porphyric attacks in patients with acute porphyria. Ranitidine hydrochloride should therefore be avoided in patients with a history of acute porphyria.

[#printed] => 1 ) [#title] => [#description] => [#children] => [#printed] => 1 ) [field_drug_interactions] => Array ( [#type_name] => product [#context] => full [#field_name] => field_drug_interactions [#post_render] => Array ( [0] => content_field_wrapper_post_render ) [#weight] => 9 [field] => Array ( [#description] => [items] => Array ( [0] => Array ( [#formatter] => default [#node] => stdClass Object *RECURSION* [#type_name] => product [#field_name] => field_drug_interactions [#weight] => 0 [#theme] => text_formatter_default [#item] => Array ( [value] => Ranitidine has been reported to affect the bioavailability of other drugs through several different mechanisms such as competition for renal tubular secretion, alteration of gastric pH, and inhibition of cytochrome P450 enzymes. such as Procainamide ,Warfarin ,Ketoconazole , Midazolam. [format] => 1 [safe] =>

Ranitidine has been reported to affect the bioavailability of other drugs through several different mechanisms such as competition for renal tubular secretion, alteration of gastric pH, and inhibition of cytochrome P450 enzymes. such as Procainamide ,Warfarin ,Ketoconazole , Midazolam.

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Ranitidine has been reported to affect the bioavailability of other drugs through several different mechanisms such as competition for renal tubular secretion, alteration of gastric pH, and inhibition of cytochrome P450 enzymes. such as Procainamide ,Warfarin ,Ketoconazole , Midazolam.

) [#title] => [#description] => [#children] =>

Ranitidine has been reported to affect the bioavailability of other drugs through several different mechanisms such as competition for renal tubular secretion, alteration of gastric pH, and inhibition of cytochrome P450 enzymes. such as Procainamide ,Warfarin ,Ketoconazole , Midazolam.

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Ranitidine has been reported to affect the bioavailability of other drugs through several different mechanisms such as competition for renal tubular secretion, alteration of gastric pH, and inhibition of cytochrome P450 enzymes. such as Procainamide ,Warfarin ,Ketoconazole , Midazolam.

[#printed] => 1 ) [#title] => [#description] => [#children] => [#printed] => 1 ) [field_side_effects] => Array ( [#type_name] => product [#context] => full [#field_name] => field_side_effects [#post_render] => Array ( [0] => content_field_wrapper_post_render ) [#weight] => 10 [field] => Array ( [#description] => [items] => Array ( [0] => Array ( [#formatter] => default [#node] => stdClass Object *RECURSION* [#type_name] => product [#field_name] => field_side_effects [#weight] => 0 [#theme] => text_formatter_default [#item] => Array ( [value] => Transient pain at the site of IM injection has been reported. Transient local burning or itching has been reported with IV administration of ranitidine hydrochloride. The following have been reported as events in clinical trials or in the routine management of patients treated with oral or parenteral ranitidine hydrochloride. The relationship to therapy with ranitidine hydrochloride has been unclear in many cases. Headache, sometimes severe, seems to be related to administration of ranitidine hydrochloride. [format] => 1 [safe] =>

Transient pain at the site of IM injection has been reported. Transient local burning or itching has been reported with IV administration of ranitidine hydrochloride.
The following have been reported as events in clinical trials or in the routine management of patients treated with oral or parenteral ranitidine hydrochloride. The relationship to therapy with ranitidine hydrochloride has been unclear in many cases. Headache, sometimes severe, seems to be related to administration of ranitidine hydrochloride.

[#delta] => 0 ) [#title] => [#description] => [#theme_used] => 1 [#printed] => 1 [#type] => [#value] => [#prefix] => [#suffix] => [#children] =>

Transient pain at the site of IM injection has been reported. Transient local burning or itching has been reported with IV administration of ranitidine hydrochloride.
The following have been reported as events in clinical trials or in the routine management of patients treated with oral or parenteral ranitidine hydrochloride. The relationship to therapy with ranitidine hydrochloride has been unclear in many cases. Headache, sometimes severe, seems to be related to administration of ranitidine hydrochloride.

) [#title] => [#description] => [#children] =>

Transient pain at the site of IM injection has been reported. Transient local burning or itching has been reported with IV administration of ranitidine hydrochloride.
The following have been reported as events in clinical trials or in the routine management of patients treated with oral or parenteral ranitidine hydrochloride. The relationship to therapy with ranitidine hydrochloride has been unclear in many cases. Headache, sometimes severe, seems to be related to administration of ranitidine hydrochloride.

[#printed] => 1 ) [#single] => 1 [#attributes] => Array ( ) [#required] => [#parents] => Array ( ) [#tree] => [#context] => full [#page] => 1 [#field_name] => field_side_effects [#title] => Side Effects [#access] => 1 [#label_display] => above [#teaser] => [#node] => stdClass Object *RECURSION* [#type] => content_field [#children] =>

Transient pain at the site of IM injection has been reported. Transient local burning or itching has been reported with IV administration of ranitidine hydrochloride.
The following have been reported as events in clinical trials or in the routine management of patients treated with oral or parenteral ranitidine hydrochloride. The relationship to therapy with ranitidine hydrochloride has been unclear in many cases. Headache, sometimes severe, seems to be related to administration of ranitidine hydrochloride.

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• Store below 30 C°
• Protect from light and freezing

[#delta] => 0 ) [#title] => [#description] => [#theme_used] => 1 [#printed] => 1 [#type] => [#value] => [#prefix] => [#suffix] => [#children] =>

• Store below 30 C°
• Protect from light and freezing

) [#title] => [#description] => [#children] =>

• Store below 30 C°
• Protect from light and freezing

[#printed] => 1 ) [#single] => 1 [#attributes] => Array ( ) [#required] => [#parents] => Array ( ) [#tree] => [#context] => full [#page] => 1 [#field_name] => field_storage [#title] => Storage [#access] => 1 [#label_display] => above [#teaser] => [#node] => stdClass Object *RECURSION* [#type] => content_field [#children] =>

• Store below 30 C°
• Protect from light and freezing

[#printed] => 1 ) [#title] => [#description] => [#children] => [#printed] => 1 ) [field_packing] => Array ( [#type_name] => product [#context] => full [#field_name] => field_packing [#post_render] => Array ( [0] => content_field_wrapper_post_render ) [#weight] => 12 [field] => Array ( [#description] => [items] => Array ( [0] => Array ( [#formatter] => default [#node] => stdClass Object *RECURSION* [#type_name] => product [#field_name] => field_packing [#weight] => 0 [#theme] => text_formatter_default [#item] => Array ( [value] => • Injection 50mg/2ml: Box of 10 ampoules [format] => 1 [safe] =>

• Injection 50mg/2ml: Box of 10 ampoules

[#delta] => 0 ) [#title] => [#description] => [#theme_used] => 1 [#printed] => 1 [#type] => [#value] => [#prefix] => [#suffix] => [#children] =>

• Injection 50mg/2ml: Box of 10 ampoules

) [#title] => [#description] => [#children] =>

• Injection 50mg/2ml: Box of 10 ampoules

[#printed] => 1 ) [#single] => 1 [#attributes] => Array ( ) [#required] => [#parents] => Array ( ) [#tree] => [#context] => full [#page] => 1 [#field_name] => field_packing [#title] => Packing [#access] => 1 [#label_display] => above [#teaser] => [#node] => stdClass Object *RECURSION* [#type] => content_field [#children] =>

• Injection 50mg/2ml: Box of 10 ampoules

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Ranitidine hydrochloride is a competitive, reversible inhibitor of the action of histamine at the histamine H2-receptors, including receptors on the gastric cells. Ranitidine hydrochloride does not lower serum Ca++ in hypercalcemic states. Ranitidine hydrochloride is not an anticholinergic agent.

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